Well it's not a forgone conclusion. First of all "oxidative stress" is not a simple subject. And it's not just whether you should take antioxidants but if so, how you should take them.

First things first.

What is post oxidative stress?

Oxidative stress is an imbalance between free radicals (pro-oxidant molecules) and the body's oxidative defense mechanisms. Primarily the free radicals in our bodies are derived from the consumption of oxygen but there are many possible radical species. The basic definition is a particle that contains one or more unpaired electrons and this can be true of many different substances. However the most important ones for us are those derived from oxygen or nitrogen. They are called reactive oxygen/nitrogen species or RONS for short.

How does the body deal with them?

The body has a basic antioxidant defense system composed of endogneous (produced by the body) and exognenous (coming from the diet) compounds. Examples of endogenous antioxidants are superoxide dismutases and glutathione peroxidase. You may have heard of those. In fact, glutathione is sold in supplement form by people who conveniently forget to tell you that glutathione is pretty worthless as a supplement since it is a tripeptide that does not cross the GI tract very well.

Exogenous antioxidants are the familiar nutrients like beta carotene (and other cartenoids), vitamin E and C, and various biflavonoids.

What does exercise have to do with it?

Well it's a very complex subject and scientists have a long way to go on it. But those that tell you "you must take antioxidants" misunderstand one key factor. There is a difference between the production of free radicals and oxidative stress. Yes, we know that acute exercise, both aerobic and anaerobic, results in radical species but that does not mean it automatically causes oxidative stress. Remember the definition of oxidative stress above. It is an imbalance between RONS production and the body's oxidative defense system.

The intensity and duration of the exercise, nutrition status, age, training status all seem to impact whether oxidative stress occurs. Higher intensity and duration of exercise tends to equate to more oxidative stress. But all the other factors have an impact as well and findings are inconsistent because of this as well as how the oxidative stress is measured. What tissue is looked at and when and what biomarker is chosen. It's not as cut and dry as your favorite bodybuilding guru told you, is it?

Ah, but the muscles…

Lifting them weights, commonly referred to as resistance exercise, is thought to cause an increase in free radical formation in the muscles. There are a couple of ideas as to how this occurs.

One is called the ischemia-reperfusion theory. When the muscles undergo an intense contraction there is a temporary decrease in blood supply and thus oxygen resulting in ischemia. As the muscles relax undergo reperfusion which means that blood and thus oxygen and nutrients rush back into them. The resulting inflammation and oxidative damage is sometimes called reperfusion_injury. Usually this theory is reserved for actual muscle injury but it is thought that reperfusion after intense contraction may give rise to an abundance of free radicals that damage muscle tissue.

The other theory is that mechanical stress being placed on the muscles physically damages them (high eccentric forces particularly) and that this causes and inflammatory process that produces free radicals.

Whatever the theory the common prescription is to take vitamin E, and C with special attention usually given to vitamin E. The idea should be clear enough. You workouts produce free radicals that damage your muscle cells so lots of antioxidants should help protect them thus helping them recover faster.

Unfortunately there are few studies that actually test whether vitamin E actually reduces post resistance exercise lipid peroxidation in muscle tissue and there is not enough evidence to conclude that supplementation with E and C actually protects against this damage. As is usual with these types of things the results have been mixed and of course the protocols have as well.

Well shouldn't I take antioxidants just in case?

You should not take any supplements "just in case". There is a huge problem right now between the rationale for supplement use and the actual reason people take supplements with "just in case" being near the top of the list. It is not that clear how good for you long term supplementation with antioxidants is for you. And it is not really even that clear if they work as advertised.

Assuming that they work and that we should take them to reduce post exercise oxidative stress we must also assume that this stress is harmful. No, not all stress is ultimately harmful. Some stress is "adaptive". Good, or adaptive stress such as this is sometimes called eustress (as opposed to distress).

Exercise is a physical stress on the body but when done correctly it is a health producing stress not a health damaging one. Yes, it has been shown, at least to some extent, that exercise results in increased oxidative stress. But that does not mean that this is detrimental to health in the long term.

And remember what I said about training status? Well there is more and more evidence that when training results in oxidative stress this stress is hormetic. Hormesis is a phenomenom by which low doses of toxic substances produce favorable, and ultimately protective, responses. Eustress is really another name for this general idea.

Hormesis Dose Responses Graph

In terms of healthful states, too much RONS production and not enough defense is termed an oxidizing environment. Conversely, a healthful state would be thought to be a reducing environment. And environment that favored the destruction of free radicals because of increased antioxidant defense.

It just so happens that regular moderate intensity exercise appears to do just that. We know that exercise makes us healthier. Well increased antioxidant defense may be one of the ways this happens.

Moderate Intensity? I'm Hardcore!

Chill out, tough guy. It's the median intensity we are talking about. Just because you go "all out" some of the time, or work at percentages of greater than 90 percent maximum load sometimes, etc.. and so on, it does not mean you need to down a bottle of vitamin E after or before you next workout.

First of all intensity is relative to the individual and if you are able to work at insanely intense levels every time you exercise you probably don't exercise "regularly". And regular is just as important as "intensity". It all evens out in the wash.

Most of the research concerning post exercise oxidative stress is examining acute exercise. In other words what happens as an immediate result of an exercise session. But the beneficial effects of exercise happen because of chronic exercise…exercise performed habitually over time at levels that can be sustained and recovered from. You'd need some really long term studies.

Exercise certainly seems to increase oxidative stress in untrained subjects but the problem is it has become simple dogma that the oxidative stress from exercise is bad thing that needs to be combated with pills. Are you seeing the dichotomy here? Exercise is good. Exercise makes you a patient in need of intervention to protect you from it's damaging effects. It doesn't make a lot of sense but there is still a debate going on. One side saying that antioxidant protection is needed to protect against these chronic effects and the other saying that but long-term exercise may counter the effect of oxidative stress by increasing the activity of antioxidant enzymes and reducing oxidant production. Leading to greater health than what you started with. You'll have to decide which side to put your money with.

Vitamin E or C?

Vitamin E is the supplement most frequently written about in bodybuilding articles because it is the main chain breaking antioxidant in lipid peroxidation. Since the cell walls are made of lipids vitamin E can help prevent oxidation of the lipids in cell walls and protect the stability and fluidity of the membrane.

However, vitamin C prevent lipid peroxidation in the fluild outside the cell walls and thus is equally important. What's more, the two work together. when vitamin E reacts to RONS it becomes a radical itself. Vitamin C is used to regenerate it. This produces a vitamin C radical which is reduced by glutathione. Ain't it rad?

So what should I do?

Read and research. Decide for yourself. I'll tell you what I do. I take a multivitamin and mineral supplement and that's about it. At times a take extra antioxidants in the form of vitamin E, C, beta carotene and some others but I don't beleive it to be a make or break proposition and I doubt that I need it to protect myself from oxidative stress from my workouts. No, I don't believe that it has any impact on recovery.

The findings are all over the place but the most consistent results come from supplementation during or right after exercise rather than daily chronic ingestion over time, which takes high doses.

You don't need my opinion, though, and giving you my stamp of approval or a thumbs down is nothing more than an ego trip on my part. Instead, how about starting with Acute exercise and oxidative stress: a 30 year history. This article should be a perfect spring board to further research. Maybe you can come back and tell me a thing or two.

Comments

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Major Sources

1. Groff, James L., and Sareen Annora Stepnick. Gropper. Advanced Nutrition and Human Metabolism. Belmont, CA: West/Wadsworth, 2000. Print.
2. Fisher-Wellma, Kelsey, and Richard J. Bloomer. "| Full Text | Acute Exercise and Oxidative Stress: a 30 Year History." Dynamic Medicine. Biomed Central, 1 Aug. 2009. Web. 11 Mar. 2010. <http://www.dynamic-med.com/content/8/1/1>.
3. Viitala, Peter, Et Al. E. "The Effects of Antioxidant Vitamin Supplementation on Resistance Exercise Induced Lipid Peroxidation in Trained and Untrained Participants." | Full Text | Lipids in Health and Disease (2004). Biomed Central, 14 Mar. 2004. Web. 10 Mar. 2010. <http://www.lipidworld.com/content/3/1/14>.

by EricT

Meinrad Peterlik¹, Steven Boonen², Heide S. Cross³and Christel Lamberg-Allardt⁴

Intl. Journal of Environmental Research and Public Health

Vitamin D and calcium insufficiencies are risk factors for multiple chronic diseases. Data from 46 recent studies from Europe, North America, South-East Asia and the South Pacific area clearly indicate that a low vitamin D status and inadequate calcium nutrition are highly prevalent in the general population (30–80%), affecting both genders. The extent of insufficiencies is particularly high in older populations, and in some geographical areas, also in children and in young women of child-bearing age, in ethnic minorities and immigrants, as well as in people of low socio-economic status. Enrichment of cereal grain products with vitamin D and calcium would be a viable approach to increase consumption and improve health outcomes in the general population worldwide.

Introduction

An inadequate supply of vitamin D and calcium has negative effects on bone health at all ages, inasmuch as it causes rickets in infants, retards acquisition of an adequate bone mass during skeletal development in adolescents, and is finally responsible for accelerated bone loss in adulthood in both women and men, leading to the development of osteoporosis. Importantly, there is also evidence from epidemiological studies, clinical intervention trials as well as from studies with animal models of human diseases that a compromised vitamin D status and inadequate calcium nutrition are predisposing conditions for a great number of other diseases, including various types of cancer, chronic infectious, inflammatory and autoimmune diseases, metabolic disorders, as well as hypertension and cardiovascular diseases (Table 1 omitted ; for details, [1-3]

Why a Low Vitamin D Status and a Nutritional Calcium Deficit are Risk Factors for many Chronic Diseases

Vitamin D comes from two sources in humans, it could either be synthesized in form of vitamin D3 (cholecalciferol) under the influence of solar UV-B radiation in the epidermis, or be absorbed from the diet or from supplements and food additives, which in some countries may contain vitamin D2 (ergocalciferol). In any form, vitamin D is transferred to the liver, where it is metabolized to 25-hydroxyvitamin D (25-(OH)D). The term 25-(OH)D is used to denote the sum of 25-(OH)D3 and 25-(OH)D2. Thus, the plasma level of this metabolite reflects the sum of vitamin D from endogenous synthesis and from dietary intake, and is therefore a reliable indicator of an individual’s vitamin D status.

Conversion of 25-(OH)D3 to the biologically most active metabolite, 25-dihydroxyvitamin D3 (1,25-(OH)2D3), is catalyzed by the CYP27B1-encoded enzyme, 25-(OH)D-1-hydroxylase, and takes place predominantly in the kidney, but also at many extra-renal sites [4] (see Figure 1): Omitted

Examples are normal and neoplastic epithelial cells of the skin [5], of the gastrointestinal tract [6,7] and of female and male reproductive organs [8-10] as well as osteoblasts and osteoclasts [11,12] and cells of the vascular [13], the central nervous [14] and the immune system [15,16]. 1,25-(OH)2D3 bound to the nuclear high-affinity vitamin D receptor (VDR) functions as a transactivating regulator of gene expression. Circulating 1,25-(OH)2D3, which is produced by up to 90% in the kidney, plays a key role in systemic calcium and phosphate homeostasis by regulating ion fluxes in its classical target organs, i.e., small intestine, kidney and bone. 1,25-(OH)2D3 is also an important local regulator of cellular proliferation, differentiation and function in many organs and cell systems that express the 25-(OH)D-1-hydroxylase [4] (Figure 1 omitted). The extent of intracellular synthesis of 1,25-(OH)2D3 at extra-renal sites depends largely on ambient 25-(OH)D3 levels and is not associated with circulating 1,25-(OH)2D3 concentrations (e.g., [17]). Therefore, at low serum levels of 25-(OH)D, 25-(OH)D-1-hydroxylase activity may not be sufficient to maintain tissue concentrations of 1,25-(OH)2D3 necessary for efficient autocrine/paracrine regulation of cellular growth and function. This explains why many chronic diseases, as listed in Table 1 omitted, show significant negative associations with serum 25-(OH)D [1,3,18]. Importantly, low serum 25-(OH)D has been shown to be a reliable predictor of all-cause mortality [19].

Table 1. Rating of evidence for association of vitamin D and/or calcium insufficiency with frequent chronic diseases (for details, [1,3]).

There is evidence from many human and animal studies for a significant inverse relationship between dietary calcium and risk of multiple chronic diseases [1]. This is difficult to understand because the effect of even large variations in calcium intake levels on extracellular calcium concentrations [Ca2+]o is attenuated by the systemic actions of calcium-regulating hormones allowing physiological variations in [Ca2+]o to occur only within a narrow range. However, many types of cells express a calcium-sensing receptor (CaR), which senses even minute changes in [Ca2+]o and thus allows Ca2+ to function as a “first messenger” for various cellular responses [20].

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An important feature of the CaR is the high cooperativity between multiple Ca2+-binding sites in its extracellular domain. This results in amplification of signals from extracellular Ca2+ , which, by cell-specific coupling to stimulatory and inhibitory G proteins, are transduced into various intracellular signalling pathways. Expression of a functioning CaR thus allows cell-specific reactions to physiological changes in [Ca2+]o. The CaR not only controls PTH secretion from parathyroid gland cells but plays key roles in normal cartilage and bone formation [21-23], as well as in limitation of cellular growth of normal and neoplastic cells [2,24]. Conversely, low dietary calcium causes hyperparathyroidism by impairment of CaR activity and, by the same token, can be linked to the development of not only osteoporosis and various malignancies, but possibly other calcium-insufficiency-related chronic diseases (Table 1 omitted) (for details, [1,3]; see also Figure 2 omitted).

Relevant for our understanding how vitamin D and calcium status interact in the pathogenesis of chronic diseases, is the observation that most cell types jointly express the 25-(OH)D-1-hydroxylase and the CaR. Therefore, cell-specific cooperative signalling from 1,25-(OH)2D3/VDR and CaR, which is necessary to maintain normal cell functions (as detailed in [1,3]), is impaired under conditions of vitamin D and calcium insufficiency (Figure 2 omitted). This has been shown particularly for osteoporosis and many malignancies, particularly colorectal and breast cancer (as detailed in the following). Low serum 25-(OH)D and inadequate calcium intake reportedly are associated with cardiovascular risk factors such as hypertension [25-27], obesity [28-30], metabolic syndrome and diabetes mellitus type II [31,32]. Vitamin D and calcium insufficiencies have also been correlated with incident cardiovascular symptoms, including angina, coronary insufficiency, myocardial infarction, transient ischemic attack, and stroke [33], as well as with greater mortality from chronic cardiovascular disease [19,34,35].

Vitamin D Insufficiency: A World-Wide Phenomenon

Definition of Vitamin D Insufficiency

The vitamin D status of an individual is a composite of UV-B mediated synthesis of vitamin D3 in the epidermis and of intake and absorption from the gut. Outright vitamin D deficiency is indicated by plasma 25-(OH)D levels below 10-15 nM [36]. In this situation, 1,25-(OH)2D production in the kidney is severely limited because of substrate depletion, causing a decrease in intestinal calcium absorption with rickets or osteomalacia as a consequence. At 25-(OH)D serum concentrations above 15 nM, the kidney produces enough 1,25-(OH)2D3 to maintain systemic mineral ion homeostasis [37], but availability of 25-(OH)D for intracellular production of 1,25-(OH)2D3 at extra-renal sites may be insufficient for autocrine/paracrine control of cellular functions [1]. The definition of vitamin D insufficiency is still a matter of debate. At one time, a serum 25-(OH)D concentration of ~30 nM was thought to be the delimitation between vitamin D insufficiency and adequate vitamin D supply [38]. Now there is growing agreement that serum 25(OH)D should be at least 50 nM [39] (see also Tables 2-4 omitted). Even higher cut-offs, e.g. 60-100 nM, are supported by studies on optimal health outcomes [40].

Epidemiology of Vitamin D Insufficiency

Considering reasons for vitamin D insufficiency, one has to take into account that cutaneous UV-Bmediated production of vitamin D3 is affected by many factors, such as time of the day, season of the year, latitude, altitude, skin pigmentation or use of sunscreens. Also aging can markedly reduce the capacity of the skin to produce vitamin D3 [41]. Geographical differences in vitamin D status result from varying contributions to the vitamin D supply from exposure to solar UV-B but also from intake of dietary and supplemental vitamin D [42,43]. Table 2 (omitted) lists the results of the available nationally representative studies on prevalence of vitamin D insufficiency in the normal adult population in Europe, North America, East Asia and in the South Pacific area.

In Europe, 7-27% of the adult population have a serum 25-(OH)D concentration below 25-30 nM [26,38,44-47]. In South-East Asia and in Australia, incidence of vitamin D insufficiency varies between 8-17% [48-50]. A relatively low value of 5% has been reported for the USA [51]. However,if 50 nM 25-(OH)D is considered the upper reference limit, on the average one-half of the adult population in Europe [26,38,44-47], Western Canada [52], Australia [53,54] and New Zealand [55] presents with vitamin D insufficiency, whereas only one-third is afflicted in the USA [51] (Table 2 omitted).

It must be noted that the proportion of the general population with serum 25-(OH)D below the desirable level of 70–80 nM [40,56] is 73% in the USA [51], 84–87% in Europe and in the South Pacific area [44,46,55] and up to 97% in Canada [52]. 3.3. Vitamin D Insufficiency in Different Population Segments Elderly people: It has been known for decades that vitamin D insufficiency is common in people, who are immobilized because of chronic diseases or are housebound due to old age. However, recent nationally representative data show that vitamin D insufficiency is present in a substantial portion of old age ambulant people worldwide (Table 3 omitted): For example, the European SENECA Study on diet and health of elderly people from 19 towns in 12 European countries revealed that overall 36% of men and 47% of women had serum 25-(OH)D concentrations below 30 nM [57]. In the Netherlands, 50% of people aged 65 years and older had serum levels of 25-(OH)D below 50 nM [58]. Similar values were reported for elderly women in Belgium [59]. According to the OPTIFORD Study [60], 50-92 % of elderly women in Denmark, Finland, Ireland and Poland had wintertime 25-(OH)D concentrations lower than 50 nM. On the average, prevalence of vitamin D insufficiency in elderly people in North America [51,61], Australia [62], New Zealand [55] and Japan [63] seems to be lower than in Europe (Table 3 omitted).

Children, adolescents and young adults: In some European countries such as Denmark, Finland, Ireland and Poland [60], 37% of 12-year old girls had 25-(OH)D concentrations lower than 25 nM (Table 4 omitted). By using a broader definition, i.e., <50 nM, 92% had to be considered vitamin Dinsufficient. Comparative values are much lower in Germany [64], but considerably higher in France [65].

In the USA, the proportion of male and female adolescents between 12-19 years, who had 25-(OH)D values below 50 nM, ranged from 24 to 31%, respectively [51]. Incidence of vitamin D insufficiency in younger women is low in Canada [66], compared to Indonesia, Malaysia [67] or Japan [50]. Alarmingly high rates were found in older girls and young women at child-bearing age in India [68] and China [69,70] (Table 4 omitted).

Pregnant women and neonates: In Europe and in the USA, a poor vitamin D status is observed with increasing frequency in pregnant women [71] and consequently in their neonates causing a high risk of not only rickets, but also non-skeletal diseases in later life, e.g. type 1 diabetes [72]. Obesity deserves a special note as a condition frequently associated with vitamin D and calcium insufficiency. A number of earlier studies have well documented a high prevalence of vitamin D insufficiency in morbidly obese women. Now evidence is emerging that in otherwise healthy women and men, body fat mass is frequently inversely associated with vitamin D insufficiency [29,73]. Sequestration of vitamin D in the subcutaneous fat, which alters its release into the circulation, could be one by which obesity could contribute to vitamin D insufficiency [74].

Ethnic groups: The immigrant population is at high risk for vitamin D insufficiency in many European countries such as Denmark, Norway and Great Britain [75-77]. In Germany, the proportion of vitamin D inadequacy in children and adolescents, aged 2-17 years, is higher in immigrant than in non-immigrant girls and boys at any time. Notably, after termination of vitamin D supplementation for prophylaxis of rickets between the age of 1-2 years, serum 25-(OH)-D levels fell rapidly below 50 nM in both groups [64]. In the USA, prevalence of vitamin D insufficiency in Mexican American and Non-Hispanic black people is higher than in Non-Hispanic White individuals [51]. Analogous skin pigmentation and degree of vitamin D inadequacy has been reported for three ethnic groups in New Zealand, i.e., Pacific people, Maori and people of European origin [55]. In Australia, dark-skinned and “veiled” women, particularly when pregnant, belong to the group with the highest risk for vitamin D insufficiency [78]

Inadequate Calcium Intake: A World-Wide Problem

Recommended Calcium Intake Levels

Different intake levels for calcium are recommended by FAO/WHO experts for infants, children and adults [79] to assure optimal whole body calcium retention and consequently adequate development and maintenance of bone mass and mineral density. For children and adolescents between 10–18 years of age, consumption of 1,300 mg per day is recommended, while 1,000 mg per day apply for men between 25–50 years of age and also for women in the same age group, except when higher intake is necessary during pregnancy or after menopause. Recommended calcium allowance per day for males over 65 years and postmenopausal women is 1,300 mg [79].

Epidemiology of Calcium Intake

Findings listed in Table 5 (omitted) indicate that in Europe daily calcium intake from nutrient sources is consistently low. For example, 84% of the adult population in Austria fail to meet recommended intake levels [44]. The situation is apparently better in Germany [80,81], with one study reporting daily calcium intake even at recommended levels [26]. This seems to be also the case in Great Britain [82]

In contrast, 40% of the population does not meet adequacy in the USA [83]. Similar values probably pertain for Australia [84] and New Zealand [85]. Special consideration must be given to the nutritional calcium deficit in South-East Asian countries such as Indonesia, Malaysia [67] and Bangladesh [86]: The situation is particularly alarming in Bangladesh, where 47% of premenopausal women in the higher socio-economic brackets failed to meet a daily allowance of 400–500 mg calcium, and 63% of women of low socio-economic standing had calcium intake even lower than 200 mg/day [86].

Population Segments with Low Habitual Calcium Intake

Chronically ill people: A chronically negative calcium balance due to malabsorption develops, for example, in the many individuals suffering worldwide from lactose intolerance or from inflammatory bowel disease (Crohn’s disease, ulcerative colitis). In addition, calcium malabsorption must be reckoned with in all cases of vitamin D insufficiency resulting from intestinal, hepatic, renal or endocrine disorders as well as in the group of bariatric surgery patients who increase in numbers as a result of the obesity epidemic in the affluent parts of the world.

Individuals with reduced physical activity: It must be noted that immobilization even for a short period, e.g. 1-2 weeks of bed rest leads to mobilization of calcium from bone and consequently to net calcium loss [87]. Therefore not only patients in geriatric, psychiatric or neurological care, but also healthy individuals with low habitual physical activity have an increased risk of calcium insufficiency.

Elderly people: The data collated in Table 6 (omitted) confirm the long-standing assumption that particularly the elderly ingest significantly less calcium in their diet than the recommended amount, which is currently considered 1,300 mg per day for this age group [79]. In the European SENECA Study [88], the overall mean calcium intake by elderly people was 894 mg per day, with variations from 600-1,100 mg between different study sites. In the OPTIFORD Study, the median calcium intake among elderly women was 632 mg per day, being lowest in Poland (325 mg) and highest in Finland (925 mg) [60]. In the USA, the mean intake of calcium in women after age 55 is only ~600 mg/day [61]. Daily consumption of ~500 mg by elderly Japanese women [89] is far below a recommended level of 1,200 mg, although daily calcium requirements of East Asian populations may be lower for ethnic reasons [79]

Children, adolescents and young adults: In the European OPTIFORD study the median daily calcium intake of girls at a mean age of ~13 years was 823 mg, ranging from 524 mg in Poland to 1,092 mg in Finland [60] (Table 7 omitted). Data from the USA indicate that after the age of 10, calcium malnutrition is a common phenomenon. For example, average daily calcium intake in a group of young adolescents (12.7 ± 1.0 yr of age) was found to be 906 mg [90]. Grossly inadequate calcium intake was observed also in young adults in Canada [91]. Average daily calcium intake by schoolgirls in India between 400–500 mg [68], though corresponding to recommended daily allowances for Indians, nevertheless is far below current FAO/WHO recommendations of 1,000–1,300 mg/day [79].

Ethnic groups: It has to be borne in mind that not only vitamin D deficiency but also a nutritional calcium deficit is an important cause of rickets [92]. So-called calcium deficiency rickets are prevalent in Middle Eastern and many sub-tropical and tropical countries, such as Nigeria, Ethiopia, South Africa, India and Bangladesh, despite the fact that such countries have ample sunlight [93-95]. Under this condition, the disease is attributable to low dietary calcium intake from mainly cereal-based diets.

Strategies for disease prevention

Studies on the vitamin D intake in different parts of the world cannot be directly compared because results may be confounded to some extent by differences in life style and clothing habits, consumption of traditional foods or supplement intake. Exact determination of the extent of calcium malnutrition is also difficult, because different methods are used for evaluation of daily calcium intake from nutrient sources and, in addition, for ethnic, dietary and geographical reasons different recommendations apply for different parts of the world [79]. However, combined evidence from all the studies that are included in the present survey clearly indicates that vitamin D insufficiency and calcium malnutrition are common in both genders worldwide, not only in elderly people as previously believed but also in younger adults. Importantly, the highest rates of insufficiencies are found in children and adolescents as well as in women of child bearing age.

Need to Increase Combined Intakes to Daily 800 IU Vitamin D and 1,200 mg Calcium

Vitamin D: A recent survey on world-wide vitamin D intake [96] clearly indicates that in many countries vitamin D supply from nutrient sources is too low to sustain mean 25-(OH)D levels in the general population between 40-100 nM, which are considered sufficiently high to achieve a better health outcome [97]. Cashman et al. [98] calculated that in 20-40 yr old adults, depending on the extent of sun exposure in summer, daily intakes of vitamin D between 300 and 1,600 IU are required to maintain an adequate vitamin D status in wintertime. Notably, Nelson et al. [56] reported that daily doses of 800 IU vitamin D3 were sufficient to sustain “optimal” 25-(OH)D serum concentrations (≥75nM) in 80% of a group of pre-menopausal women. With approximately the same daily dose of vitamin D3, serum 25-(OH)D levels could be maintained at 50 nM in 97.5% of a group of elderly people in the absence of sufficient sun exposure [99]. The beneficial effects of 800 IU supplemental vitamin D for various health outcomes are well documented. Daily intake of 700-800 IU vitamin D3 maintains normal bone turnover in healthy men at wintertime [100], and reduces the risk for colorectal or breast cancer by 50% [101,102].

Calcium: The suggestion to raise daily consumption of calcium to an average of 1,200 mg per day is based not only on physiological considerations [103] but can be deduced also from considerations of optimal health outcomes: For example, daily doses of 1,200 mg calcium effectively prevent osteoporotic bone loss and fractures in people aged 50 years or older [104], and cause a 40-50% risk reduction of colorectal cancer in men and of breast cancer in premenopausal women [105,106].

Rationale for Advocating Combined Intake of Vitamin D and Calcium

Simultaneous correction of nutritional vitamin D and calcium deficits for prevention or amelioration of many chronic diseases is necessary for two reasons: First, dietary intakes of vitamin D and calcium are strongly associated [107] and therefore vitamin D insufficiency is frequently associated with low calcium intake [1,44]. Second, because vitamin D and calcium interact positively in modulation of cellular proliferation, differentiation and function, as detailed before [3,18], it can be expected that an adequate vitamin D status is required to achieve the nutritional benefits of calcium and vice versa.

Osteoporosis: Combined supplementation with daily 800 IU vitamin D and 1,200 mg calcium is the essential basis for pharmacological prevention and treatment of osteoporosis. From a meta-analysis of 10 randomized controlled trials of oral vitamin D with or without calcium supplementation vs placebo/no treatment on the risk of hip fracture in elderly people, Boonen et al. [108] concluded that oral vitamin D appears to reduce the risk of hip fractures only when calcium supplementation is added.

Cancer: Lappe et al. [109] reported evidence from a randomized placebo-controlled trial that in post-menopausal women combined high-dose calcium and vitamin D3 supplementation, i.e., 1,400–1,500 mg calcium plus 1,100 IU vitamin D3, reduced the cumulative risk of cancer of the breast, lung, colon, uterus, lymphoid and myeloid system to 0.232 after four years of trial. Cho et al. [110] concluded from an analysis of pooled primary data from 10 cohort studies with a follow-up of more than half a million individuals for 6–16 years, that optimal risk reduction for colorectal cancer necessitates high intake levels of both vitamin D and calcium. This notion was shown to be valid not only for Western but also for Asian populations [111]. In pre-menopausal women, Bérubé et al. [112] found highly significant inverse relations between total intakes of vitamin D and calcium and breast density, which is a surrogate marker for breast cancer risk. It is noteworthy, that higher intake of one nutrient was related to lower breast density only in the presence of higher intake of the other nutrient.

What can be Done?

Simultaneous supplementation of vitamin D and calcium represents a safe and inexpensive strategy for prevention of osteoporosis, colorectal and breast cancer and possibly of many other chronic diseases (Table 1). It must be emphasized that daily consumption of 800 IU vitamin D and 1,200 mg calcium is well below the currently accepted tolerable upper intake levels of 2,000 IU (=50 g) vitamin D3 and 3,000 mg calcium [79].

Supplementation by Fixed Vitamin D/Calcium Combination Tablets

Osteoporotic fractures can be effectively prevented at relatively low cost by combined
supplementation with 1,200 mg/d calcium and 800 IU/d vitamin D3. However, a significant effect of vitamin D/calcium treatment is only seen in cohorts with at least 80% compliance [104]. Low compliance and lack of adherence seen with any long-term medication certainly will limit the usefulness of combined vitamin D and calcium supplementation for correction of respective insufficiencies in the general population. Therefore, combined vitamin D and calcium supplementation should be promoted specifically for disease prevention in high risk groups, i.e., individuals, who otherwise are unable to attain a normal vitamin D and calcium status due to specific living conditions (immobilization, physical incapacitation, advanced age, chronic diseases), traditional or personal nutritional habits, preferred lifestyle (lack of physical activity, indoor dwelling) etc.

Vitamin D and Calcium Enrichment in Single Foodstuffs

Fortified foods are an important source of vitamin D for those who consume them [113]. In a recent survey on the efficacy of food fortification on serum 25-(OH)D concentrations [114], doseeffect relations for vitamin D from food sources were found equivalent to those reported for vitamin D supplements. Vitamin D-fortified milk has been found to be a safe, effective and acceptable method of administering vitamin D, particularly to the elderly, community-based population. Orange juice fortified with vitamin D2 (1,000 IU/240 ml) was tested for its suitability to serve as an alternative for vitamin D-fortified milk. Fortification with vitamin D3 of wheat and rye bread is technically easy, and stability and bioavailability of vitamin D is good [115]. Consumption of bread fortified with 5,000 IU vitamin D3 and 320 mg calcium per daily serving for 12 months improved the vitamin D status of sundeprived nursing home residents. Together with suppression of secondary hyperparathyroidism this apparently caused a significant increase in bone mineral density at the lumbar spine and the hip [116].

Calcium fortification is in use all over the world: Staples and food stuffs that are enriched with calcium include flour, cereals, milk, orange juice, mineral waters, soymilk etc. [117]. Calcium- and vitamin D-fortified milk, when providing 800 IU vitamin D and 1,000 mg calcium per day, has a significant positive effect on bone mass and strength in older men [118,119].

It is apparent that fortification of traditional and widely consumed foodstuffs (milk and milk products, bread, orange juice etc.) will guarantee a minimum additional supply of vitamin D and calcium.

Vitamin D and Calcium Addition to Cereal Grain Products

At present, cereal grain products, such as flour, corn meal, noodles and the like, are enriched with vitamin D and calcium in some countries in Europe and in the USA. Newmark et al. [117] summarized the rationale, data, efficacy, safety, cost and practicality of the addition of both calcium and vitamin D to cereal grain products to reduce the risk of osteoporosis and colon cancer. The authors estimate that, if cereal grain products were uniformly enriched with 90 IU/100g vitamin D, average daily intake of vitamin D could increase by up to 200 IU vitamin D. Enrichment of cereal grain products with 1,200-1,800 mg/kg calcium could raise dietary intake by about 200-400 mg/day. A conservative estimate suggests that through these measures at least a 20% reduction of the rate of osteoporotic fractures and of colorectal incidence can be achieved [117].

Enrichment of cereal grain products with vitamin D and calcium at indicated levels would be possible within current legal regulations in the USA [117]. It also conforms to legislation introduced in the European Union as of 2007. However, some important member states such as Germany have not yet changed their national law accordingly.

In summary, enrichment with vitamin D and calcium of cereal grain products is an effective and safe measure at very low cost to broaden the range of commonly consumed foods as dietary sources of vitamin D and calcium. This will guarantee at least some modest improvement in both vitamin D and calcium nutrition at the same time without necessitating a change in traditional eating habits. To fulfill individual needs for vitamin D and calcium however, additional consumption of particularly vitamin D- and calcium-rich food and food products or even supplement use is certainly indicated.

Acknowledgment

We thank Sandra E. Guggino, Johns Hopkins University Medical School (Baltimore, USA) for
critical reading of the manuscript.

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J.M.; Kiely, M. Estimation of the dietary requirement for vitamin D in healthy adults. Am. J. Clin. Nutr. 2008, 88, 1535-1542.
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100. Viljakainen, H.T.; Vaisanen, M.; Kemi, V.; Rikkonen, T.; Kroger, H.; Laitinen, E.; Rita, H.; Lamberg-Allardt, C. Wintertime vitamin D supplementation inhibits seasonal variation of calcitropic hormones and maintains bone turnover in healthy men. J. Bone Miner. Res. 2009, 24, 346-352.
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mammographic breast densities. Cancer Epidemiol. Biomarkers Prev. 2004, 13, 1466-1472.
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110. Cho, E.; Smith-Warner, S.A.; Spiegelman, D.; Beeson, W.L.; van den Brandt, P.A.; Colditz, G.A.; Folsom, A.R.; Fraser, G.E.; Freudenheim, J.L.; Giovannucci, E.; Goldbohm, R.A.; Graham, S.; Miller, A.B.; Pietinen, P.; Potter, J.D.; Rohan, T.E.; Terry, P.; Toniolo, P.; Virtanen, M.J.; Willett, W.C.; Wolk, A.; Wu, K.; Yaun, S.S.; Zeleniuch-Jacquotte, A.; Hunter, D.J. Dairy foods, calcium, and colorectal cancer: a pooled analysis of 10 cohort studies. J. Natl. Cancer Inst. 2004, 96, 1015-1022.
111. Ishihara, J.; Inoue, M.; Iwasaki, M.; Sasazuki, S.; Tsugane, S. Dietary calcium, vitamin D, and the risk of colorectal cancer. Am. J. Clin. Nutr. 2008, 88, 1576-1583.
112. Berube, S.; Diorio, C.; Masse, B.; Hebert-Croteau, N.; Byrne, C.; Cote, G.; Pollak, M.; Yaffe, M.; Brisson, J. Vitamin D and calcium intakes from food or supplements and mammographic breast density. Cancer Epidemiol. Biomarkers Prev. 2005, 14, 1653-1659.
113. Lamberg-Allardt, C. Vitamin D in foods and as supplements. Prog. Biophys. Mol. Biol. 2006, 92, 33-38.
114. O'Donnell, S.; Cranney, A.; Horsley, T.; Weiler, H.A.; Atkinson, S.A.; Hanley, D.A.; Ooi, D.S.; Ward, L.; Barrowman, N.; Fang, M.; Sampson, M.; Tsertsvadze, A.; Yazdi, F. Efficacy of food fortification on serum 25-hydroxyvitamin D concentrations: systematic review. Am. J. Clin. Nutr. 2008, 88, 1528-1534.
115. Natri, A.M.; Salo, P.; Vikstedt, T.; Palssa, A.; Huttunen, M.; Karkkainen, M.U.; Salovaara, H.; Piironen, V.; Jakobsen, J.; Lamberg-Allardt, C.J. Bread fortified with cholecalciferol increases the serum 25-hydroxyvitamin D concentration in women as effectively as a cholecalciferol supplement. J. Nutr. 2006, 136, 123-127.
116. Mocanu, V.; Stitt, P.A.; Costan, A.R.; Voroniuc, O.; Zbranca, E.; Luca, V.; Vieth, R. Long-term effects of giving nursing home residents bread fortified with 125 microg (5000 IU) vitamin D3 per daily serving. Am. J. Clin. Nutr. 2009, 89, 1132-1137.
117. Newmark, H.L.; Heaney, R.P.; Lachance, P.A. Should calcium and vitamin D be added to the current enrichment program for cereal-grain products? Am. J. Clin. Nutr. 2004, 80, 264-270.
118. Daly, R.M.; Bass, S.; Nowson, C. Long-term effects of calcium-vitamin-D3-fortified milk on bone geometry and strength in older men. Bone 2006, 39, 946-953.
119. Daly, R.M.; Brown, M.; Bass, S.; Kukuljan, S.; Nowson, C. Calcium- and vitamin D3-fortified milk reduces bone loss at clinically relevant skeletal sites in older men: a 2-year randomized controlled trial. J. Bone Miner. Res. 2006, 21, 397-405.

© 2009 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.

This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

by EricT

The original Gripper Guide focused on the beginnings of gripper training. In that post I used CoC grippers as my standard gripper (hence the table is based on CoC resistances only) and laid out some suggestions for picking resistances and how to train. The reason I use CoC is simple. They were among the first to take grippers to the next level and they have a very good product. This part of my guide is centered around the very first thing you will do in your grip training. Buying a gripper! I've also got some other training tidbits and advice thrown into the mix.

Casual Grip Training

For those that are not interested in peak crushing grip but have grown tired of the weak and easy department store grippers, this section is for you. Grippers may be an accessory as opposed to a necessity to you but you can still use the information here to find what you need. The key to casual grip training is to have a gripper, or grippers, that will challenge you but can be readily closed. You're not doing maximal work so you'll want something you can perform low rep sets (~4) now and higher rep sets (~10) down the road.

Even if you're only interested in a single gripper, you still want a quality gripper that won't season or weaken on you. That will compromise your progression. The cost of a gripper is anywhere from $10-50 dollars. I'm not suggesting you buy a $50 gripper but something of good quality in the $20 range will do. The good ones last a long time and are very consistent so why not pay an extra couple of bucks for quality and consistency? Between this article and my original Gripper Guide, even a casual grip trainer can find what they need.

Gripper Brands

Trying to find a brand of gripper can be a daunting task. There are many brands to choose from and unless you're into grip training it is hard to evaluate them. All of the heavy resistance grippers I've seen have a rating associated with them. While I'll be talking about ratings later on it's important to know two things before buying grippers: 1) What is my starting level? and 2) What are my short and long term goals? If the brand you are considering doesn't have resistances that satisfy these two questions, you should pick another brand.

Along the same lines, you can learn a lot by what products a company offers. For instance if you notice a particular company has 40 different grippers you should ask why you need so many grippers when other companies get by with less than 12. Gimmicks are prevalent when it comes to the fitness industry and grip training is no exception.

Examples of gimmicks:

* Grippers that have an extended handle for negatives…probably not the best way to spend your money.
* Chrome plated grippers. You're going to cover them with chalk, not put them on the hood of your car. Chrome is not a perfect alloy either, it can flake off and if it does you've got an unsightly gripper handle.
* Thicker handles. The only advantage to a thicker handle, in my opinion, is that the closing gap is smaller (proportional to the increase in handle size) but that also happens to be it's greatest weakness. Thicker handles have a more difficult starting position (hand is "more open") but I see no advantage to increasing the difficulty of a no-set close (setting defeats the purpose of having an open hand) at the expense of closing distance. Static holds are another story, but with a thick handled gripper you're moving into the realm of open hand supporting grip. Something that a gripper was not designed to train. Why not put that money towards a thick handle (i.e. Rolling Thunder or thick bar) instead?

While spotting gimmicks you should also be on the lookout for desirable traits. Like anything else you have to weigh the pros and cons.

Examples of desirable traits:

* Grip texture/knurling. The grips or texture of the handles is important. You don't want something so coarse that its going to rip your skin to shreds but at the same time you don't want a powder coated finish. IronMind's CoC gripper seems to be the middle road approach, while Heavy Grips and Beef Builders (and Mash Monster) represent a finer and coarser knurling, respectively.
* High level of quality control. It sounds dated but there are a lot of things that aren't built like they are in North America.
* Price. Dirt cheap grippers may not be the way to go and a 'top shelf' priced gripper may be equally as bad in terms of cost effectiveness.

When it comes time to build your gripper arsenal, try to pick a brand. Consistency makes progression easier and can save money on shipping costs. If you stick with the same brand you can also expect a similar performance over time. A set of cheap grippers will most likely become easier with time, while a set of good grippers will be the same from day 1 and onward. Mixing a cheap gripper in with good grippers may give you the illusion of progress as the cheap gripper becomes weaker while the stronger gripper remains the same. This is especially prevalent when your cheap gripper is in the mid-high range of resistance within your set. The nature of gripper training is patience, consistency, and a bit of creativity (and oh yeah, lots of chalk). You want to progress because your hands are stronger, not because your gripper is weaker.

If you do mix brands, it's best to keep the cheaper or lower quality grippers in the lowest range of resistance within your set. Use them for warmup and close each brand separately. Meaning if you have 3 from Brand A and 3 from Brand B, all 3 from Brand A should be closed before you move to Brand B. Purchase resistances accordingly.

Here's a barbell analogy to illustrate: You're goal is to deadlift 400lbs but everyday someone is filing off a bit of weight. One day you finally do it. Just because the marking on the barbell plates add up to 400lbs doesn't make it so.

Remember, the internet is a very useful tool. Doing a quick search of a gripper brand can lead you to customer reviews, FAQ's from the manufacturer, as well as vendors.

Left Handed Gripper

Recently I came across an ad for a "left handed" gripper. I covered the left handedness myth in a previous post titled Myths and Misconceptions: Torsion Springs, The Dog Leg, and 'Handedness' however that was geared towards the physics of a torsion spring and the forces you get in each handle. However in this ad the argument of varying ROMs arises. My first reaction was to agree with the claim however I had no concrete reasoning or science that could back it up. After some thought and some very informal 'scientific evaluation' (read: me closing a bunch of grippers with my left and right hand) I came to the conclusion that there may be a difference. What I also concluded was that this difference, if any, would be negligible. However I was not totally convinced so I contacted IronMind and in talking with Randall Strossen1 we both agreed that any difference would be negligible and would change neither the function of the gripper nor the resistance it took to close it.

The best analogy I can think of is a deadlift. Imagine we have a loaded barbell and one side is loaded with plates at their lower tolerance for weight (-2%) and the other at the ceiling (+2%). You perform the lift with the bar as is, but then you flip it for the next attempt. Overall the movement is the same and while there is a slight difference, the overall affect is the same. You wouldn't even know there was a difference.

Money is always a factor. For the same money you can buy two grippers of varying resistance or two grippers of the same resistance, one for each hand. If you have a set of four different resistances, you pay double for the novelty of having a gripper dedicated to each hand. Don't forget to label them either, lest you forget and close your left hand wound gripper with your left hand!

'N' Designation

Grippers with an 'N' designation typically mean that they are a Narrow spread (hence the N). What this means is that the handles, compared to a regular gripper, are closer together when the gripper is open. Originally I thought that the 'N' stood for Newtons and I'd hate for someone else to pay, literally, for that same mistake.

The advantage of a narrow gripper is that you don't have to set it. However, that is also it's greatest weakness since a no-set close doesn't allow the same ROM as a regular gripper. In my opinion the benefit of the no-set close ROM from a regular gripper is worth having to set a gripper once in a while. I don't find it difficult to set a gripper anyway so that isn't high on my list of desirable gripper characteristics.

Gripper Ratings

Every gripper has a rating. But what does that rating mean? During my conversation with Mr. Strossen we also discussed gripper ratings, more importantly their interpretation. If you have a 400lb barbell, you know what you've got, if you have a 240lb gripper…what does that mean? Couple that with the fact that evaluation techniques vary and you have a very muddied system for identifying the resistance level of a gripper. Case in point is Heavy Grips:

The above quote is taken directly from heavy grips' website. Without a standardized system I can produce a gripper which is tested at the base of the gripper (more specifically, the base of the handle) or at the top of the gripper. Both tests will produce drastically different results, proportional to the length of the handle. I can also report my results as a force (which some companies do) rather than a torque (which Heavy Grips prefers). Or I can modify my unit of measure for marketing purposes. ALL are legal as no standard exists to govern it. Looking at Heavy Grips again. Read the following three statements carefully. Pay attention to what they are actually saying about the resistance of their grippers.

In the first statement they state most strong people can do reps with the 150 and find the difficulty begins with the 200, meanwhile people of average hand strength have trouble closing the 200 for reps. Pay attention to this phrase from the third statement: "those with no grip training experience will most likely find it very difficult to close the HG200 at the beginning of their training".

Let us assume I have no experience with grippers. Reading those statements I would have no clue whether or not I should buy a 200. From my strength training I may consider myself a strong person of average hand strength but have never done any dedicated grip training. It boils down to this. Who can close a 200?

Aside from those contradictory statements, let's examine this quote: "When training their hand like other body-parts with reps under 20, most athletes, including women, are surprised at how fast they can master the HG 200 and HG250 and some athletes do reps with the HG 300 and HG 350."

Obviously the ratings system is very similar to the CoC grippers. Without going through their website and finding their unit of measure, you may assume that a HG 350 is a 350lb gripper. If you buy this gripper thinking you've got a #3.5-#4 CoC, you're mistaken. Units aside the quickest way to tell is right here: "some athletes do reps with the HG 300 and HG 350". A 300 is between a #3 and #3.5. People have enough trouble closing a 3, let alone repping with it. A #4 has only ever been 'officially' closed by 5 people!

I know I picked on Heavy Grips a bit. I have nothing against them, they just so happen to provide a good example for me to use.

Rather than compare a 100lb gripper to a 100lb gripper, or a 200lb gripper, it's easier to compare to a brand. Use the resistance, or certification system if possible, as a 'step in the right direction'. Couple that with a bit of research on the manufacturer, some customer reviews, and you have a gripper for your skill level. If you mix, fit your grippers into your training and progression based on the relative resistances within your set. Just remember what I said earlier about mixing brands.

I dream that one day there will be a unified method for evaluating a gripper's resistance, but until that day I'll stick with my favorite brand. :)

Seasoning

Seasoning has been around for a while. The idea behind it is that a gripper's resistance and spread will decrease over a certain amount of closes. To have a consistent resistance/performance, and a means of measuring progress, it is supposedly required to season your gripper. If you imagine having to season a No. 3, or even 4, level of resistance…Seasoning becomes daunting as those grippers are no easy task to close, even with two hands. Not to mention the fact that seasoning occurs (if you believe the legends) after approximately 100 closes.

My personal view is that it has no place in today's grippers. There is a marriage between material and design. The result of a bad marriage is a divorce. You pair a gripper designed for X amount of resistance but the material is not truly saying "I do", you get a gripper with a first time promise and a life time of shortcomings.

Of course, this wouldn't be a gripper article without some solid math and science. So here goes. The whole idea of seasoning is that over time the spring will lose strength and the gap will decrease a bit. The end result is a gripper with a shorter set and a weakened resistance, neither of which are a good thing. Why does this happen? It goes back to the altar (the marriage analogy). A proper design would ensure that the spring remained within the elastic range of stresses on the material's stress-strain curve. If the spring were improperly designed, then every time you closed the gripper it would exceed the elastic range ever so slightly. Every time you exceed that range, you get plastic deformation (read: permanent, unrecoverable movement). In the case of a gripper the handles no longer sit as far apart as they used to.

Resistance loss comes in because it is now easier to strain the gripper. Suppose the first time you close your gripper it starts at 0 strain and at close it reaches a strain of X and a stress of Y. This is slightly outside the elastic range. When you close it a second time it is already at a non-zero level of strain and to increase it to a strain of X takes less stress (for arguments sake, this is the resistance), owing to the non-zero strain component.

Graphically, our initial gripper is represented (below) by the black curve and upon closing reaches the red line. Upon the second close the gripper now takes on the dashed line. Drawing a line from the black-red intersection to the dashed line we have the vertical gray line representing equal strain values. Looking at the blue line we see the reduction in strength (the distance between the red and blue lines).

Now, this does not have to occur right away. It can occur after several uses. In fact I've exaggerated the effect in the above curve for ease of interpretation. This can be due to the endurance limit of the steel, which falls under the fatigue properties of the material. In a nutshell, everything has a limit as to how many times you can apply a certain stress. Think of a paper clip. You can bend it all the way back and forth only a few times before it breaks or quite a few times if you only bend it a little bit. The stresses in the latter are less, thus more cycles can be performed. The endurance limit refers to the minimum level of stress at which, theoretically, infinite cycles can be performed without failure occurring. Continually stressing a material, slightly above the endurance limit stress, will still allow the material to exhibit a large number of cycles before failure but each cycle is 'taking something' from the material performance. Don't be concerned that your gripper will break after 10 closes, fatigue cycles just about the endurance limit of steel can be in the millions.

Degradation over time can also be explained by the fact that plastic strains are very small. Along the same lines as looking in the mirror. If you're gaining or losing weight and using the mirror everyday you won't see a change but if you look at a before and after photo the difference is usually quite visible. Chronic exposure and slight differences make it very difficult to notice long term changes.

Seasoning may have been meant for steel which was not up to today's standards of quality control or as a means of justifying the use of cheap steel or improper design. With today's technology there is no reason why a gripper cannot perform its task well within the elastic range of stresses and strains. Thus making your gripper perform the same from day 1 to day 1000. To use ANOTHER barbell analogy: Think of 2 barbells. One is top quality and the other is cheaply made, both are calibrated to Olympic standards. You put 400lbs on each bar and the chances of the cheap one bending, permanently, are pretty good. You put even more on and the cheap one is frowning while the top quality one is straight as an arrow.

Hand Extensions

We endeavour to find balance in our regular gym training. Matching push and pull, chest and back, quads and hamstrings, but sometimes forget that opening the hand is the opposite, antagonist, of closing the hand. To keep your hands and grip healthy you need to train both functions of the hand. Problems in your hand can lead to problems in your wrist, your forearm, and even your bicep! If you don't believe me then you haven't got a copy of the trigger point manual by Claire Davies.

Extensions are simple exercises and not as boring as you might think. In my previous Gripper Guide article I mentioned using pails/buckets of sand or rice and working the hands that way. I also mentioned broccoli elastics (simply thick rubber bands) and to illustrate the technique Anuj (aka Wolf) has made a video demonstrating the exercise:

The beauty of using elastic bands is that micro loading is very easy. Placing the elastic closer to the base of the fingers provides the least resistance while placing them at the tip provides the most. When one elastic becomes too easy but 2 is too difficult, you can place one at the regular distance and the other closer to the base of the fingers. Don't forget about regular elastic bands either. They're a light resistance and you can add just about as many as you can keep in place.

Static Holds

I mentioned using grippers to perform static holds in my first gripper guide. While I stand by that recommendation there are a couple of things I would like to explain further. Static holds can damage the skin and tissue of your hands. I suffered a particularly nasty injury trying to squeeze a couple of seconds after I began to lose my grip. The gripper shifted slightly as it opened my hand and the result was a missing patch of skin between my pinky's 1st and 2nd knuckle. Lesson learned. Stop shy of failure or if you feel the gripper begin to slip. Grippers are different than a static barbell hold because a barbell doesn't push back like a gripper does.

Another solution I have found is to wear a leather palm work glove. It protects your hand. It's not 'legal' but since you're working supporting grip and you're not in a competition setting, who cares. :)

Even something as minor as a blister can interfere with your grip training. Regular barbell and dumbbell style training may not suffer since you can just resort to gloves and straps, but it sure has a way of messing with your grip training schedule.

As always thank you for reading. If you have any questions or comments (or if you would like to debate my explanations), please feel free to comment as either a guest or a user.

Comments

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by JoeWeir

Gregory R Waryasz¹ and Ann Y McDermott²

Dynamic Medicine 2008

Patellofemoral Pain Syndrome (PFPS), a common cause of anterior knee pain, is successfully treated in over 2/3 of patients through rehabilitation protocols designed to reduce pain and return function to the individual. Applying preventive medicine strategies, the majority of cases of PFPS may be avoided if a pre-diagnosis can be made by clinician or certified athletic trainer testing the current researched potential risk factors during a Preparticipation Screening Evaluation (PPSE). We provide a detailed and comprehensive review of the soft tissue, arterial system, and innervation to the patellofemoral joint in order to supply the clinician with the knowledge required to assess the anatomy and make recommendations to patients identified as potentially at risk. The purpose of this article is to review knee anatomy and the literature regarding potential risk factors associated with patellofemoral pain syndrome and prehabilitation strategies. A comprehensive review of knee anatomy will present the relationships of arterial collateralization, innervations, and soft tissue alignment to the possible multifactoral mechanism involved in PFPS, while attempting to advocate future use of different treatments aimed at non-soft tissue causes of PFPS.

A systematic database search of English language PubMed, SportDiscus, Ovid MEDLINE, Web of Science, LexisNexis, and EBM reviews, plus hand searching the reference lists of these retrieved articles was performed to determine possible risk factors for patellofemoral pain syndrome.

Positive potential risk factors identified included: weakness in functional testing; gastrocnemius, hamstring, quadriceps or iliotibial band tightness; generalized ligamentous laxity; deficient hamstring or quadriceps strength; hip musculature weakness; an excessive quadriceps (Q) angle; patellar compression or tilting; and an abnormal VMO/VL reflex timing. An evidence-based medicine model was utilized to report evaluation criteria to determine the at-risk individuals, then a defined prehabilitation program was proposed that begins with a dynamic warm-up followed by stretches, power and multi-joint exercises, and culminates with isolation exercises. The prehabilitation program is performed at lower intensity level ranges and can be conducted 3 days per week in conjunction with general strength training. Based on an objective one repetition maximum (1RM) test which determines the amount an individual can lift in good form through a full range of motion, prehabilitation exercises are performed at 50–60% intensity.

To reduce the likelihood of developing PFPS, any individual, especially those with positive potential risk factors, can perform the proposed prehabilitation program.

Background

Patellofemoral Pain Syndrome (PFPS) is a term for a variety of pathologies or anatomical abnormalities leading to a type of anterior knee pain [1]. Knowledge of the anatomy of the patellofemoral (PF) joint is essential to developing an understanding of the pathogenesis of PFPS. The symptom of anterior knee pain is associated with the conditions listed in Table 1. Pain may be caused by increased subcondral bone stress attributed to the stress of articulation or from cartilaginous lesions on the patella or distal femur [2-4]. Nearly 10% of all sports injury clinic visits by physically active individuals are attributed to PFPS [5], with more than 2/3 of patients being successfully treated through rehabilitation protocols [6-8].

Table 1. Common Pathologies Leading to Anterior Knee Pain (AKP)*

• Based on research presented by S. Dixit 2007, P. Brukner 2002, R.H. Miller 1998, J.P. Fulkerson 2000, W.E. Prentice 2001, T.A. Peters 2000, R. Khaund 2005, A. Haim 2006

Physical training including sport-specific cardiovascular training, plyometrics, sport cord drills, strength and flexibility training has been found in adolescent female soccer players to significantly reduce lower body injury incidence from 33.7% to 14.3%, allowing athletes to be game-ready [9]. Injuries cannot be prevented entirely, however practitioners can attempt to avoid some types and keep more severe injuries to a minimum [9]. Also, participating with injuries due to insufficient recovery time increases the risk of new injury [10]. Concern over the long term consequences of anterior knee pain in adolescence and young adulthood includes a predisposition to patellofemoral osteoarthritis in later life [11]. The goal of sports medicine should be to keep athletes and patients healthy, pain free, and able to enjoy their sport and physical activity for years to come.

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Physical rehabilitation programs to treat anterior knee pain have proven to be a highly effective non-operative option [6-8]. Results have ranged from an 82% success rate in decreasing the severity of symptoms in athletes with chondromalacia patella [7], to an 87% initial success rate for a combination physical therapy and NSAIDs intervention, with 68% maintaining improvements for a mean of 16 months post-rehabilitation [8]. In treating chronic patellofemoral pain syndrome, continuous rehabilitation conducted over seven years had a 67% success rate of complete subjective and functional recovery [6]. These high rehabilitation success rates for anterior knee pain due to either cartilaginous injury or anatomical abnormalities suggest the potential for the prevention of a majority of anterior knee pain using a prehabilitation approach.

PFPS is a condition of both malalignment and muscular dysfunction [1]. Unlike a surgical distal realignment procedure [12,13], rehabilitation exercises can restore PF joint homeostasis although the anatomical malalignment of PFPS may not be corrected [1]. In comparison, prehabilitation aims to optimize function and pain measures before a stressful event [14]. Because the symptoms of anterior knee pain are brought on by overuse stress [15], PFPS is an ideal condition for prehabilitation. It should be noted that the shape and size of the patella and trochlear groove are limiting factors in the outcome of a rehabilitation program [16], and therefore would likely limit the outcome of a prehabilitation program. Based on anatomical, functional, and biomechanical parameters known to occur in symptomatic athletes before overuse resulted in pain, prehabilitation involves a pre-diagnosis in asymptomatic individuals. The Preparticipation Screening Evaluation (PPSE) offers an opportune time to make a pre-diagnosis and initiate a prehabilitation protocol [17].

Anatomy of the Patellofemoral Region

The patella (Figure 1), the largest sesamoid bone in the human body [18], functions to improve flexion efficiency and to protect the tibiofemoral joint [18]. The combination of the quadriceps tendon, lateral retinaculum, medial retinaculum, and the patella tendon help stabilize the patella [19]. Because the patella is not completely engaged in the patellar groove during the first 0–30 degrees of flexion, instability and the potential for subluxation/dislocation injury increases if patellar stabilizers are weak or malaligned [19].

Figure 1. Cadaver Patellofemoral Computed Tomography Scan. P- Patella; LR- Lateral Retinaculum; MR- Medial Retinaculum; LFC- Lateral femoral condyle; MFC- Medial femoral condyle.

Arterial System

Arterial blood flow to the knee is accomplished by an intricate system of anastomoses between five major arteries: superior medial and lateral, the middle (posterior), and the inferior medial and lateral genicular arteries [20]. An anastomosis occurs between the anterior tibial recurrent artery and the descending genicular arteries [20]. The genicular arteries except for the middle genicular artery make a contribution to the circumpatellar anastomosis [20]. The cirumpatellar anastomosis extends into the superficial and deep structures of the bone, synovium, capsule, retinaculum, and subcutaneous fascia [20]. The arterial supply to the patella arises from the circumpatellar anastomosis [20].

Arising from the popliteal artery, the medial superior genicular artery lies anterior to the semimembranous and semitendinosus muscles, and the lateral superior genicular artery will then anastomose with the descending branch of the lateral collateral femoral artery to supply the vastus lateralis, vastus intermedius, and branches of the femoral nerve [20]. The middle genicular artery passes anterior to the joint line and into the posterior joint capsule to supply the anterior cruciate ligament (ACL) and the posterior cruciate ligament (PCL) [20,21].

The medial inferior and lateral genicular arteries arise from the popliteal artery distal to the posterior joint line and proceed to the deep collateral ligaments [21]. The medial inferior genicular artery provides blood supply to the tibial (medial) collateral ligament, anastomoses with the saphenous branch of the descending genicular branch, and anastomoses with the anterior tibial recurrent artery [20]. The lateral inferior genicular artery forms an anastomosis with the anterior tibial recurrent artery and supplies the fibular (lateral) collateral ligament at the joint line [20].

Gross arterial anatomy is similar between adults and children, however on a microscopic level, there are childhood differences in blood supply to the epiphyseal plate [20]. The pathology of PFPS may be related to decreased pulsatile blood flow in skeletally mature individuals [22]. Tissue ischemia resulting from mechanical forces that reduce genicular arterial flow during passive flexion from 20 to 90 degrees may be a cause or consequence of the pain associated with PFPS [22]. Surgical disruption of the genicular arterial system has not been reported to cause permanent vascular abnormalities to the patella, because the arterial supply appears able to revascularize the patella adequately after a surgical insult during ligamentous reconstruction procedures involving the knee [23]. Such surgical disruption can occur during a lateral retinculum release of the patella [23], a common surgical procedure for the alleviation of PFPS pain. If ischemia is an issue in the pathogenesis of PFPS, an arteriogram or other sophisticated test may detect defects in the collateral flow that could warrant the use surgical or medical revascularization to treat PFPS.

Quadriceps Force Vector

The quadriceps force vector (Figure 2) includes forces from the fiber orientation of the vastus lateralis (VL), vastus intermedius (VI), rectus femoris (RF), and the vastus medialis (VM). The vastus lateralis is composed of two force vector components, the vastus lateralis longus (VLL) and vastus lateralis obliquus (VLO) [19]. The vastus medialis is composed of two force vector components, the vastus medialis longus (VML) and vastus medialis obliquus (VMO) [19]. In the coronal plane, the quadriceps force vector angles are made by the VLO at 35 degrees and the VLL at 14 degrees laterally, by the VI and RF at 0 deg, and medially by VMO at 47 degrees and VML at 15 degrees. Overall the quadriceps force has a posterior pull sagitally to keep the patella in proper articulation with the trochlear groove [19].

Figure 2. Quadriceps-Patellar Force Diagram.
VMO- Vastus medialis obliquus;
VML- Vastus medialis longus;
RF- Rectus femoris;
VI- Vastus intermedius;
VLL- Vastus lateralis longus;
VLO- Vastus lateralis obliquus;
P- Patella; TT- Tibial Tubercle;
T- Tibia; MR- Medial retinaculum;
LR- Lateral retinaculum.

The lateral retinaculum is two layers; the superficial oblique retinaculum and a deep transverse retinaculum. The superficial oblique retinaculum is the culmination of the interdigitating of the patellar tendon, the VL group, and the iliotibial (IT) band [16,21,24-26]. The IT band originates from the tensor fascia lata and the gluteus maximus [21], with its attachment on the lateral epicondyle of the femur [12] and Gerdy's Tubercle on the anterior promixal tibia [12,21].

The deep transverse retinaculum consists of three structures; the epicondylopatellar band or lateral patellofemoral ligament, the midportion, and the patellotibial band [26]. The epicondylopatellar band provides superolateral support, the midportion provides lateral support, and the patellotibial band provides inferolateral support to the patella [16,21,24-26]. The midportion originates from the IT band and attaches to the lateral patella [26].

The lateral retinaculum is often released arthroscopically to alleviate its lateral displacement force [27]. To avoid complications, the procedure involves an incision through the superficial oblique retinaculum and deep transverse retinaculum without violating the joint capsule [26].

The medial retinaculum is much thinner than the lateral retinaculum and consists of three ligaments beneath the retinaculum; the medial patellofemoral ligament (MPFL), medial patellomeniscal ligament (MPML), and medial patellotibial ligament (MPTL). The MPFL merges with the VMO forming the primary restrictive mechanism for excessive lateral patella deviation, especially during lower degrees of knee flexion approaching full extension [16], the time when the patella is at greater risk of dislocation/subluxation [19]. Acute lateral patellar dislocation can occur if the MPFL is torn away from the femur or if the VMO muscle is torn from the adductor magnus tendon [28]. There is controversy as to validity of the VMO as being anatomically distinct and functionally separate from the VML [29]. The VM muscle group is both a knee extensor and patellar stabilizer dependent on the task performed [30]. The MPML and MPTL are thought to be less important in PF joint stability than the MPFL [16,19,31,32].

A cadaveric study demonstrated that static medial stability contributions were 50% from the MPFL, 24% from the MPML, 13% from the MPTL, and 13% from the medial retinaculum [33]. Due to the interdigitation with the VMO, the MPFL contributes over 50% against lateral dislocation as it assists to maintain the patella in the trochlear groove during the initial 20–30 degrees of flexion [33].

Sensory Receptors

The patellofemoral joint contains a variety of sensory receptors not distinct to this specific joint including: bare nerve endings, Pacinian corpuscles, Ruffini endings, Golgi receptors, and muscle spindles [34]. The major sensory nerves supplying the knee joint are the posterior articular (PAN), lateral articular (LAN), medial articular (MAN), intramuscular, and muscle nerves [34]. PAN is a branch of the tibial nerve that supplies the posterior cruciate ligament, anterior cruciate ligament, posterior oblique ligament, insertion of the annular ligament at the mediolateral menisci, posterior fat pad, posterior capsule, fibular collateral ligament, and the tibial collateral ligament [34]. LAN is a branch of the common peroneal nerve that inconsistently innervates the tibiofibular joint capsule and the lateral knee tissues. MAN is a branch of the saphenous nerve that supplies the anterior and medial capsule, medial meniscus, tibial collateral ligrament, posterior capsule, patellar fat pad, and patellar tendon [34]. The intramuscular and muscle nerves include the golgi tendon organs and muscle spindles supplied by branches of the femoral, obturator, or sciatic nerve depending on the location of the myotome [21,34,35].

The lateral patellar nerve innervates the patella at the lateral anterior border at the 11 o'clock position [36]. The medial patellar nerve innervates the patella at the medial anterior border at the 2 o'clock position. Both the medial and lateral patellar nerves are distal branches of the femoral nerve [36]. The medial based neurovascular bundle is the primary interosseous innervation to the patella [37]. The medial and central portions of the patella are densely interosseosly innervated in comparison to the lateral patella [37].

The innervation to the skin in the anterior region of the knee is from the lateral and anterior cutaneous branches of the femoral nerve and the infrapatellar branch of the saphenous nerve [21,35]. Posterior skin overlying the knee is supplied by the posterior cutaneous nerve, and cutaneous branches of the obturator nerve [21,35].

There is substance-P in the soft tissue supports of the patella including the fat pad, retinaculum, and periosteum, which is evidence for the soft tissue role in anterior knee pain [38]. Substance-P is involved in nociceptive input to the spinal cord and functionis as a vasodilator producing inflammation [38]. Woijtys (1990) observed that substance-P fibers may be denser in the lateral than the medial retinaculum, however the study did not specifically quantify the observation [38]. Substance-P fibers have also been found in the patellar marrow cavity in degenerative knees [38]. Identifying possible nerve defects or increased sensitivity to pain could alter treatment to include corticosteroid injections through regional nerve block techniques that are highly specific to the region of pain.

Methods

A systematic database search of PubMed, SportDiscus, Ovid MEDLINE, Web of Science, LexisNexis, and EBM reviews, plus hand searching the reference lists of these retrieved articles was performed to determine potential risk factors for patellofemoral pain syndrome. Key words searched were "patellofemoral pain syndrome", "patellofemoral", "anterior knee pain", "chondromalacia patella", "knee", and "patella". Articles were included based upon availability through the Tufts Hirsch Health Science Library and Interlibrary Loan. Selection criteria were based on a subject population with PFPS or a description of anterior knee pain not consistent with other pathologies listed in Table 1 and based on inclusion criteria presented in the article. Articles included were prospective cohorts, case-control, and case series. The articles included were limited to the English language and published between January 1984 and July 2007. Excluded from analysis were articles involving a treatment intervention.

Results

A total of 24 articles were included in Additional File 1: Review of Potential Patellofemoral Pain Syndrome Risk Factors. There are 3 prospective cohorts [39-41], 17 case-controls [42-58], and 4 case series articles [59-62] included in Additional File 1: Review of Potential Patellofemoral Pain Syndrome Risk Factors. Two articles were included that did not report P values [51,59]. Seven articles were included that did not have a patient population described specifically as PFPS [40,51,55,56,59,63,64], however the articles met the review inclusion criteria presented in the methods section. The articles were included to present the extent of research into the potential risk factors of PFPS that has been performed from January 1984 to July 2007.

Additional file 1. Review of Potential Patellofemoral Pain Syndrome Risk Factors. Comprehensive table of the articles discussed in the results section of the manuscript that review the potential risk factors for Patellofemoral Pain Syndrome. Format: DOC Size: 107KB

Electromyography (EMG) Measured Neuro-Motor Dysfunction

Using electromyography (EMG) to measure neuro-motor dysfunction in PFPS has been analyzed in 5 studies. All 5 studies have determined that when comparing PFPS subjects to controls, there is significant neuro-motor dysfunction in PFPS. Thomee (1996) demonstrated that the vastus medialis muscle was less active on EMG in PFPS patients, while the rectus femoris was equally active to healthy controls while standing [45]. Cowan (2001) and Cowan (2002) determined that during activities of daily living there was a difference in EMG onset in PFPS compared to controls [42,43]. Witvrouw (2000) found VMO/VL reflex response time to be a significant finding in PFPS [39]. The VMO/VL reflex response time was determined by electromyography unit with skin electrodes over the VL and VMO muscle bellies. Readings were taken using the patellar tendon reflex with the test performed 10 times per knee [39]. The VMO/VL muscles responded faster in the PFPS group compared to the controls [39]. Although not statistically significant, the group noticed that the VMO fired earlier compared to the VL in the control group [39], which would equate to an earlier activation of the medial force vector preventing lateral patella displacement. The authors concluded that an altered VMO/VL response time was a risk factor for PFPS [39]. The authors found no statistical difference when the VL response time was subtracted from the VMO response time (VMO-VL) between the PFPS group and the control group [39]. Crossley (2004) states that although the magnitude differences measured by EMG may be small, but statistically significant detecting these differences may influence treatment [44].

Foot Abnormalities

The characteristics of genu varum, genu valgum, pes cavus, and pes planus have not been found to contribute to PFPS [39,48] or other related conditions [15,47,65]. Arch index was determined in one study to be significantly lower for only a discriminant analysis of anterior knee pain not specifically classified as PFPS [63]. The arch index was calculated by forming three equal foot sections (forefoot, midfoot, and rearfoot), then dividing the midfoot area by the total footprint area and serves as a marker that the anterior knee pain group had a higher arched foot (cavus) which may produce greater pressures during running on the PF joint [63]. Other literature does suggest an increased risk of running injuries may be due to genu varum, genu valgum, and foot postural abnormalities, including excessive pronation, valgus ankles, and lowered foot arches [12,66-68]. Additional research is needed to clarify the validity of these characteristics as potential risk factors for PFPS.

Functional Testing

Functional testing may show that PFPS patients have lower strength capacity [39] as demonstrated by decreased vertical jump performance [39,46], anteromedial lunge [49], step-down [49], single-leg press [49], and balance and reach tests [49]. No difference was appreciated between the PFPS patients and controls for Flamingo balance, standing broad jump, bent arm hang, shuttle run, plate tapping, arm pull, leg lifts, sit and reach, sit ups, and maximal oxygen uptake[39]. No research has definitively suggested that PFPS is due to the lower strength capacity or rather a result of lower strength capacity. For this reason, functional testing deficits are a potential risk factor until proven otherwise.

Gastrocnemius Tightness

Gastrocnemius and soleus tightness reduces the amount of dorsiflexion leading to excessive subtalar joint pronation and tibial internal rotation which will cause femoral internal rotation to increase the Q angle [50]. Therefore, one mechanism to PFPS pathogenesis is by increasing Q angle and increased PF joint stresses [50]. Gastrocnemius tightness was significant in two studies comparing PFPS patients to controls [39,50], but was not significant in another study comparing anterior knee pain subjects to controls [63].

Generalized Ligamentous/Joint Laxity

Generalized ligamentous laxity is proposed to increase the total patellar mobility which would alter patellar tracking and lead to symptoms [64]. Generalized ligamentous laxity was significantly increased in PFPS patients in two out of three studies. Al-Rawi (1997) found significant generalized ligamentous laxity in chondromalacie patella knees [64]. Witvrouw (2000) was only able to find significance in the thumb-forearm mobility exam, the rest of the exam was not significant [39]. Fairbank (1984) found the relationship between knee pain and generalized ligamentous laxity not to be significant [51].

Hamstring Strength

The mechanism behind hamstring strength and pathogenesis of PFPS is not well understood, however overall lower body strength is recommended for a runner's exercise program [63] and the hamstrings are involved in power activities such as the vertical jump [69]. Hamstring strength was examined in one study and determined that running athletes with a "syndrome complex" have an 81% absolute strength deficiency at 60 degrees per second and 73% had a deficiency at 240 degrees per second when using a Cybex dynamometer [59]. "Syndrome complex" refers to pain in the anterior aspect of the knee in the soft tissues or around the patellar tendon, pain upon running, mild retropatellar pain upon compression with minimal crepitus, and no clinical evidence of patellar subluxability, chondromalacia, plica, increased Q angle, or increased foot pronation [59]. The data however was not presented as a research article, and no P values were reported [59].

Hamstring Tightness

Hamstring tightness has been theorized to either cause slight knee flexion during activities or to necessitate higher quadriceps forces to overcome the passive resistance of the hamstring, both of which may increase PF joint reaction forces [50]. Hamstring tightness was evaluated in four articles [39,40,50,59]. Two of the four articles found hamstring tightness in anterior knee pain/PFPS athletes [40,50], one study found no significance [39], and one study stated that 23% of "syndrome complex" athletes had appreciable hamstring tightness [59].

Hip Musculature Weakness

The iliopsoas muscle, a hip flexor and secondary femoral external rotator, if weak de-stabilizes the pelvis [70,71]. The individual then compensates by developing an anterior pelvic tilt with an internally rotated femur [70,71], the Q angle is then increased, leading to increased PF joint stresses [50]. For the small number of patients who show asymmetrical hip rotation with diminished medial rotation and excessive lateral rotation, a program designed to create a balance in internal and external rotation hip strength is required [72]. A strong VMO with weak hip adductors results in the adductor magnus tendon being drawn to the patella; therefore, strong hip adductors serve as a stable origin for VMO contraction [73].

Two of three studies evaluating hip musculature found weakness [52,53]. Hip abductor strength was determined to be significantly decreased in both studies when comparing PFPS patients to control subjects [52,53]. Piva (2005) found hip external rotation strength and hip abduction strength not be significant [50].

Balanced hip strength is very important for PFPS prevention, as the IT band originates from the lateral hip musculature [12] and the VMO has a relationship to the adductor magnus tendon [28]. A 6-week treatment program designed to improve hip flexion, adduction, and abduction strengths in patients with PFPS (n = 35) led to a combination of improved hip flexion strength with a normalized Ober Test and Thomas Test in 93% of successfully treated PFPS cases defined by a decrease in VAS pain score [74].

Iliotibial (IT) Band Tightness

IT band tightness through anatomical correlations to the lateral retinaculum and patella will increase the lateral force vector on the patella during flexion to increase the lateral PF joint stresses [54,75]. Iliotibial band tightness was found in PFPS athletes in three articles evaluating the IT band [54,59,60]. An early study Kibler (1987) reported 67% of running athletes with "syndrome complex" had IT band tightness, although there was no P value reported [59]. Piva (2005) reported no tightness in the IT band/tensor fascia lata complex [50].

Quadriceps Angle (Q-Angle)

A greater Q angle is believed to change the location of contact and pressure in the PF joint, resulting in areas experiencing excessive stresses that are not physiologically manageable [63]. Huberti (1984) using cadaver knees and a special loading fixture found that both an increased and a decreased Q angle increased peak patellofemoral pressures [76]. These increased pressures may predispose an individual to degenerative pathological changes [76]. Increasing the Q angle is associated with increased lateral patellofemoral contact pressures and patellar dislocation, while decreasing the Q angle may not shift the patella medially, but rather increases the medial tibiofemoral contact pressure through increasing the varus orientation of the knee [77]. The effect of Q angle has been examined in a number of studies [39,47,48,55-57,63]. Three studies reported the Q-angle to be significantly increased in PFPS subjects against controls [48,55,57], while four studies reported no difference in Q angle [39,47,56,63].

Haim (2006) reported an abnormal Q angle of greater than 20 degrees was statistically associated with anterior knee pain [48]. Q angle has been believed to differ between males and females, however the slight difference of only 2.3 degrees appears to be related to height rather than pelvic dimensions [78]. Shorter statured individuals appear to have larger Q angles and therefore the slight difference between genders may be attributed to men being taller than women [78].

Quadriceps Tightness

Witvrouw (2000) states that the decreased quadriceps flexibility existed prior to developing the symptomatic syndrome, and therefore is not necessarily a result of PFPS [39]. Quadriceps tightness may cause high patellofemoral stresses that predispose individuals to developing symptoms [39,79]. The presence of quadriceps tightness was reported in all five studies that evaluated quadriceps tightness [39,40,50,59,63]. While Kibler (1987) reported 61% of "syndrome complex" patients had rectus femoris tightness, no P value was reported [59].

Quadriceps Weakness

Quadriceps weakness, specifically VMO weakness in comparison to the VL, can lead to lateral displacement of the patella causing the articulating pressure to be on the lateral facet [16,19]. The quadriceps force vector (Figure 2) explains how an imbalance in strength can lead to improper patella alignment as a weak VMO cannot adequately support medial patellar stability [16,19]. A total of six studies evaluated quadriceps weakness on anterior knee pain/PFPS. Two studies reported quadriceps weakness was a non-significant finding [41,57]. Three studies found weakness to be a significant finding [46,58,62]. Kibler (1987) reported that 39% of "syndrome complex" athletes had appreciable quadriceps weakness (no P value reported) [59].

Patellar Compression/Crepitus

Patellar compression/crepitus was examined in two studies [48,61]. Testing using the patellar tracking test was determined to be 56% sensitive and 55% specific as confirmed by arthroscopy [61]. The patellar tracking test is performed by compressing the patella in the trochlear groove while moving the patella up and down, with pain during the test indicating a positive result for chondromalacia [61]. Haim (2006) found patellofemoral crepitation significantly associated with reduced mobility in PFPS patients [48]. Crepitus alone may be a non-specific finding [75], and therefore may not be useful as a potential risk factor based on the current research.

Patellar Mediolateral Glide/Mobility

While two studies reported reduced patellar mobility in PFPS patients [48,60], Witvrouw (2000) reported that medial, lateral, and total patellar mobility were greater in PFPS, however the findings were not significant [39]. After assessment of the research of patellar glide/mobility as a risk for PFPS, data appears to be inconclusive at the current time.

Patellar Tilting

Excess patellar tilting laterally can lead to patellar medial hypomobility resulting in high stresses between the lateral facet of the patella and the lateral trochlea [75]. Excessive tightness of the lateral structures inhibits the patella from reentering the trochlear groove when the pathologic lateral tilt is in excess of 20 degrees when the knee is in extension as measured by CT scan [19]. Haim (2006) reported a positive patellar tilt was significant for PFPS subjects compared to controls with 92% specificity and 43% sensitivity [48].

Discussion

Recommendations for Pre-Diagnostic Physical Examination

A number of identifiable and diagnostically accurate risk factors exist that can be determined without radiographic imaging (Table 2) [75]. General visualization of the patellar movement through flexion extension may be helpful in detecting malalignment if there is a "J sign" [80,81] as result of lateral retinacular tightness or medial retinacular weakness. Decreased quadriceps flexibility, specifically rectus femoris tightness, can be assessed by using the Ely Test [82].

Decreased IT band flexibility is evaluated using the Ober Test [74,79]. Decreased hip flexor flexibility is assessed using the Thomas Test [74,83-85]. Weak hip abductors are evaluated using the Trendelenburg Test [86].

A Q angle measurement in excess of 20 degrees may increase PFPS risk [48], however studies have demonstrated slight differences in Q angle between PFPS and control at lower Q angle values [55,57].

Weak quadriceps or quadriceps atrophy can be determined visually or by using a tape-measure to check for asymmetry between sides. Quadriceps circumference is measured proximal to the patella. The diagnostic parameters have not been well-defined, as the level of atrophy may be minimal [58], however athletes should have near bilateral symmetry. Utilizing the quadriceps atrophy criteria may be left to the opinion of the clinician as to whether there is enough quadriceps tone or if the asymmetry warrants a prehabilitation program prescription.

Altered VMO muscle reflex time compared to VL is assessed by simultaneous VMO and VL palpation during knee extension. In normal patients, no timing difference between the contraction of the VMO and VL exists. In some patients, a marked delayed onset of VMO is evident on palpation [1]. Electromyography using skin electrodes over the VMO and VL could be used to more accurately ascertain the reflex time difference during an elicited patellar tendon reflex using a reflex hammer [39], however this may not be feasible financially for most clinicians.

Decreased vertical jump is assessed by direct measurement, preferably using a Vertec device, however the criteria for jump height, type of jump surface, and specific testing technique are not developed well enough for pre-diagnostic use. Rather, comparison with previous vertical jump testing and a decrease in performance may indicate decreased power production which may translates to an increased risk for developing PFPS [39]. Other functional tests can be performed (see Additional File 1: Review of Potential Patellofemoral Pain Syndrome Risk Factors), however the vertical jump test is a practical way to track athletic progress as a prehabilitation is initiated.

Generalized ligamentous laxity is determined by a variety of tests listed in Table 2. Having any generalized ligamentous laxity characteristics may be a positive indication for PFPS prehabilitation, as studies have showed a significant correlation with generalized ligamentous laxity tests and symptomatic PFPS [39,64,75].

A patellar tilt test can also show lateral retinacular tightness if the lateral patella cannot be raised to horizontal while compressing the medial patella posteriorly [39,80]. There is still the clinician's opinion as to whether or not the athlete has a hypomobile patella even if the criteria are not met. Other pre-diagnostic criteria may be developed or the current criteria altered as larger prospective PFPS studies are conducted and more information is learned. Radiographic measurements are more accurate, but cost effectiveness is a concern.

Proposed Prehabilitation Intervention

The prehabilitation program is derived from common practices in PFPS rehabilitation and from strength and conditioning trends designed to increase power output, create balanced strength, and reduce overuse injuries associated with symptomatic PFPS (Tables 3 and Additional File 2: Patellofemoral Pain Syndrome (PFPS) Exercises and Prescription Recommendations and Instructions). As with diagnosis, it is important to consider factors in a joint proximal and in a joint distal to the joint of interest. The program consists of a general dynamic warm-up, stretching (13 total), power exercises (1 total), multi-joint exercises (2 total), and isolation exercises (1 total) for each of the defined muscle groups.

Isolation exercises described have a major effect on a single muscle group, although have minor effects on other muscle groups as a true isolation is difficult to achieve during exercise. Athletes are encouraged to incorporate this program 3 days per week at rehabilitation intensity levels [light (50% intensity of 1 repetition maximum (1 RM)/heavy (60% intensity of 1 RM)/moderate (55% intensity of 1 RM)], as a supplement to general weight lifting and stretching activities. This intensity is in contrast to "heavy week" training in which the strength and conditioning professional or certified athletic trainer prescribed intensity levels reach up to or near a 1 RM.

A variety of general weight lifting programs are outlined by the National Strength and Conditioning Association (NSCA) [69] and should be the primary program of the athlete, with the PFPS prehabilitation program serving as additional, less intense exercises performed to develop symmetrical lower body strength and flexibility. The proposed program is based on a non-linear periodization model and can be made flexible based on athletic training demands. A 1 RM can be determined by a formal maximal weight lift if the athlete demonstrates proper form for a back squat and leg press. The athlete should not experience pain during the 1 RM lift. Other exercises listed in Additional File 2: Patellofemoral Pain Syndrome (PFPS) Exercises and Prescription Recommendations and Instructions require the athlete and fitness practitioner to determine an appropriate weight that pushes the athlete at a targeted rate of perceived exertion (Borg RPE scale) [87]. The 1 RM lift for exercises such as lunges, resistance band training, Romanian Dead Lift (RDL), and box jumps also involve RPE, rather than by actual maximal lift.

Additional file 2. Patellofemoral Pain Syndrome (PFPS) Exercises and Prescription Recommendations and Instructions. Table of recommendations and instructions for exercises and stretches suggested to possibly prevent Patellofemoral Pain Syndrome. Format: DOC Size: 99KB

Once identified as "at risk for developing symptomatic PFPS", the athlete should 1) continually perform the prehabilitation program as long as the athlete wishes to remain physically active, with 2) periodic vertical jump testing to ensure there is no decrease in power production. Due to bone growth changing the lower leg moment of inertia in children [88], the prehabilitation program may not be necessary or appropriate for anterior knee pain prevention in skeletally immature individuals.

Dynamic and static methods of stretching increase both ROM and flexibility for injury prevention, and are both incorporated in rehabilitation [89]. Dynamic stretching is performed during the general dynamic warm-up (Table 3) taught by the certified athletic trainer or strength and conditioning specialist [69]. Dynamic stretching involves controlled movements that gradually increase in speed and range of motion, mimicking the athletic activity to follow so as to increase muscle memory [69]. This is in contrast to ballistic stretching which uses the momentum of a moving limb in a spring-like manner, attempting to force it beyond its normal range of motion [69]. The dynamic warm-up does not include any ballistic stretching, as ballistic stretching has been associated with injury [69]. Static stretching and Active Isolated Stretching (AIS) are performed after the dynamic warm-up [69,90]. Stretching the IT Band, hamstrings, quadriceps, hip adductors, hip abductors, hip external rotators, hip internal rotators, quadriceps, gastrocnemius/soleus, and hip flexors is prescribed for PFPS rehabilitation and therefore is appropriate for prehabilitation [16,74,79,89,91,92].

Power exercises, such as the power clean, snatch, or push jerk, can increase power production if the athlete has the proper instruction and equipment available [69]. The power clean is an Olympic style lift that involves a quick and forceful lift of a bar off the ground to the final position in front of the shoulders through one movement [69]. The snatch is an Olympic style lift that involves quickly and forcefully lifting a bar off the floor to an overhead position in one uninterrupted motion, ending with the elbows in full extension [69]. The push jerk involves rapidly moving the bar from the shoulders to an overhead position using an explosive extension of the hips and knees to accelerate the bar to its final overhead position ending with elbows extended. [69]. Due to the potential for injury from improperly performing Olympic lifting exercises, the box jump and resisted squat jump are included in the supplemental program to improve power output [69]. It is recommended these exercises be performed on an Olympic-style platform with hard-soled shoes, preferably Olympic-style weight lifting shoes.

Rehabilitation protocols have determined that both closed kinetic chain (CKC) and open kinetic chain (OKC) do not create supraphysiologic stresses and are advantageous to the individual with PFPS [28,91,93]. Lower body CKC exercises involve many muscle groups, are typically weight bearing and involve the foot remaining in a fixed position without movement. Examples include the back squat and leg press. CKC exercises are considered superior for athletic purposes [93] based on mimicking functional movements in sport and involving many muscle groups.

In comparison, lower body OKC exercises isolate a specific muscle, are typically non-weight bearing and involve free movement of the foot. Examples include straight leg raises and knee extensions. Both CKC and OKC are included in PFPS rehabilitation programs [91,92,94], with adjusted ranges of motion on traditional exercises (Additional File 2: Patellofemoral Pain Syndrome (PFPS) Exercises and Prescription Recommendations and Instructions).

VMO training is important to improve VL and VMO onset timing differences [95]. Retraining the vasti with eccentric exercises such as squats has been noted to improve PFPS rehabilitation outcomes [96]. VMO muscle isolation has been difficult to prove possible without the use of electrode stimulation [97], however it is generally believed that VMO activity is greater with the hip in external rotation [97]. Hip external rotators have been determined to be weaker in PFPS patients as diagnosed by the single-leg squat test, therefore loading in external rotation is beneficial [13], even if there is no added benefit to the VMO. Many protocols have successfully emphasized the use of a 10 o'clock and 2 o'clock (between 30–45 degrees) position of femoral external rotation [98].

The hip's external/internal rotation, flexion/extension, and abduction/adduction groups need to be both stretched and strengthened [74,79,89,91,99,100]. Isolation exercises for these groups, as well as multi-joint exercises that focus on eccentric loading and isometric contraction, are important [99].

Historically, patellar taping has been advocated in treating PFPS patients to increase VMO activity and decrease VL activity [101]. In asymptomatic individuals the data are limited and conflicting, with patellar taping noted to be effective [102] or detrimental [101], therefore the prehabilitation program does not promote use of patellar taping until supported by additional research.

Summary

In skeletally mature patients, anatomical abnormalities may be pre-diagnosed during the Preparticipation Screening Evaluation (PPSE) by using the evidence-based criteria for potential PFPS risk factors. The clinician with a proper knowledge of the neurovascular, bony, and muscular anatomy has the knowledge to appropriately assess malalignment of the PF joint and therefore perform a screening physical examination for PFPS based on potential risk factors. The anatomy section also serves as a reference point to 1) explain exactly how anatomical deviations can potentiate PFPS pathogenesis and 2) stimulate thought about other possible therapies, including addressing vascular insufficiency and neuropathic pain.

In an effort to prevent the onset of debilitating knee pain, a positive finding in any pre-diagnostic category or asymptomatic PFPS that concerns the physician results in prophylactic treatment prescribing a prehabilitation exercise protocol based upon proven, successful rehabilitation techniques that create balanced lower body strength, increased flexibility, and increased power production. As more research is conducted on PFPS risk factors and potential risk factors, the pre-diagnostic criteria should be updated and changes made to the supplemental prehabilitation program. By conducting prospective cohort studies in healthy individuals, research could determine whether the risk factors listed in this article serve to initiate or contribute to PFPS, or rather result from PFPS development. The proposed supplemental prehabilitation program offers a safe and effective means to develop balanced lower body strength and flexibility in any individual and should be considered along with a more intense strength training program as necessary for injury prevention and performance enhancement. The proposed program is to be understood as an example of a possible program, other programs can be made that accomplish a similar task of attempting to prevent PFPS. Practitioners are encouraged to alter the program to make it more specific to the athlete and utilize available resources.

Abbreviations

AIS: Active isolated stretch; Deg: degree(s); MR: Manual resistance; RDL: Romanian dead lift; Yd: Yard

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

GRW conceptualized the idea of the pre-diagnostic criteria, prehabilitation exercise protocol, and was the principal author of the manuscript, AYM was responsible for significant reviewing and assistance with the writing and final formatting of the article.

Acknowledgements

The authors would like to acknowledge Dr. Stanley Jacobson, PhD of the Tufts University School of Medicine, Department of Anatomy and Cellular Biology for the Cadaver Patellofemoral Computed Tomography Scan and the VolView cadaver image.

© 2008 Waryasz and McDermott; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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by EricT

Previously I've called upper chest breathing either inverted or paradoxical breathing. In case you haven't gotten the news flash, it's bad. Now, I'm seeing something called 'reverse breathing' being promoted for martial artists. Wikipedia says that it is "Ancient Chinese Secret".

The practice appears to be an almost perfect instruction on incorrect breathing. The idea is to expand your abdomen while breathing out and pull your stomach in while breathing in. Absolutely ridiculous and a good way to 'gas out' for a martial artist. Here is a some excerpts from an article at DragonDoor. It's full of nonsensical gobbledygook but these are the highlights of the instruction:

From DragonDoor by Tim Heurtz:

"To begin, stand with your feet shoulders wide, relax your shoulders into their sockets and “swallow” your chest (swallowing your chest is believed to stimulate the thymus gland which aids in the immune system)."

Let's stop there. What? Double what? I believe, I believe.

"Tilt the pelvis up and touch your tongue lightly to the roof of your mouth. Tuck the chin in a bit and you’re ready to start."

Incidentally, the tongue thing is also how you can ward off the death touch.

"Expel all your air and push not only your stomach out, but also your sides and lower back… Inhale slowly through the nose and pull your stomach in while lifting the perineum (that no-man’s land that separates the front from the back – just another way of working the anal lock or the squeezing and lifting of the anal sphincter and sex organs)."

While your busy trying to lift your perineum let me rant just a bit on how very WRONG that is. That is textbook bad breathing. No wonder they have a disclaimer after every article. The abdomen should never pull in during inhalation and when it does you have lapsed into an unhealthy breathing pattern which is physiologically reverse of what it should be. Who promotes practices that are 'reverse' of what our body's are made to do?

Learn how breathing is supposed to work with this handy category called breathing.

Comments

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by EricT

The last post in the series discussed what we assume and how we must assume. In this post I want to talk about what we know.

What do we know?

We don't know a whole lot. If we are willing to take the time and do a little Critical Thinking we can come close to the best conclusion based on the state of knowledge at the time. Knowledge is not static. Evidence is not static. So here is what to look for:

Author's recommendations and viewpoints never seem to change

As you peruse the internet you will come across fitness and strength writers who have written a great many articles or at least whose opinions are freely available in some form. Chances are you'll find someone who was writing articles in the year 2000 and is still writing them today, in 2010. Pay attention to the dates. Pay attention to the evolution. Ten years is a long time. Heck even five years is a long time and for me one year is long enough to turn my thinking on a subject one hundred sixty degrees.

You may find that our hypothetical writer is saying the same things now as he or she was in 2000. That is a bad fitness writer, my friends. The state of knowledge has changed too much for anyone to still be saying the same things.

This statement out of all that I've made thus far may be the hardest for many to except. Experience tells me that most people view those whose opinions never waiver as having more authority. Someone who seems more sure of themselves and their opinions will be viewed as more of an expert than those who don't always take a concrete stand (another article?). They have less because they have simply stopped learning. Stopped thinking. Stopped applying.

Do not attach yourself to dinossaurs and sticks in the mud.

Not a day goes by that someone does not ask a question, get ten contradictory answers and wonder, rightly so: "Who do I listen to?". The purpose of these posts are to help those very people. The beginner has very little foundation on which to proceed. They are very prone to falling victim to those who shout, rant, and rave rather than reason, discuss, and LISTEN. Well, those who pound the fist are those who have little voice.

So here is a simple research tool. Take some time and examine the history of your information source. The ones to avoid are the ones who never seem to change on anything. They say the same things through the years albeit louder and louder. It's alright to be wrong. As a matter of fact, the next time a writer proclaims, I WAS WRONG, in an article, mark them down as a go to source.

But all that is just about researching and learning. We need a specific practice or habit to serve as a spot for our bad fitness article list. Well these writers will tend to discuss everything as if its "for sure". Phrases such as "it's been proven" or "we have known for a long time" will be prevalent. Other favorites are the appealing to common knowledge or common practice. Everybody knows this or everybody does this. Some writers will be so blatant as to say things like "I am right about this and nothing anybody can say will make me believe otherwise. In fact, if you think differently you are not even worth listening to. So the spot is:

The author talks about what he KNOWS rather than what he THINKS.

Above I brought up old articles versus new articles. I want to be clear that I am not making a value judgment about new things being superior to older ones. An older article can still be valid and educational. The point is to compare the evolution in one author's thinking and not to say that old articles are not valuable. Just because an author changes their stance often does not make them right or wrong. That should be obvious. But if they never change their stance then you can bet they have much fewer chances of ever being right, or at least as right as anyone can be.

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Other posts in this series:

by EricT

The bodyweight boom is on. To hear people talk you'd think that calisthenics and bodyweight exercises in general had just been invented last year and were the best thing since the camp fire.

Gymnastics skills have been joined to the traditional and well known exercises to create a very popular market. A perfect example is the handstand pushup. A google search will reveal countless articles and also a great many very expensive products supposed to teach you to achieve one.

Handstand pushups certainly look impressive. They create this wide eyed wonder effect and the idea of achieving this type of skill can create instant motivation in many. Handstand pushups are only one of many. We like the Pistol (one-legged) squat here at GUS and it's no slouch either in terms of impressing your friends.

The video below would probably motivate many couch potatoes to instantly get up and stand on their hands. Those are impressive skills and they may have as much sell in the strength training world as Arnold in "Pumping Iron" did in the bodybuilding world.

By the tone of this post so far you've probably guessed that I have a problem with some of this. But it is not my intention to tear down any kind of bodyweight training and in fact I think the average strength trainee needs to be doing MUCH more of it.

Strength and Skills

Strength is skills, right? Well, that depends on who you ask. I've said many times that we are all allowed our own personal definition of strength, within reason. And reasonably, equating displays of skill to strength is failing to perform a cost benefit analysis. By that definition dramatic and awe-inspiring skill will tend to win out, which is the advantage certain bodyweight skills have over weighted exercises. Yet, displays of specific strength as strength defined seems to be a theme these days.

Although many of these bodyweight skills are borrowed and modified from gymnastics they are essentially 'closed skills' which are skills that are executed in a predictable setting under rote conditions. When you hear talk about 'real world strength' keep in mind that this implies open skills which means that the conditions may be unpredictable. The real world requires quick and precise adaptations to those conditions.

So you may notice that the above comparison of a powerlifter to a martial artist is an apple and oranges one. Martial arts combat relies on open skills. After all, your opponent is a changing and unpredictable factor. Performing a deadlift, squat, or bench press is a closed skill. These are two decidedly different competitive environments.

Skills as strength is a subject for an entire article but consider that most strength training movements are meant to improve different aspects of strength development and one of those aspects is fundamental movement. Skills themselves are the specific abilities needed to perform in one's chosen sport or activity. So to simply say that skills are strength is like saying that an MMA fighter who beats a powerlifter is stronger than the powerlifter. After all it was the fighters skills that got him the win. But when the powerlifter out-lifts the fighter, of course, he is stronger. In reality both of them are very strong but neither is skilled at the other's sport. Sounds like a no-brainer when I put it like that doesn't it? Yet, the idea that simply mastering a set of skills not only makes you 'strong' but that this strength is superior to other 'types' of strength is at the heart of bodyweight propaganda.

There is so much ability needed just to control and stabilize your bodyweight in various ways, let alone perform movements, that the skills involved have a built in mystique and attraction. But let's look at some of the assumptions that the more vocal of bodyweight only crowd works from:

• Bodyweight exercises are inherently superior to weighted exercises

• Bodyweight exercises are inherently safer

• Bodyweight exercises equate to "real-world" strength better than weighted exercises - they have more functional carryover into every day activities

• Bodyweight exercises improve core strength and stability

• Bodyweight exercises improve balance and coordination

In some cases these assumptions are valid and in others they are not. Most of the claim made for the more dramatic skills are so generic they could be pasted on to any skill.

Balance and coordination

Balance and coordination from handstand pushups? Really. Is this in case you lose both your legs and must walk on your hands? Handstands pushups make you balanced and coordinated ON YOUR HANDS. Yet I have read aficionados asserting that this skill, among others, will actually improve your general balance and coordination. It's a ridiculous idea. Balance is as specific as anything else

Right now, assuming you can stand up and walk around normally, you have balance and coordination. If you want to be able to jump from one post to another Ninja style you'll have to practice your Ninja post jumping. Handstand pushups won't help you walk better nor will they make you a Ninja.

Core strength and stability

Could something like a handstand push-up improve your core strength and stability in a general way? Absolutely. The problem is in the claim that it has special efficacy in terms of core strength. The biggest areas of improvement will come in the area of the specific skill with a small carryover into other skills. The further removed one skill is from another the less carryover.

Superior to Weighted Exercises

Some bodyweight exercises can be demonstrated to be superior to their weighted counterparts in some instances. The bodybuilding "movement" likes to claim that all bodyweight exercises are more effective than alternative. In this way they are much like generic fitness claims. The key is the misuse of the word effective.

Effective, as a word, could actually be considered one of the spots like I talk about in the Bad Fitness Articles series. When someone says bodyweight exercises are effective but they fail to say what they are effective FOR..that is a spot. Effective, in the general sense, means something produces a certain effect. So what is the effect? One exercise could have several effects.

For instance, handstand pushups are effective at increasing upper body strength. Especially upper body vertical push type strength.

But are they efficacious? Well they would probably efficacious for gymnasts. The difference is that efficacious implies that something is effective for a certain population given certain goals or needs and that it is efficient. There is not a lot of wasted time and effort.

Do you see the difference? Many things can be said to be effective. Pushing my car is effective at getting my car to move. Since handstand pushups are directly compared to the overhead press, we have to ask before we compare.

People say they are superior to overhead press for increasing upper body strength. The two movements are contrasted but not compared. They are both similar. One has you pressing your body weight and the other pressing an implement. If you goal is pushing something overhead then you can do probably do that already with an appropriately weighted barbell or dumbbell, provided proper instruction and some initial quality practice with the press.

So, acquiring the skill (and safely) is relatively straightforward. Progression is simple and quick so it is efficient. And the result is increased overhead pushing strength so overhead pressing is effective and efficacious if your goal is to increase vertical pushing strength.

Let's assume right now that you cannot do a handstand and that you cannot even support your bodyweight. You maybe do not like being upside down and have a fear of landing on your head. With a proper plan and a lot of time, effort, and risk you will eventually achieve ONE free handstand pushup.

Let's assume also, that you can overhead press a certain weight a certain amount of times. Since we are comparing the exercises for the handstand pushup to be superior to the overhead press all the effort toward one should have resulted in considerable improvement in the other. After all, the movement is the same except for the distal end being fixed or free. So how much does acquiring that one handstand pushup improve your military press? No telling. You won't know until you invest a considerable amount of time and effort into acquiring the skill.

Much of that time will be spent on simply supporting your bodyweight, then balancing it statically, then dynamically while developing the great amount of strength needed just to move the body in this way. In terms of just pushing strength it is by no means efficient and there are many risks involved, not the least of which is knocking yourself out or worse.

The problem, to my way of thinking, is the focus on the acquisition of dramatic skills rather than on efficient ways to get the benefits from the movement. The fact is that most will lose interest and give up long before acquiring these skills and even when they do achieve them they've expended a lot of resources to achieve what amounts to a party trick.

On the other hand, a simple jackknife pushup, such as shown here can be learned very quickly and easily and simply progressed, resulting in much of the supposed benefits of the handstand pushup. They can be fitted in to a training routine without undue changes to the existing setup and the benefits and cost of them toward your strength and conditioning as a whole can be weighted much sooner. The only benefits that one would not achieve are those that are quite specific toward achieving the handstand push-up itself.

So, if your goal is to increase upper body strength than putting forth herculean efforts to learn a fancy skill may not be very efficacious for you considering the fact that simply grabbing some dumbbells or a barbell, learning to press it overhead properly and then progressing in a straightforward manner will begin increasing your upper body strength from day one. And considering the fact that you are more likely to carry a free object overhead than you are to stand on your hands and press it is sensible.

Why Am I Knocking Fancy Bodyweight Skills?

I'm not! To be honest I think handstand pushups and other such skills are way cool. I find such achievements impressive and inspiring and I think that choosing to develop such skills, if that is your wish, is quite valid. You will be stronger. You will develop great torso control (provided variety). You will have a lot of fun and you will likely feel great about it.

On one hand you have guys like Matt Furey who uses, for lack of a better word, propaganda and "poisoning the well" to try to shove bodyweight skills down people's throats and on the other you have guys like Jim from Beastskills who feels no need to tear other types of training down to build himself up. As a matter of fact, I just checked before finalizing this post and he recommends a foundation in general strength training for beginners and even that he doesn't get all precious about. Furey's ad for his handstand pushup course, which costs over 70 bucks (for ONE exercise folks!) starts by letting you in on a 'secret' and proclaims in HUGE letters: BENCH PRESSING SUCKS!

Among his many fantastical claims are that his course will instantly double your balance and coordination and will correct the ratio between arm and leg strength in which he seems to be claiming he will make your arms as strong as your legs or at least alluding to such. Of course there is no usable information in these types of ads only inflated and overwrought claims and emotive language designed to sell you something. He even manages to make "fear of being upside" down sound like a general problem that handstand pushups will solve rather than just an obstacle for the skill itself.

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by EricT

PLoS Biol 2004

Skeletal muscle demonstrates a remarkable plasticity, adapting to a variety of external stimuli (Booth and Thomason 1991; Chibalin et al. 2000; Hawley 2002; Flück and Hoppeler 2003), including habitual level of contractile activity (e.g., endurance exercise training), loading state (e.g., resistance exercise training), substrate availability (e.g., macronutrient supply), and the prevailing environmental conditions (e.g., thermal stress). This phenomenon of plasticity is common to all vertebrates (Schiaffino and Reggiani 1996). However, there exists a large variation in the magnitude of adaptability among species, and between individuals within a species. Such variability partly explains the marked differences in aspects of physical performance, such as endurance or strength, between individuals, as well as the relationship of skeletal muscle fiber type composition to certain chronic disease states, including obesity and insulin resistance.

In most mammals, skeletal muscle comprises about 55% of individual body mass and plays vital roles in locomotion, heat production during periods of cold stress, and overall metabolism (Figure 1). Thus, knowledge of the molecular and cellular events that regulate skeletal muscle plasticity can define the potential for adaptation in performance and metabolism, as well as lead to the discovery of novel genes and pathways in common clinical disease states.

Figure 1: Individual bundles of muscle fibers are called fascicles. The cell membrane surrounding the muscle cell is the sarcolemma, and beneath the sarcolemma lies the sarcoplasm, which contains the cellular proteins, organelles, and myofibrils. The myofibrils are composed of two major types of protein filaments: the thinner actin filament, and the thicker myosin filament. The arrangement of these two protein filaments gives skeletal muscle its striated appearance.

How Is Skeletal Muscle Fiber Type Classified?

Much of our early understanding of the plasticity of skeletal muscle has been derived from studies undertaken by exercise physiologists (e.g., Holloszy 1967). With the application of surgical techniques to exercise physiology in the late 1960s (Bergstrom and Hultman 1966), it became possible to obtain biopsy samples (~150 mg) of human skeletal muscle, and by means of histological and biochemical analyses, specific morphological, contractile, and metabolic properties were identified. In 1873, the French anatomist Louis Antoine Ranvier had already observed that some muscles of the rabbit were redder in color, and contracted in a slower, more sustained manner, than paler muscles of the same animal. These early observations formed the basis of the classical terminology of red and white muscle fibers, which was subsequently found to be related to myoglobin (an iron-containing oxygen-transport protein in the red cells of the blood) content (Needham 1926). Based upon histochemical staining (Engel 1962), muscle fibers are now commonly distinguished as slow-twitch (ST), which stain dark or red, and fast-twitch (FT), which stain light or pale. In humans, a further subdivision of the FT fibers is made (Brooke and Kasier 1970), whereby the more aerobic (or oxidative) FT fiber is designated FTa, and the more anaerobic (glycolytic) fiber is termed FTb. Under aerobic conditions (sufficient oxygen supply to the working muscles), energy is produced without the production of lactate. Under anaerobic conditions (insufficient oxygen supply to the working muscles), energy is produced via the glycolytic pathway, which results in lactate accumulation and in turn limits anaerobic exercise. Thus, muscle fibers can be classified in terms of contractile and metabolic properties (Table 1).

Table 1. Contractile Characteristics, Selected Enzyme Activities, and Morphological and Metabolic Properties of Human Skeletal Muscle Fiber Types

All individuals have different capacities to perform aerobic or anaerobic exercise, partly depending on their muscle fiber composition. In untrained individuals, the proportion of ST fibers in the vastus lateralis muscle (the largest of the quadriceps muscles and the most commonly studied muscle in humans), is typically around 55%, with FTa fibers being twice as common as FTb fibers (Saltin et al. 1977). While marked differences in the metabolic potentials between FTa and FTb fibers are observed in untrained humans, the absolute level for the activities of oxidative and glycolytic enzymes in all fiber types is large enough to accommodate substantial aerobic and anaerobic metabolism (Saltin et al. 1977). While there is a large degree of homogeneity within individual skeletal muscles from rodents (Delp and Duan 1996), this is not the case for humans (Saltin et al. 1977). The dramatic heterogeneity of fiber type composition between people may explain their remarkable variation in exercise performance.

Does Muscle Fiber Type Composition Influence Athletic Performance?

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In this regard, the results of Fink et al. (1977) are important. These researchers determined the fiber composition from the gastrocnemius muscle (the muscle of the calf of the leg) of 14 elite male long distance runners, 18 good (but not world-class) male long distance runners, and 19 untrained men. The elite group included Olympic medal winners (Figure 2) and American record holders at the time. Muscle from the elite runners contained a larger proportion of ST fibers than either the good runners or the untrained men (79.0% ± 3.5% versus 61.8% ± 2.9% versus 57.7% ± 2.5% respectively; p < 0.05). The values found for several of the elite runners were the highest observed in human muscle (> 92% ST). Moreover, the ST fibers from the elite runners were 29% larger than FT fibers (p < 0.05), and both ST and FT fibers were larger in the good runners than in the untrained men. Because of the marked hypertrophy (bulk increase) of the ST fibers in the elite runners, the cross-sectional area composed of these fibers was greater than either the good runners or the untrained subjects (82.9% ± 3.1% versus 62.1% ± 2.6% versus 60.0% ± 2.7% respectively; p < 0.05). When the data from the elite and good runners was combined, a positive correlation between the proportion of ST fibers and the best 6-mile performance time was noted (r = -0.62, p < 0.05).

However, fiber type alone did not determine the performances of the elite athletes. For example, two athletes with similar best times for the 42.2 km marathon distance (approximately 2 hr 18 min) had 50% versus 98% ST muscle fibers. Subsequent work (Foster et al. 1978) revealed that endurance running performance was better related to an athlete's maximal O2 uptake (VO2max; r= -0.84, -0.87, and -0.88 for 1-, 2-, and 6-mile times, respectively). Indeed, while an athlete's muscle fiber type is an important morphological component and is related to several contractile and metabolic properties (see Table 1), other physiological factors (e.g., VO2max, maximal cardiac output, and speed/power output at the lactate threshold) are more likely to determine the upper limits of endurance capacity (Coyle 1995; Hawley and Stepto 2001).

Do Alterations in Skeletal Muscle Fiber Type Contribute to Metabolic Disease?

The close coupling between muscle fiber type and associated morphological, metabolic, and functional properties is not confined to athletic ability. Insulin sensitivity also correlates with the proportion of ST oxidative fibers (Lillioja et al. 1987). Specifically, insulin-stimulated glucose transport is greater in skeletal muscle enriched with ST muscle fibers (Henriksen et al. 1990; Song et al. 1999; Daugaard et al. 2000), thus priming ST muscle for accelerated glucose uptake and metabolism. A shift in fiber distribution from ST to FT fibers gives rise to altered activities of key oxidative and glycolytic enzymes (Pette and Hofer 1980). Indeed, the ratio between glycolytic and oxidative enzyme activities in the skeletal muscle of non-insulin-dependent diabetic or obese individuals is related to insulin resistance (Simoneau et al. 1995; Simoneau and Kelley 1997). Similarly, with ageing and physical inactivity, two other conditions associated with ST-toFT fiber-type transformation, oxidative capacity and insulin sensitivity, are diminished (Papa 1996).

Genes That Define Skeletal Muscle Phenotype

Skeletal muscle fiber-type phenotype is regulated by several independent signaling pathways (Figure 3). These include pathways involved with the Ras/mitogen-activated protein kinase (MAPK) (Murgia et al. 2000), calcineurin (Chin et al. 1998; Naya et al. 2000), calcium/calmodulin-dependent protein kinase IV (Wu et al. 2002), and the peroxisome proliferator ? coactivator 1 (PGC-1) (Lin et al. 2002). The Ras/MAPK signaling pathway links the motor neurons and signaling systems, coupling excitation and transcription regulation to promote the nerve-dependent induction of the slow program in regenerating muscle (Murgia et al. 2000). Calcineurin, a Ca2+/calmodulin-activated phosphatase implicated in nerve activity-dependent fiber-type specification in skeletal muscle, directly controls the phosphorylation state of the transcription factor NFAT, allowing for its translocation to the nucleus and leading to the activation of slow-type muscle proteins in cooperation with myocyte enhancer factor 2 (MEF2) proteins and other regulatory proteins (Chin et al. 1998; Serrano et al. 2001). Calcium-dependent Ca2+/calmodulin kinase activity is also upregulated by slow motor neuron activity, possibly because it amplifies the slow-type calcineurin-generated responses by promoting MEF2 transactivator functions and enhancing oxidative capacity through stimulation of mitochondrial biogenesis (Wu et al. 2002).

Figure 3. Exercise-Included Signaling Pathways in Skeletal Muscle That Determine Specialized Characteristics of ST and FT Muscle Fibers Contraction-induced changes in intracellular calcium or reactive oxygen species provide signals to diverse pathways that include the MAPKs, calcineurin and calcium/calmodulin-dependent protein kinase IV to activate transcription factors that regulate gene expression and enzyme activity in skeletal muscle.

PGC1-a, a transcriptional coactivator of nuclear receptors important to the regulation of a number of mitochondrial genes involved in oxidative metabolism, directly interacts with MEF2 to synergistically activate selective ST muscle genes and also serves as a target for calcineurin signaling (Lin et al. 2002; Wu et al. 2001). New data presented in this issue of PLoS Biology (Wang et al. 2004) reveals that a peroxisome proliferator-activated receptor d (PPARd)-mediated transcriptional pathway is involved in the regulation of the skeletal musclefiber phenotype. Mice that harbor an activated form of PPARd display an “endurance” phenotype, with a coordinated increase in oxidative enzymes and mitochondrial biogenesis and an increased proportion of ST fibers. Thus—through functional genomics—calcineurin, calmodulin-dependent kinase, PGC-1a, and activated PPARd form the basis of a signaling network that controls skeletal muscle fiber-type transformation and metabolic profiles that protect against insulin resistance and obesity.

The transition from aerobic to anaerobic metabolism during intense work requires that several systems are rapidly activated to ensure a constant supply of ATP for the working muscles. These include a switch from fat-based to carbohydrate-based fuels, a redistribution of blood flow from nonworking to exercising muscles, and the removal of several of the byproducts of anaerobic metabolism, such as carbon dioxide and lactic acid. Some of these responses are governed by transcriptional control of the FT glycolytic phenotype. For example, skeletal muscle reprogramming from a ST glycolytic phenotype to a FT glycolytic phenotype involves the Six1/Eya1 complex, composed of members of the Six protein family (Grifone et al. 2004). Moreover, the Hypoxia Inducible Factor-1a (HIF-1a) has been identified as a master regulator for the expression of genes involved in essential hypoxic responses that maintain ATP levels in cells. In this issue of PLoS Biology (Mason et al. 2004), a key role for HIF-1a in mediating exercise-induced gene regulatory responses of glycolytic enzymes is revealed. Ablation of HIF-1a in skeletal muscle was associated with an increase in the activity of rate-limiting enzymes of the mitochondria, indicating that the citric acid cycle and increased fatty acid oxidation may be compensating for decreased flow through the glycolytic pathway in these animals. However, hypoxia-mediated HIF-1a responses are also linked to the regulation of mitochondrial dysfunction through the formation of excessive reactive oxygen species in mitochondria.

Can You Become a Slow-Twitcher?

With the 2004 Olympics still fresh on our minds, many will ask: Who has the right stuff to go the distance? Athletes like Olympic champion Frank Shorter are clearly exceptional and represent an extreme in human skeletal muscle phenotype. Realistically, few of us can ever hope to run a marathon in world-class time. However, there may be cause for some optimism for the average mortal, since endurance exercise training in healthy humans leads to fiber-type specific increases in the abundance of PGC-1 and PPAR-a protein in skeletal muscle (Russell et al. 2003). Moreover, functional genomics support the concept that skeletal muscle remodeling to a ST phenotype, either through activated calcineurin or PPARd, can protect against the development of dietary-induced insulin resistance (Ryder et al. 2003) and obesity (Wang et al. 2004). The results of these studies have clinical relevance since insulin-resistant elderly subjects and offspring of patients with type 2 diabetes mellitus have skeletal muscle mitochondrial dysfunction (Petersen et al. 2003; Petersen et al. 2004). Clearly, further translational studies in humans are required to test the hypothesis that increasing the proportion of ST oxidative muscle fibers will overcome the mitochondrial dysfunction and metabolic defects associated with insulin-resistant states.

Abbreviations

FT, fast-twitch; FTa, aerobic FT fiber; FTb, anaerobic FT fiber; HIF-1a, Hypoxia Inducible Factor-1a; MAPK, mitogen-activated protein kinase; MEF2, myocyte enhancer factor 2; PGC-1, peroxisome proliferator ? coactivator 1; PPARd, peroxisome proliferator-activated receptor d; ST, slow-twitch; VO2max, maximal O2 uptake

Copyright: © 2004 Juleen R. Zierath and John A. Hawley. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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by EricT

Journal of the International Society of Sports Nutrition January 2010

Caffeine Position Statement

The position of The Society regarding caffeine supplementation and sport performance is summarized by the following seven points: 1.) Caffeine is effective for enhancing sport performance in trained athletes when consumed in low-to-moderate dosages (~3-6 mg/kg) and overall does not result in further enhancement in performance when consumed in higher dosages ( ≥ 9 mg/kg). 2.) Caffeine exerts a greater ergogenic effect when consumed in an anhydrous state as compared to coffee. 3.) It has been shown that caffeine can enhance vigilance during bouts of extended exhaustive exercise, as well as periods of sustained sleep deprivation. 4.) Caffeine is ergogenic for sustained maximal endurance exercise, and has been shown to be highly effective for time-trial performance. 5.) Caffeine supplementation is beneficial for highintensity exercise, including team sports such as soccer and rugby, both of which are categorized by intermittent activity within a period of prolonged duration. 6.) The literature is equivocal when considering the effects of caffeine supplementation on strength-power performance, and additional research in this area is warranted. 7.) The scientific literature does not support caffeine-induced diuresis during exercise, or any harmful change in fluid balance that would negatively affect performance.

Introduction

Research on the physiological effects of caffeine in relation to human sport performance is extensive. In fact, investigations continue to emerge that serve to delineate and expand existing science. Caffeine research in specific areas of interest, such as endurance, strength, team sport, recovery, and hydration is vast and at times, conflicting. Therefore, the intention of this position statement is to summarize and highlight the scientific literature, and effectively guide researchers, practitioners, coaches, and athletes on the most suitable and efficient means to apply caffeine supplementation to mode of exercise, intensity, and duration.

Caffeine and mechanism of action

To understand the effect of caffeine supplementation in its entirety it is necessary to discuss its chemical nature and how the compound is physiologically absorbed into the body. Caffeine is quickly absorbed through the gastrointestinal tract [1-3], and moves through cellular membranes with the same efficiency that it is absorbed and circulated to tissue [4, 5]. Caffeine (1,3,7-trimethylxanthine) is metabolized by the liver and through enzymatic action results in three metabolites: paraxanthine, theophylline, and theobromine [1, 6-8]. Elevated levels can appear in the bloodstream within 15-45 min of consumption, and peak concentrations are evident one hour post ingestion [1, 3, 9, 10]. Due to its lipid solubility, caffeine also crosses the bloodbrain barrier without difficulty [5, 11]. Meanwhile, caffeine and its metabolites are excreted by the kidneys, with approximately 3-10% expelled from the body unaltered in urine [1, 7, 12]. Based on tissue uptake and urinary clearance circulating concentrations are decreased by 50-75% within 3-6 hours of consumption [3, 13]. Thus, clearance from the bloodstream is analogous to the rate at which caffeine is absorbed and metabolized.

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Clearly, one of caffeine’s primary sites of action is the central nervous system (CNS). Moreover, theophylline and paraxanthine can also contribute to the pharmacological effect on the CNS through specific signaling pathways [5]. However, as noted above, rarely is there a single mechanism that fully explains the physiological effects of any one nutritional supplement. Because caffeine easily crosses the blood brain barrier as well as cellular membranes of all tissues in the body [15], it is exceedingly difficult to determine in which system in particular (i.e. nervous or skeletal muscle) caffeine has the greatest effect [15].

In addition to its impact on the CNS, caffeine can affect substrate utilization during exercise. In particular, research findings suggest that during exercise caffeine acts to decrease reliance on glycogen utilization and increase dependence on free fatty acid mobilization [16-19]. Essig and colleagues [19] reported a significant increase in intramuscular fat oxidation during leg ergometer cycling when subjects consumed caffeine at an approximate dose of 5 mg/kg. Additionally, Spriet et al. [18] demonstrated that following ingestion of a high dose of caffeine (9 mg/kg) net glycogenolysis was reduced at the beginning of exercise (cycling to exhaustion at 80% VO2max). Consequently, performance was significantly improved and results of this study [18] suggested an enhanced reliance on both intra- and extramuscular fat oxidation.

Another possible mechanism through which caffeine may improve endurance performance is by increasing the secretion of β-endorphins. Laurent et al. [20] demonstrated that when compared to the placebo group caffeine consumption (6 mg/kg) significantly increased plasma β-endorphin concentrations following two hours of cycling at 65% VO2peak and a subsequent bout of high intensity sprint activity. It has been established that plasma endorphin concentrations are enhanced during exercise and their analgesic properties may lead to a decrease in pain perception [21].

Research has also demonstrated that caffeine may result in alterations of neuromuscular function and/or skeletal muscular contraction [22, 23]. For example, Kalmar and Cafarelli [22] indicated a moderate dose of caffeine (6 mg/kg) significantly enhanced both isometric leg extension strength as well as the time to fatigue during a submaximal isometric leg extension.

Caffeine consumption also promotes a significant thermogenic response. In fact, caffeine consumption at a dose of 100 mg resulted in a significant thermogenic effect despite the fact that subjects in that particular investigation had a habitual caffeine intake of 100-200 mg per day [24]. The increase in energy expenditure subsequent to caffeine ingestion had not returned to baseline 3 hours post-consumption.

Overall, the findings of research studies involving caffeine supplementation and physical performance indicate a combined effect on both the central and peripheral systems. Therefore, it is possible that caffeine acts on the central nervous system as an adenosine antagonist, but may also have an effect on substrate metabolism and neuromuscular function. Research in all areas of caffeine supplementation continues to emerge and it is necessary to understand that as a supplement, caffeine has wide ranging physiological effects on the body that may or may not result in an enhancement in performance. Caffeine supplementation can improve sport performance but this is dependent upon various factors including, but not limited to, the condition of the athlete, exercise (i.e. mode, intensity, duration) and dose of caffeine.

Caffeine and Cognitive Performance

Caffeine has been shown to enhance several different modes of exercise performance including endurance [8, 16, 25-28], high-intensity team sport activity [29-34], and strengthpower performance [30, 35]. Additionally, the use of caffeine has also been studied for its contribution to special force operations, which routinely require military personnel to undergo periods of sustained vigilance and wakefulness. In a series of investigations, McLellan et al. [36-38] examined the effects of caffeine in special force military units who routinely undergo training and real life operations in sleep deprived conditions, where alertness and diligent observation are crucial to assignment.

In the McLellan et al. investigations [36-38], soldiers performed a series of tasks over several days, where opportunities for sleep were exceedingly diminished. Experimental challenges included a 4 or 6.3 km run, as well as tests for marksmanship, observation and reconnaissance, and psychomotor vigilance [36-38]. During periods of sustained wakefulness, subjects were provided caffeine in the range of 600-800 mg, and in the form of chewing gum.

The caffeine supplement was consumed in this manner as it has been shown to be more readily absorbed, than if it was provided within a pill based on the proximity to the buccal tissue [39]. In all three studies [36-38], vigilance was either maintained or enhanced for caffeine conditions in comparison to placebo. Additionally, physical performance measures such as run times and completion of an obstacle course were also improved by the effects of caffeine consumption [36, 38]

Lieberman et al. [40] examined the effects of caffeine on cognitive performance during sleep deprivation in U.S. Navy Seals [40]. However, in this investigation [40] the participants were randomly assigned varying doses of caffeine in capsule form delivering either 100, 200, or 300 mg. In a manner similar to previous investigations, participants received either the caffeine or placebo treatment and one hour post consumption performed a battery of assessments related to vigilance, reaction time, working memory, and motor learning and memory. In addition, the participants were evaluated at eight hours post consumption to assess duration of treatment effect in parallel to the half-life of caffeine, in a manner similar to a study conducted by Bell et al. [41].

As to be expected, caffeine had the most significant effect on tasks related to alertness[40]. However, results were also significant for assessments related to vigilance and choice reaction time for those participants who received the caffeine treatment. Of particular importance are the post-hoc results for the 200 and 300 mg doses. Specifically, there was no statistical advantage for consuming 300, as opposed to 200 mg [40]. In other words, those trainees who received the 300 mg (~4 mg/kg) dose did not perform significantly better than those participants who received 200 mg (~2.5 mg/kg). Meanwhile, a 200 mg dose did result in significant improvements in performance, as compared to 100 mg. In fact, it was evident from post-hoc results that 100 mg was at no point statistically different or more advantageous for performance than a placebo. These studies [36-38, 40] demonstrate the effects of caffeine on vigilance and reaction time in a sleep deprived state, in a distinct and highly trained population. These findings suggest that the general population may benefit from similar effects of caffeine, but at moderate dosages in somewhat similar conditions where sleep is limited.

An additional outcome of the Lieberman et al. [40] study is the fact that caffeine continued to enhance performance in terms of repeated acquisition (assessment of motor learning and short-term memory) and Profile of Mood States fatigue eight hours following consumption. These results are in agreement with Bell et al. [41], where aerobic capacity was assessed 1, 3, and 6 hours following caffeine consumption (6 mg/kg). Caffeine had a positive effect on performance for participants classified as users ( ≥ 300 mg/d) and nonusers ( ≤ 50 mg/d); however, nonusers had a treatment effect at 6 hours post-consumption, which was not the case for users – this group only had a significant increase in performance at 1 and 3 hours postconsumption. Taken together, results of these studies [40, 41] provide some indication, as well as application for the general consumer and athlete. Specifically, while caffeine is said to have a half-life of 2.5-10 hours [42], it is possible performance-enhancing effects may extend beyond that time point as individual response and habituation among consumers varies greatly.

Finally, it was suggested by Lieberman and colleagues [40] that the performance enhancing
effects of caffeine supplementation on motor learning and short-term memory may be related to an increased ability to sustain concentration, as opposed to an actual effect on working memory. Lieberman et al. [40] attributed the effects of caffeine to actions on the central nervous system, specifically the supplement’s ability to modulate inhibitory actions, especially those of adenosine. In fact, it was suggested that because caffeine has the ability to act as an antagonist to adenosine, alterations in arousal would explain the compound’s discriminatory effect on behaviors relating vigilance, fatigue and alertness [40].

Recently, it was also suggested that caffeine can positively affect both cognitive and endurance performance [25]. Trained cyclists, who were moderate caffeine consumers (approximated at 170 mg/d) participated in three experimental trials consisting of 150 min of cycling at 60% VO2max followed by five minutes of rest and then a ride to exhaustion at 75% VO2max. On three separate days, subjects consumed a commercially available performance bar that contained either 44.9 g of carbohydrates and 100 mg of caffeine, non-caffeinated carbohydrate and isocaloric, or flavored water. Results from a repeated series of cognitive function tests favored the caffeine treatment in that subjects performed significantly faster during both the Stroop and Rapid Visual Information Processing Task following 140 min of submaximal cycling as well as after a ride to exhaustion. In addition, participant time increased for the ride to exhaustion on the caffeine treatment, as compared to both the non-caffeinated bar and flavored water [25].

Overall, the literature examining the effects of caffeine on anaerobic exercise is equivocal, with some studies reporting a benefit [29-32, 43, 44] and others suggesting that caffeine provides no significant advantage [45, 46]. As with all sports nutrition research, results can vary depending on the protocol used, and in particular, the training status of the athlete as well as intensity and duration of exercise. For example, Crowe et al. [47] examined the effects of caffeine at a dose of 6 mg/kg on cognitive parameters in recreationally active team sport individuals, who performed two maximal 60-second bouts of cycling on an air-braked cycle ergometer. In this investigation [47], untrained, moderately habituated (80-200 mg/d) participants completed three trials (caffeine, placebo, control) and underwent cognitive assessments prior to consumption of each treatment, post-ingestion at approximately 72-90 min, and immediately following exercise. Cognitive testing consisted of simple visual reaction time and number recall tests. Participants performed two 60-second maximal cycle tests interspersed by three min of passive rest. The results were in contrast to other studies that investigated cognitive parameters and the use of caffeine [25, 36-38, 40] in that caffeine had no significant impact on reaction time or number recall, and there was no additional benefit for measurements of power. In fact, in this study [47], the caffeine treatment resulted in significantly slower times to reach peak power in the second bout of maximal cycling.

Elsewhere, Foskett and colleagues [48] investigated the potential benefits of caffeine on cognitive parameters and intermittent sprint activity and determined that a moderate dose (6 mg/kg) of caffeine improved a soccer player’s ball passing accuracy and control, thereby attributing the increase in accuracy to an enhancement of fine motor skills.

Based on some of the research cited above, it appears that caffeine is an effective ergogenic aid for individuals either involved in special force military units or who may routinely undergo stress including, but not limited to, extended periods of sleep deprivation. Caffeine in these conditions has been shown to enhance cognitive parameters of concentration and alertness. It has been shown that caffeine may also benefit endurance athletes both physically and cognitively. However, the research is conflicting when extrapolating the benefits of caffeine to cognition and shorter bouts of high-intensity exercise. A discussion will follow examining the effects of caffeine and high-intensity exercise in trained and non-trained individuals, which may partially explain a difference in the literature as it pertains to short-term high-intensity exercise.

Caffeine and Carbohydrate

An extensive body of research has provided compelling evidence to support the theory that caffeine’s primary ergogenic mode of action is on the CNS. However, caffeine may also be 1979, Ivy et al. [16] published an investigation that supported the latter concept [16]. Trained cyclists were subjected to two hours of isokinetic cycling and received three treatments on separate occasions: caffeine, glucose polymer, and placebo. Caffeine was consumed in an absolute dose of 500 mg, 250 mg one hour prior to cycling and the remainder in divided doses beginning 15 min prior to onset of exercise. Results indicated a significant advantage in work produced following caffeine consumption. Specifically, work produced was 7.4% greater over control and 5.3% greater than the glucose polymer treatment. Midway into two hours of cycling, fat oxidation was significantly increased above that of the control and glucose trials. Fat oxidation was maintained during the last hour of exercise and it was suggested this substrate utilization was in part responsible for the increased work production. Moreover, following caffeine consumption and a two-hour bout of isokinetic cycling, plasma free fatty acid (FFA) levels were 30% greater than those for placebo.

Results of the Ivy et al. [16] study, as well as others [18, 49], provide a persuasive argument for the use of caffeine as a means to increase work production by way of increased fat oxidation. However, Ivy et al. [16] suggested caffeine also had an effect on the CNS. Specifically, when subjects consumed caffeine, they began the exercise bout at a higher intensity, but perceived this effort to be no different than when they ingested the placebo and glucose conditions. Furthermore, Ivy et al. [16] also suggested participants were able to perform at this increased work rate due to a greater ability to rely on fat metabolism.

In a study performed by Jackman et al. [50] subjects consumed either caffeine at a dose of 6 mg/kg or placebo and performed high-intensity work with both the power output and total work done held constant. In total, subjects performed approximately 4-6 min of high intensity work (2-min bouts of cycling interspersed with 6 min of rest and a final ride to voluntary exhaustion). Results indicated an increase in plasma epinephrine for the caffeine treatment, which is consistent with other caffeine supplementation studies [8, 29, 46, 51, 52]. Even though epinephrine promotes glycogenolysis, the data from this study demonstrated an increase in both muscle lactate and plasma epinephrine without a subsequent affect on net muscle glycogenolysis following the first two bouts of controlled maximal cycling. Epinephrine can up-regulate lipolysis in adipocytes as well as glycogenolysis in muscle and liver; therefore, a direct relationship between increases in the hormone and enhanced substrate catabolism is somewhat ambiguous. Greer et al. [53] reported in 2000 that theophylline is more potent than caffeine as an adenosine antagonist. Whereas adenosine can act to inhibit lipolysis in vivo [54], theophylline
consumption at 4.5 mg/kg resulted in increased blood glycerol levels, even more so than caffeine at 6 mg/kg and placebo. Indeed, it is possible that both theophylline and caffeine act to regulate substrate metabolism via mechanisms other than those that are catecholamine-induced [53].

Graham and Spriet [8] examined varying doses of caffeine consumption at 3, 6, and 9 mg/kg on endurance capacity (run to exhaustion at 85% VO2max). Results from this study demonstrated an enhancement in performance, but only with the 3 and 6 mg/kg dose. Concurrently, the 6 and 9 mg/kg dosages were the only measured quantities that resulted in increased plasma epinephrine levels, with significant increases in glycerol and free fatty acids measured only at the 9 mg/kg dose. Therefore, results of this investigation present quite a paradox in that a low dose of caffeine (3 mg/kg) was adequate for enhancing performance, but did not lead to increased levels of epinephrine or subsequent effect of free fatty acid mobilization.

Hulston and Jeukendrup [55] published data that indicated caffeine at 5.3 mg/kg co-ingested with a 6.4% glucose solution had no significant effect on increasing plasma FFA levels or glycerol concentrations, nor did it substantially enhance rates of whole-body fat oxidation during endurance exercise even though performance was significantly improved with the caffeine + glucose solution [55]. Therefore, the results of some research studies lend substantiation to the premise that caffeine may act to increase performance by altering substrate utilization [16, 18], while results of additional investigations serve to suggest other mechanisms of action [50, 56, 57].

Carbohydrate consumption during exercise can decrease the body’s dependence on endogenous carbohydrate stores and lead to enhanced endurance performance [58, 59]. Therefore, it is beneficial to determine an optimal method of enhancing rates of exogenous carbohydrate delivery and oxidation. Exogenous carbohydrate delivery is determined by various factors including, but not limited to, the rate of gastric emptying and intestinal absorption [58]. However, it has been suggested that during exercise intestinal absorption seems to have the greatest influence on the rate of exogenous carbohydrate oxidation [58, 60].

In 1987 Sasaki et al. [61] reported that in trained distance runners 100g sucrose in combination with approximately 400 mg (~6 mg/kg) of caffeine had no additive effect on endurance performance, when compared to consumption of either substrate alone. In addition, Jacobson et al. [62] reported that caffeine (6 mg/kg) combined with carbohydrate (2.6 g/kg), had no significant enhancement on exercise performance or substrate utilization in trained cyclists.

However, Yeo et al. [63] reported that during the final 30 min of a 2-hr steady state bout of cycling (64% V02max) a 5.8% glucose solution (48 g/hr), in addition to 5 mg/kg of caffeine, significantly enhanced exogenous carbohydrate oxidation (~26% higher than glucose alone). It was suggested by these authors [63] and others [64] that this was the result of enhanced intestinal glucose absorption.

Finally, Hulston et al. [55] found that a 6.4% glucose solution in addition to a moderate dose of caffeine (5.3 mg/kg) significantly enhanced time trial performance in trained cyclists. The caffeine-glucose solution improved performance by 9% when compared to placebo and 4.6% in comparison to glucose. However, it was also reported that caffeine consumption had no affect on exogenous carbohydrate oxidation [55]. In addition, Kovacs et al. [56] demonstrated that after consuming caffeine at a dose of either 225 mg or 320 mg in combination with a carbohydrate-electrolyte solution participants were able to perform significantly faster during a time trial protocol. In contrast, Desbrow and colleagues [65] found a low dose of caffeine (1.5 and 3 mg/kg), in addition to glucose consumption every 20 min had no significant affect on time trial performance nor did caffeine in combination with glucose, affect maximal exogenous carbohydrate oxidation [65].

Strategies that may enhance exogenous carbohydrate absorption and oxidation during exercise are clearly defined in the literature [58-60]. The combined effect of caffeine and exogenous carbohydrate intake during endurance exercise is less understood. Therefore, future research should continue to investigate this potential ergogenic effect, as well as any corresponding physiological mechanisms.

Caffeine, carbohydrate, and recovery

Recently, the combination of caffeine and carbohydrate has been examined as a potential means to enhance recovery by increasing the rate of glycogen synthesis post exercise. In 2004, Battram et al. [66] demonstrated that following carbohydrate depleting exercise, exogenous carbohydrate and caffeine supplementation did not hinder either proglycogen (small particles) or macroglycogen (large, acid soluble) production. It was postulated that the fractions respond differently to the recovery phase of exercise and thus glycogen resynthesis. Prior to, as well as during exhaustive exercise, subjects consumed in divided doses a total of 6 mg/kg of either caffeine or placebo in capsule form. Following exercise and throughout the 5-hr recovery period subjects consumed in total 375 g of exogenous carbohydrate. Muscle biopsies and blood samples revealed caffeine ingestion did not obstruct proglycogen or macroglycogen resynthesis following exhaustive, glycogen depleting exercise [66]. It is imperative to recognize that each person may respond differently to supplements and compounds containing caffeine. An individual at rest, and even sedentary in nature, is likely to have a different response compared to a trained, conditioned athlete, or physically active person. According to the data presented by Battram et al. [66], caffeine supplementation followed by exogenous carbohydrate in the recovery phase did not negatively impact glycogen resynthesis.

In a more recent study, Pedersen et al. [67] investigated the role of caffeine plus carbohydrate as a post-exercise method for enhancing glycogen synthesis. Following an overnight fast, trained cyclists and triathletes performed exhaustive exercise on a cycle ergometer at 70% VO2peak. In a crossover manner, subjects consumed 4 g CHO/kg (gels, sports bars, carbohydrate-containing drinks) and on another day 4 g CHO/kg in the same form, in addition to caffeine at 8 mg/kg, which was added to a carbohydrate-containing sports drink and consumed in two divided doses. Following a 4-hr recovery period, results were definitive in that glycogen resynthesis was increased by 66% for the carbohydrate-caffeine treatment, as compared to the carbohydrate-only condition [67].

The data presented in these studies [66, 67] indicate that caffeine is not detrimental to glycogen repletion, and in combination with exogenous carbohydrate may actually act to enhance synthesis in the recovery phase of exercise. From a practical standpoint, however, it should be considered that most athletes or recreationally trained individuals would choose to supplement with caffeine prior to competition for the purpose of enhancing performance. Moreover, clearance of caffeine in the bloodstream occurs between 3 and 6 hours, and may extend beyond that time point depending on the individual. Therefore, caffeine consumption pre and post-exercise would have to be precisely timed so as not to interrupt sleep patterns of the athlete, which in itself could negatively affect overall recovery.

Caffeine: Form, Dose, and Endurance Exercise

Caffeinated coffee, anhydrous caffeine and endurance exercise

Various methods of caffeine supplementation have been explored and results have provided considerable insight into appropriate form and dosage of the compound. One of the most acknowledged studies, published by Graham et al. [26] demonstrated a range of effects when caffeine (at 4.45 mg/kg) was consumed in varying forms. In their study, aerobically conditioned runners performed five treadmill runs to exhaustion at approximately 85% VO2max after receiving one of the following treatments 60 minutes prior: caffeine capsules plus water, regular coffee, decaffeinated coffee, decaffeinated coffee plus caffeine in capsule form, and placebo. Caffeine in capsule form significantly increased work capacity allowing them to run an additional 2-3 km [26], as compared to the four other treatments.

It was also proposed by Graham and colleagues [26] that perhaps other indistinguishable compounds within coffee rendered caffeine less effective than when consumed in anhydrous form. This suggestion was supported by de Paulis et al. [68] in a 2002 publication which indicated derivatives of chlorogenic acids are produced from the roasting process of coffee. In turn, these derivatives may have the potential for altering the affects of caffeine as an adenosine antagonist, possibly reducing the drug’s ability to diminish the inhibitory action of adenosine [68].

As such, McLellan and Bell [27] examined whether a morning cup of coffee just prior to anhydrous caffeine supplementation would have any negative impact on the compound’s ergogenic effect. Subjects were physically active and considered to be moderate-to-high daily consumers of caffeine. In a crossover design consisting of six separate testing days, rides to exhaustion were performed at approximately 80% VO2max. Subjects consumed one cup of coffee with a caffeine dosage that was approximately 1.0 mg/kg, and 30 min later ingested either of the following six conditions: decaffeinated coffee + placebo capsules; decaffeinated coffee + caffeine capsules at 5 mg/kg, coffee at 1.1 mg/kg + caffeine capsules at 5 mg/kg, coffee + caffeine capsules at 3 mg/kg, coffee + caffeine capsules at 7 mg/kg, water + caffeine capsules at 5 mg/kg. The results indicated caffeine supplementation significantly increased exercise time to exhaustion regardless of whether caffeine in anhydrous form was consumed after a cup of regular or decaffeinated coffee [27]. Taken together the available research suggests that caffeine supplemented in capsule form in a range of 3 to 7 mg/kg provided an average increase in performance of 24% over placebo [27]. While caffeine supplemented from a cup of coffee might be less effective than when consumed in anhydrous form, coffee consumption prior to anhydrous upplementation does not interfere with the ergogenic effect provided from low to moderate dosages.

Caffeinated coffee, decaffeinated coffee, and endurance exercise

Wiles et al. [69] examined the effect of 3 g of coffee, which contained approximately 150-200 mg of caffeine, on treadmill running time. This form and dose was used to mimic the real life habits of an athlete prior to competition. Subjects performed a 1500-m treadmill time trial. Ten subjects with a VO2max of 63.9-88.1 ml/kg/min also completed a second protocol designed to simulate a “finishing burst” of approximately 400 m. In addition, six subjects also completed a third protocol to investigate the effect of caffeinated coffee on sustained highintensity exercise. Results indicated a 4.2 s faster run time for the caffeinated coffee treatment, as compared to decaffeinated coffee. For the “final burst” simulation, all 10 subjects achieved significantly faster run speeds following ingestion of caffeinated coffee. Finally, during the sustained high-intensity effort, eight of ten subjects had increased VO2 values [69].

In a more recent publication, Demura et al. [70] examined the effect of coffee, which contained a moderate dose of caffeine at 6 mg/kg, on submaximal cycling. Subjects consumed either caffeinated or decaffeinated coffee 60 min prior to exercise. The only significant finding was a decreased RPE for the caffeinated coffee as compared to the decaffeinated treatment [70].

Coffee contains multiple biologically active compounds; however, it is unknown if these compounds are of benefit to human performance [71]. However, it is apparent that consuming an anhydrous form of caffeine, as compared to coffee, prior to athletic competition would be more advantageous for enhancing sport performance. Nevertheless, the form of supplementation is not the only factor to consider as appropriate dosage is also a necessary variable.

Low, moderate, and high dosages of anhydrous caffeine and endurance exercise Pasman and colleagues [28] examined the effect of varying quantities of caffeine on endurance performance. Nine aerobically trained cyclists performed six rides to exhaustion at approximately 80% maximal power output. Subjects consumed four treatments on separate occasions: placebo, 5, 9, and 13 mg/kg of caffeine in capsule form. Results were conclusive in that all three caffeine treatments significantly increased endurance performance as compared to placebo. Moreover, there was no statistical difference between caffeine trials. Therefore, increases in performance were comparable for both the moderate dose of 5 mg/kg as well as the high dose of 13 mg/kg [28]. The average increase in performance time was 27% for all three caffeine treatments [28], and are analogous to the U.S. Navy SEAL training study published by Lieberman et al [40]. Results from that paper indicated no statistical advantage for consuming an absolute dose of 300 mg, as opposed to 200 mg. However, the 200 mg dose did result in significant improvements in performance, as compared to 100 mg, and 100 mg was at no point statistically different or more advantageous for performance than placebo [40]

As previously discussed, Graham and Spriet [8], examined the effects of varying quantities of caffeine on metabolism and endurance exercise and reported a significant increase in performance for a low (3 mg/kg) and moderate dose (6 mg/kg) of caffeine but not for 9 mg/kg. In response to why a low and moderate dose of caffeine significantly enhanced performance, as compared to a high dose, Graham and Spriet [8] suggested that, “On the basis of subjective reports of some subjects it would appear that at that high dose the caffeine may have stimulated the central nervous system to the point at which the usually positive ergogenic responses were overridden”. This is a very pertinent issue in that with all sports nutrition great individuality exists between athletes, such as level of training, habituation to caffeine, and mode of exercise. Therefore, these variables should be considered when incorporating caffeine supplementation into an athlete’s training program.

Anhydrous caffeine and endurance exercise

In an earlier study published by Graham and Spriet [52], seven elite runners performed a total of four trials, two cycling to exhaustion and two running to exhaustion at approximately 85% VO2max. Times for running and cycling were both significantly improved, running increased from ~49 min for placebo to 71 min for 9 mg/kg of caffeine, cycling increased from ~39 min for placebo to ~59 min for 9 mg/kg of caffeine [52].

Results were comparable in a separate 1992 Spriet et al. publication [18]. In a crossover design eight subjects consumed both a placebo and caffeine treatment at 9 mg/kg and 60 minutes later cycled to exhaustion at ~80% VO2max. Once again, following caffeine supplementation times to exhaustion were significantly increased. Results indicated subjects were able to cycle for 96 min during the caffeine trial, as compared to 75 min for placebo [18].

Recently McNaughton et al. [72] reported the effects of a moderate dose of caffeine (6 mg/kg) on 1-hour time trial performance. This investigation is unique to the research because, while continuous, the protocol also included a number of hill simulations to best represent the maximal work undertaken by a cyclist during daily training. The caffeine condition resulted in the cyclists riding significantly further during the hour-long time trial, as compared to placebo and control. In fact, time trial performance was improved 4-5% by the caffeine treatment over the other two treatments [72].

The use of caffeine in anhydrous form, as compared to a cup of caffeinated coffee, seems to be of greater benefit for the purpose of enhancing endurance performance. In addition, a low to-moderate dose of caffeine between 3 and 6 mg/kg appears to be sufficient for enhancing performance in a maximal sustained endurance effort.

Caffeine: High-Intensity and Team Sport Exercise

It is evident that caffeine supplementation provides an ergogenic response for sustained aerobic efforts in moderate-to-highly trained endurance athletes. The research is more varied, however, when pertaining to bursts of high-intensity maximal efforts. Collomp et al. [46] reported results for a group of untrained subjects, who participated in only 2-3 hours per week of non-specific sport activity. In a fasted state, and in a crossover design, subjects consumed caffeine at a dose of 5 mg/kg as well as a placebo condition, and performed a 30-second Wingate test. Compared to a placebo, caffeine did not result in any significant increase in performance for peak power or total work performed [46]. These results are in agreement with Greer and colleagues [45], where in addition to a lack of performance enhancement with caffeine supplementation (6 mg/kg), subjects classified as non-trained experienced a decline in power, as compared to placebo, during the last two of four Wingate bouts [45]. As previously stated, Crowe et al. [47] reported significantly slower times to reach peak power in the second of two bouts of 60-s maximal cycling. Subjects in that study were untrained in a specific sport and consumed caffeine at a dose of 6 mg/kg [47]. Finally, Lorino et al. [47] examined the effects of caffeine at 6 mg/kg on athletic agility and the Wingate test. Results were conclusive in that nontrained males did not significantly perform better for either the pro-agility run or 30-s Wingate test [73]. In contrast, a study published by Woolf et al. [30] demonstrated that participants who were conditioned athletes achieved greater peak power during the Wingate after consuming caffeine at a moderate dose of 5 mg/kg [30]. It is exceedingly apparent that caffeine is not effective for non-trained individuals participating in high-intensity exercise. This may be due to the high variability in performance that is typical for untrained subjects.

Results, however, are strikingly different for highly-trained athletes consuming moderate doses of caffeine. Collomp et al. [46] examined the use of 250 mg of caffeine (4.3 mg/kg) in trained and untrained swimmers. Swimmers participated in two maximal 100 m freestyle swims; significant increases in swim velocity were only recorded for the trained swimmers. Similar results were reported by MacIntosh and Wright [74] in a study that examined the effects of caffeine in trained swimmers, but the caffeine treatment was provided at a higher dose (6 mg/kg) and the protocol involved a 1,500-meter swim. Results indicated a significant improvement in swim times for those subjects who consumed caffeine, as compared to placebo. Moreover, time was measured at 500-m splits, which resulted in significantly faster times for each of the three splits for the caffeine condition [74]. As suggested by Collomp et al., [29] it is possible that specific physiologic adaptations present in highly trained anaerobic athletes, such as enhanced regulation of acid-base balance (i.e., intracellular buffering of H+), is intrinsic for caffeine to exert an ergogenic effect [29].

Participants in a study published by Woolf et al. [30] were highly trained anaerobic athletes, and results of that investigation demonstrated a significant increase in peak power with a moderate dose of caffeine (5 mg/kg) as compared to placebo [30]. Wiles et al. [44] reported a 3.1% improvement in performance time for a 1-kilometer time trial (71.1s for caffeine; 73.4s for placebo) at a caffeine dose of 5 mg/kg, and results also included a significant increase in both mean and peak power [44]. Wiles et al. [44] indicated that subjects in the study reported regular interval sprint training, which may support the theory that caffeine is most beneficial in trained athletes who possess physiological adaptations to specific high-intensity training [44].

A recent study published by Glaister et al. [31] examined a 5mg/kg dose of caffeine on sprint interval performance. Subjects were defined as physically active trained men and performed 12 x 30 m sprints at 35 s intervals. Results indicated a significant improvement in sprint time for the first three sprints, with a consequential increase in fatigue for the caffeine condition [31]. The authors suggested that the increase in fatigue was due to the enhanced ergogenic response of the caffeine in the beginning stages of the protocol and, therefore, was not meant to be interpreted as a potential negative response to the supplement [31].

Bruce et al. [32] tested two doses of caffeine (6 mg/kg, 9 mg/kg) on 2000 m rowing performance in competitively trained oarsmen. Results of the study revealed an increase in performance for both time trial completion and average power output for caffeine, as compared to placebo (500 mg glucose). Time trial completion improved by 1.3% for caffeine intake at 6 mg/kg. The 9 mg/kg dose did not result in additional increases in performance. The average of the 6 and 9 mg/kg caffeine treatments was 1.2% faster as compared to placebo [32]. Anderson and colleagues [75] tested these same doses of caffeine in competitively trained oarswomen, who also performed a 2,000-m row. In women, the higher dose of 9 mg/kg of caffeine resulted in a significant improvement in time by 1.3%, with performance enhancement most evident in the first 500 m of the row [75].

Team sport performance, such as soccer or field hockey, involves a period of prolonged duration with intermittent bouts of high-intensity playing time. As such, Stuart et al. [33] examined the effects of a moderate dose of caffeine (of 6 mg/kg) in well-trained amateur union rugby players. Subjects participated in circuits that were designed to simulate the actions of a rugby player, which included sprinting and ball passing, and each activity took an average 3-14 seconds to complete. In total, the circuits were designed to represent the time it takes to complete two halves of a game, with a 10 min rest period. Results demonstrated a 10% improvement in ball-passing accuracy [33]. An improvement in ball passing accuracy is applicable to a real-life setting as it is necessary to pass the ball both rapidly and accurately under high-pressure conditions [33]. In addition, throughout the duration of the protocol, those subjects on the caffeine condition successfully passed the ball 90% of the time as compared to 83% for placebo [33]. This study [33] was the first to show an improvement in a team sport skill related task as it relates to caffeine supplementation. Results of this study [33] also indicated that for the caffeine condition subjects were able to maintain sprint times at the end of the circuit, relative to the beginning of the protocol.

Schneiker et al. [34] also examined the effects of caffeine supplementation on repeated sprint ability common to sports such as soccer and field hockey. Ten male recreationally competitive team sport athletes took part in an intermittent-sprint test lasting approximately 80 minutes in duration. Results of the study indicated a caffeine dose of 6 mg/kg was successful in inducing more total sprint work, as compared to placebo. Specifically, total sprint work was 8.5% greater in the first half and 7.6% greater in the second respectively [34]. Based on the research presented [29, 30, 33, 34, 74], it is apparent that moderate caffeine supplementation in the range of 4-6 mg/kg can be advantageous to either short term or intermittent/prolonged duration high-intensity performance, but only in trained athletes. The training and conditioning of these athletes may result in specific physiologic adaptations which, in combination with caffeine supplementation, may lead to performance enhancement, or the variability in performance of untrained subjects may mask the effect of the caffeine.

Caffeine: Strength- Power Performance

In the area of caffeine supplementation, strength research is still emerging and results of published studies are varied. As previously mentioned, Woolf and colleagues [30] examined the effects of 5 mg/kg of caffeine in highly conditioned team sport male athletes. The protocol consisted of a leg press, chest press, and Wingate. The leg and chest press consisted of repetitions to failure (i.e., muscular endurance) and all exercises were separated by 60 seconds of rest. Results indicated a significant increase in performance for the chest press and peak power on the Wingate, but no statistically significant advantage was reported for the leg press, average power, minimum power, or percent decrement [30].

Beck et al. [35] examined the acute effects of caffeine supplementation on strength, muscular endurance, and anaerobic capacity. Resistance trained males consumed caffeine (201 mg, equivalent to 2.1-3.0 mg/kg) one hour prior to testing. Subjects were tested for upper (bench press) and lower body (bilateral leg extension) strength, as well as muscular endurance, which consisted of repetitions to exhaustion at 80% of individual 1RM. Participants were also tested for peak and mean power by performing two Wingate tests separated by four minutes of rest (pedaling against zero resistance). A low dose of 2.1-3.0 mg/kg of caffeine was effective for increasing bench press 1RM (2.1 kg = 2.1%). Significant changes in performance enhancement were not found for lower body strength in either the 1RM or muscular endurance [35].

Results of the Beck et al. [35] investigation are in contrast to a recent publication by Astorino et al. [76] in which twenty-two resistance-trained men were supplemented with 6 mg/kg of caffeine and tested on the bench press and leg press [76]. Findings from Astorino and colleagues [76] revealed no significant increase for those subjects supplemented with caffeine for either bench or leg press 1RM. Astorino et al. [76] did report a nonsignificant increase in repetitions and weight lifted at 60% 1RM for both the bench and leg press [76]; however, the intensity differed between the two studies. The Beck et al. design included a 2.1-3.0 mg/kg dose of caffeine and repetitions to failure at 80% of individual 1RM, whereas subjects in the Astorino et al. investigation consumed 6 mg/kg and performed repetitions to failure at 60% of individual 1RM. Indeed it is possible that the degree of intensity between the two protocols could in some way be a resulting factor in the outcome of the two studies.

Consequently, Woolf and colleagues [77] reported no significant increase in bench press performance in collegiate football athletes who consumed a moderate dose of caffeine (5 mg/kg) 60 min prior to testing. Participants in this investigation [77] were considered non-habituated to caffeine and consumed much less than 50 mg per day.

Research on the effects of caffeine in strength-power sports or activities, while varied in results and design, suggest that supplementation may help trained strength and power athletes. Therefore, future research should examine the effect of caffeine habituation and supplementation on strength and/or high-intensity short duration exercise. Of particular interest, is the lack of significant finding for lower body strength as compared to upper body performance.

Caffeine and Women

Research investigations that have examined the role of caffeine supplementation in endurance, high-intensity, or strength-trained women is scant, especially in comparison to publications that have investigated these dynamics in men. As previously indicated, Anderson and colleagues [75] examined the effect of both a moderate and high dose (6 and 9 mg/kg) of caffeine in competitively trained oarswomen. Results from a 2,000 m row performance signified the higher dose of caffeine (9 mg/kg) resulted in a significant improvement in time by 1.3%, with performance enhancement most evident in the first 500 m of the row. In addition, no significant increase in performance was reported for the lower dose or placebo; but the 6 mg/kg dose did result in a non-significant 0.7% improvement [75].

Motl et al. [78] examined the effects of a 5 and 10 mg/kg dose of caffeine on leg muscle pain during cycling to exhaustion at 60% VO2peak. Subjects were of average physical fitness and designated as non-habituated (consumed less than 100 mg/day of caffeine). Based on a leg muscle pain ratings scale, it was found that caffeine at both the 5 and 10 mg/kg dose significantly decreased leg muscle pain ratings during exercise [78]. Moreover, there was no statistically significant difference between the 5 and 10 mg dose [78]. The lack of a dose-dependent effect is in line with previously published investigations [8, 28, 32, 40].

In two different publications, Ahrens and colleagues [79, 80] examined the effects of caffeine supplementation on aerobic exercise in women. In one study [79] recreationally active women not habituated to caffeine participated in moderately-paced (3.5 mph) treadmill walking for eight minutes. In a double-blind manner, subjects randomly consumed caffeine mixed with water at either 3 or 6 mg/kg of body weight. The initial design included a 9 mg/kg dose, but during the first lab visit seven of ten subjects who received that treatment experienced profuse sweating, body tremors, dizziness, and vomiting. Results for the caffeine treatment at 6 mg/kg, as compared to 3 mg/kg and placebo, yielded a significant increase in energy expenditure at seven additional calories per 30 minutes of moderate walking [79]. From a research standpoint the increase in VO2 (0.67 ml/kg/min, equivalent to an increase in rate of energy expenditure of 0.23 kcal/min) is significant; however, in a practical setting it seems slightly less considerable. Finally, no significant results were reported for caffeine and aerobic dance bench stepping [80].

Goldstein and colleagues [81] examined the effects of caffeine on strength and muscular endurance in resistance-trained females. Similar to results reported by Beck et al. [35] it was found that a moderate dose of caffeine (6 mg/kg) significantly enhanced upper body strength (bench press 1RM). Women in this study were required to bench press 70% of individual body weight to be identified as resistance trained [81].

The research pertaining exclusively to women is somewhat limited and exceptionally varied. Publications range from examining caffeine and competitive oarswomen [75] to others that have investigated recreationally active individuals performing moderate-intensity aerobic exercise [79, 80]. Taken together, these results indicate that a moderate dose of caffeine may be effective for increasing performance in both trained and moderately active females. Additional research is needed at all levels of sport to determine if caffeine is indeed effective for enhancing performance in women, either in a competitive or recreationally active setting.

Caffeine, Habituation, and Performance

It is standard procedure for a research protocol to account for the daily caffeine intake of all subjects included within a particular study. The purpose of accounting for this type of dietary information is to determine if caffeine consumption a.) has an effect on performance and b.) if this outcome is different between a person who does or does not consume caffeine on a regular basis. In fact, as previously discussed in this paper Bell and colleagues [41] examined the effect of a moderate dose of caffeine on persons identified as users ( ≥ 300 mg/d) and nonusers ( ≤ 50 mg/d). Results demonstrated an enhancement in performance for both groups; however, the treatment effect lasted approximately three hours longer for those persons identified as nonusers [41].

Dodd et al. [82] identified caffeine habituation between subjects in a similar manner to Bell and colleagues [41] and reported no statistical difference between groups for VO2max (subjects participated in a graded exercise protocol). The only reported differences, such as ventilation and heart rate, were at rest for those persons not habituated to caffeine [82]. Van Soeren et al. [83] also reported no significant changes between users and nonusers of caffeine, other than an increase in plasma epinephrine during exercise for persons not habituated to caffeine, as compared to placebo. Finally, it was suggested by Wiles et al. [69] that daily caffeine consumption among subjects did not have an effect on the performance outcomes of that particular study, which examined the effects of 3 g of coffee containing approximately 150-200 mg of caffeine, on treadmill running time.

What may be important to consider is how caffeine affects users and nonusers individually. For example, Astorino and colleagues [76] examined the effects of 6 mg/kg of caffeine on bench press one-repetition maximum. Thirteen of 22 subjects in that investigation described feelings of greater energy, elevated heart rate, restlessness, and tremor. It should also be noted that these feelings were enhanced in participants who consumed little caffeine on a daily basis [76]. It would seem the important factor to consider is the individual habits of the athlete and how caffeine supplementation would affect their personal ability to perform. In terms of practical application, it is the responsibility of the coach and/or athlete to determine what dose of caffeine, if any, is suitable for competition.

Caffeine and Hydration

It has been widely suggested that caffeine consumption induces an acute state of dehydration. However, consuming caffeine at rest and during exercise presents two entirely different scenarios. Specifically, studies examining the effects of caffeine-induced diuresis at rest can and should not be applied to athletic performance. To begin, a study published in 1928 by Eddy & Downs [84] examined the possible role of caffeine induced dehydration but included an n of only 3. In a review publication on caffeine and fluid balance, it was suggested by Maughan and Griffin [85] that “hydration status of the individual at the time of caffeine ingestion may also affect the response, but this has not been controlled in many of the published studies”.

Despite the unfounded, but accepted, notion that caffeine ingestion may negatively alter fluid balance during exercise, Falk and colleagues [86] found no differences in total water loss or sweat rate following consumption of a 7.5 mg/kg dose of caffeine (5 mg/kg 2 hr prior to exercise, 2.5 mg/kg 30 min prior) and treadmill walking with a 22-kg backpack (intensity of ~70-75% VO2max). The authors did caution that exercise was carried out in a thermoneutral environment and additional research is warranted to determine effects in a more stressful environmental condition [86].

Wemple et al. [87] investigated the effects of a caffeinated versus non-caffeinated electrolyte solution drink at rest and during 180 min of moderate-intensity cycling at 60% VO2max. In total, 8.7 mg/kg of caffeine was consumed in divided doses. Results indicated a significant increase in urine volume for caffeine at rest, but there was no significant difference in fluid balance for caffeine during exercise [87]. These results are noteworthy, because according to a review published by Armstrong [88], several research studies published between 1970 and 1990 reported outcome measures, such as loss of water and electrolytes, based on urine samples taken at rest and within 2-8 hours of supplementation [88].

Kovacs and colleagues [56] published similar results in a 1998 study that examined time trial performance and caffeine consumption in various dosages added to a carbohydrate electrolyte solution (CES). In total, subjects consumed each carbohydrate-electrolyte drink with the addition of 150 mg, 225 mg, and 320 mg of caffeine. In regard to performance, subjects achieved significantly faster times following ingestion of both the CES 225 mg and CES 320 mg dosages, as compared to placebo and CES without addition of caffeine [56]. Finally, Kovacs et al. [56] found no statistical difference in urine volume either before or after cycling. It should also be mentioned the authors reported wide-ranging post-exercise urinary caffeine concentrations within subjects, which could possibly be explained by inter-individual variation in caffeine liver metabolism [56]. Grandjean et al. [89] collected urine samples over a 24-hr period and found at rest there was no significant change in urine output at rest when consuming water or varying doses of caffeine in the range of 114 mg/d-253 mg/d (1.4 mg/kg – 3.13 mg/kg).

An interesting study published by Fiala and colleagues [90] investigated rehydration with the use of caffeinated and caffeine-free Coca-Cola®. In a double-blind crossover manner, and in a field setting with moderate heat conditions, subjects participated in three, twice daily, 2-hr practices. Athletes consumed water during exercise, and on separate occasions, either of the Coca-Cola© treatments post-exercise. In total, subjects consumed ~7 cans/d or ~741 mg/d of caffeine. As a result, no statistical differences were found for measures such as heart rate, rectal temperatures, change in plasma volume, or sweat rate [90]. It should be noted, however, the authors also reported a negative change in urine color for the mornings of Day 1 and 3, which was a possible indication of an altered hydration status; although, it was not evident at any other time point during the experiment. Therefore, Fiala et al. [90] suggested future research should continue to investigate the effects of rehydrating with caffeine over several consecutive days.

Roti et al. [91] examined the effects of chronic caffeine supplementation followed by an exercise heat tolerance test (EHT). The study included 59 young, active males. All subjects consumed 3 mg/kg of caffeine for six days, and during days 7-12 subjects were divided into three groups and ingested 0, 3, or 6 mg/kg of caffeine. The EHT consisted of walking on a treadmill at 1.56 m/s at a 5% grade. Results were conclusive in that sweat rates were not statistically different between groups, and chronic supplementation of 3 and 6 mg/kg of caffeine did not negatively affect fluid-electrolyte balance, thermoregulation, and thus performance[91].

Millard-Stafford and colleagues [92] published results from a study that examined the effects of exercise in warm and humid conditions when consuming a caffeinated sports drink. No significant differences were found for any of the three treatments: placebo (artificially flavored water), 6% carbohydrate-electrolyte, and 7% carbohydrate-electrolyte plus B vitamins 3, 6, and 12 in addition to 46 mg/L carnitine, 1.92 g/L taurine, and 195 mg/L caffeine for sweat rate, urine output, or percent fluid retained during exercise [92]. In fact, a significant increase in exercise intensity was reported for the final 15 min (an all out portion of the exercise bout) for the caffeine + carbohydrate and electrolyte beverage, but not for the carbohydrate + electrolyte drink, or placebo. In conclusion, no significant differences in blood volume were present for any of the three treatments; therefore, caffeine did not adversely affect hydration and thus performance of long duration in highly trained endurance athletes [92].

Finally, Del Coso and colleagues [93] examined the effects of a moderate dose of caffeine in combination with sustained cycling at 60% VO2max. Seven endurance-trained males consumed each of the following conditions during 120 min of exercise: no rehydration, water, carbohydrate-electrolytes solution, and each of these three treatments with the addition of caffeine at 6 mg/kg in capsule form. Results were conclusive, and indicated caffeine alone at 6 mg/kg did not significantly affect sweat rate during exercise, nor did ingestion of caffeine in combination with water or a carbohydrate-electrolytes solution. In addition, heat dissipation was not negatively affected [93]. Therefore, while there may be an argument for caffeine-induced dieresis at rest, the literature does not indicate any significant negative effect of caffeine on sweat loss and thus fluid balance during exercise that would adversely affect performance.

Caffeine and Doping

It has been shown that caffeine supplementation in the range of 3-6 mg/kg can significantly enhance both endurance and high-intensity performance in trained athletes. Consequently, the International Olympic Committee mandates an allowable limit of 12 μg of caffeine per ml of urine [6, 15]. A caffeine dose in the range of 9 – 13 mg/kg approximately one hour prior to performance will reach the maximum allowable urinary concentration for competition [6]. Caffeine consumption and urinary concentration is dependent on factors such as gender and body weight [94]. Therefore, consuming 6-8 cups of brewed coffee that contain approximately 100 mg per cup would result in the maximum allowable urinary concentration [15, 94]. According to The National Collegiate Athletic Association, urinary oncentrations after competition that exceed 15μg/ml are considered to be illegal [95]. In addition, the World Anti-Doping Agency does not deem caffeine to be a banned substance [96], but has instead included it as part of the monitoring program [97] which serves to establish patterns of misuse in athletic competition.

Conclusion

The scientific literature associated with caffeine supplementation is extensive. It is evident that caffeine is indeed ergogenic to sport performance but is specific to condition of the athlete as well as intensity, duration, and mode of exercise. Therefore, after reviewing the available literature, the following conclusions can be drawn:

• Caffeine is more powerful when consumed in an anhydrous state (capsule/tablet, powder), as compared to coffee.

• The majority of research has utilized a protocol where caffeine is ingested 60 min prior to performance to ensure optimal absorption; however, it has also been shown that caffeine can enhance performance when consumed 15-30 min prior to exercise.

• Caffeine is effective for enhancing various types of performance when consumed in low to-moderate doses (~3-6 mg/kg); moreover, there is no further benefit when consumed at higher dosages (≥ 9 mg/kg).

• During periods of sleep deprivation, caffeine can act to enhance alertness and vigilance, which has been shown to be an effective aid for special operations military personnel, as well as athletes during times of exhaustive exercise that requires sustained focus.

• Caffeine is an effective ergogenic aid for sustained maximal endurance activity, and has also been shown to be very effective for enhancing time trial performance.

• Recently, it has been demonstrated that caffeine can enhance, not inhibit, glycogen resynthesis during the recovery phase of exercise.

• Caffeine is beneficial for high-intensity exercise of prolonged duration (including team sports such as soccer, field hockey, rowing, etc.), but the enhancement in performance is specific to conditioned athletes.

• The literature is inconsistent when applied to strength and power activities or sports. It is not clear whether the discrepancies in results are due to differences in training protocols, training or fitness level of the subjects, etc. Nonetheless, more studies are needed to establish the effects of caffeine vis a vis strength-power sports.

• Research pertaining exclusively to women is limited; however, recent studies have shown a benefit for conditioned strength-power female athletes and a moderate increase in performance for recreationally active women.

• The scientific literature does not support caffeine-induced dieresis during exercise. In fact, several studies have failed to show any change in sweat rate, total water loss, or negative change in fluid balance that would adversely affect performance, even under conditions of heat stress.

Competing Interests

The authors declare that they have no competing interests.

Authors’ Contributions

All authors read and extensively reviewed and contributed to the final manuscript.

Acknowledgements

All authors have read and approved the final manuscript.

© 2010 Goldstein et al. , licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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by EricT

Assumptions are a perfect subject for this third post in the series. The first two I think held no real surprises. For this one, I wanted to write about something that would challenge your assumptions so I decided to write about assumptions themselves.

A good fitness article must make assumptions. There, I'll bet that threw at least some of you. I mean, aren't the best fitness writers omniscient?

Refusing to make assumptions but instead trying to cover all the bases in an article can actually do more harm than good. Many writers tend to construct different scenarios in their articles in an effort to discuss every independent variable they can imagine. They seek to achieve impossible perfection and instead of moving from the complex to the simple they make ever more complications! Although this may please the author as an intellectual exercise to the reader the result is a hodgepodge of intellectual posturing and confusing details.

Let's suppose that we are answering a direct question. "When should I do my deadlifts? At the beginning of the week or later?"

A good answer would be "It depends".

I mentioned above independent variables. An independent variable is the one variable that is not dependent on any other variable. And there is only ever one to consider in any discussion.

To answer the question about deadlifts we say it depends. Well it depends on all the dependent variables. However, the dependent variables depend on what the independent variable is. We decide, in any one discussion, what that will be. The independent variable may be the deadlift. That is the one thing that we control and does not change.

However, by making the deadlift an independent variable we are making an assumption! This is not a controlled scientific experiment, this is a training discussion. What if I asked "What is your priority?"

"I really want to bring up my squat."

At that point the squat becomes the independent variable. Everything changes.

See how muddy this all gets? What's more the dependents do not assume a neat and direct relationship to only the squat. Everything affects everything. Try to follow all the threads and you will not make progress. You will suffer "paralysis by analysis".

But the key is understanding what assumptions really are. Most people tend to think that assumptions are dogmatic beliefs or expectations based on past experience. The word assume itself is often pejorative. You know, to assume makes an ass out of u and me.

Nothing of the sort. Assumptions are critical. And they are a part of critical thinking. The failure in fitness articles is not making assumptions but failing to name them. The thing about an assumption is that it must be reasonable. Someone can reject our assumptions and so reject our entire argument but that does not mean we do not make them in the first place.

The authors who refuse to make assumptions are authors who simply want you to believe that they know everything that must be known. The rub is that in attempting to cover everything that they know, they show how unknown things can be. You do not need to know everything to move toward an answer. You must simply have realistic expectations and take them into account.

For instance, I recently wrote a long article on how to achieve your first pullup. Even though the article is long I had to make assumptions to write it. Failing to make those assumptions would have resulted in a very crappy article and an overly long one as well.

My main assumption in that article was that those using the method were not severely overweight. I mentioned that excessive body-weight was, of course, a big stumbling block for pullups. But I assumed that those attempting to achieve their first pullup were either not overweight or would be attempting to lose weight. The alternative would be to write a fat loss article. But I was writing an article about how to do your first pullup from a simple methodological perspective. The other variables that need to be considered to be able to handle your own body-weight are for other articles.

Someone who wanted to cast doubt on my method could, instead of discrediting the method itself, attempt to force me to address further and further variables. This is sometimes called moving the goalpost. The idea here is not to actually answer any questions but to move further away from the central point, ask ever more complex questions and eventually stymie me by reaching a point where my knowledge fails. And on the subject of fatloss my knowledge would fail sooner rather than later. However, this would in no way discredit my instruction on how to achieve a pullup!

So we must break this down to simple spots for bad fitness articles. The first two are:

1. Author refuses to make assumptions but rather moves a simple question or subject to ever more complex area of investigations.

2. Author makes assumptions but fails to clearly name them in the article.

The last spot needs a bit more explanation:

3. Author makes unreasonable assumptions.

Unreasonable assumptions are those that the author, nor anybody else can garner from past experience or knowledge. Unreasonable assumptions, at their extreme, are just ridiculous statements. In an article they become like the pink elephant in the room. So be the first person to acknowledge them.

A great example comes from Pavel Tsatsouline. I've mentioned this one several times because it is such an outrageous assumption. Pavel said everybody has the strength to lift a car; their muscles just don't know it yet. After a statement like that, it really doesn't matter what follows.

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by EricT

Much of the Getting in the Zone series of articles are focused on areas of sport psychology. Having psychologists help athletes perform better is a relatively new thing. While I have drawn from that, as I read some of the articles on this subject (controlling anxiety, etc) from sport psychologists, I wonder if many of them really "get it". Sure they understand the statistics and have a background in the psychology effecting performance, but have they ever been there? Do they know what it feels like? I read with interest an article in the "Mind Games" section of the NSCA's performance training journal by Suzie Tuffey Riewald entitled "Help, I'm Nervous". It's related, of course to my Getting in the Zone series of articles.

This article deals with feeling of nervousness or anxiety and the somatic anxiety symptoms that accompany that, which the author also refers to as 'bodily anxiety'.

She points out, as I did in the zone articles, that anxiety isn't always bad for performance, but unfortunately:

"it is often the case that when an athlete experiences anxiety, or nervousness before a
competition, he or she automatically thinks, “oh no, I am nervous—this isn’t good. Things are going to end badly.”

Absolutely. Right on the money. It isn't so much the anxiety inself in this case but our reaction to it or interpretation of it. In fact this is a much better view of stress in general, suited to the "Transactional Model of Stress" which places more emphasis on the individuals perception of the demand placed on them by the environment as well as their mode of thought, their behavioral tendencies, and their capacity for action.

The author makes a number of good suggestions for dealing with performance robbing anxiety, however, there are a number of common misunderstandings at work. I think they are important enough to lay out here in a separate article, which I will include as an appendix article to the zone series.

1. Think Back

The idea that an athlete should first "think back" to past performances and figure out "what levels of anxiety" were good for performance and what levels were bad. This would entail examining what they felt prior to a good performance or what they were thinking. Then compare that to poor performance trying to find a "pattern" between nervousness and poor performance.

Are you getting the idea here? You are supposed to go through a complicated mental process to SEEK out the "perfect" level of nervousness! If this sounds cumbersome and downright impossible..that's because it is.

The problem is with the idea that not all anxiety is bad and that some level of anxiety is conducive to an optimal level of personal arousal and therefore good performance. This is true to some extent. But it is a leap of logic to assume that one must therefore tune their anxiety like a radio!

I hate quoting myself but since this is related to/contrasted with the Getting in the Zone series I need to include some excerpts for purposes of explanation.

In Getting in the Zone IV, I stated:

"Over-focusing on one emotional response or trigger tends to divert attention to a self-consciousness appraisal of our emotional state. Instead of a healthy 'self-awareness' or 'mindfullness' we have rumination or preoccupation."

And in the first article:

"[the heart of flow is] you are aware of what you are doing but not in an examining way. In other words, you are aware but not aware of being aware. You don't think about it; you don't TRY. You just do. The awareness element of flow can be likened to a state of Zen awareness in that it is not a judgmental or analytical state. You do not seek to block or control thoughts but simply let them flow by without judgment or comment, completely aware without SEEKING to be aware."

I should not that those statements are not meant to say that you should not combat things like negative self talk. Of course combat is the wrong word. Most lifters should replace negative talk with positive, goal oriented directives that have been clearly visualized and enhanced through quality repetition, as I discussed in Don't Dwell on Failures. This is a much more straightforward directive than "seek your goldi-locks moment". Which will have you tied up in a knot, most likely.

Given those statements and the idea of not "dwelling" on nervousness above, perhaps you can see that trying to tune or control anxiety is really just a systematic version of the very same mental process. Not many people with anxiety problems will be able to exert some type of control over it by a complicated mental trick. The "trying" and "striving" to tune your anxiety will just result..in more anxiety or mental diversion.

I have a hard enough time getting people to squat and deadlift right. I don't think having them "determine the optimal levels of anxiety" for themselves is in the cards.

Instead of trying to turn a mental dial back and forth until you get just the right volume of anxiety, you must first learn to turn the knob all the way to the left. In other words, one must first learn to RELAX completely. Which leads us to the next fallacy:

2. Somatic Versus Cognitive Anxiety

The author separates somatic (bodily anxiety) from cognitive (mental) anxiety and suggest that some may be more bothered by one or the other:

"If you are more plagued by the physical (somatic) manifestations of anxiety, your pre-competition goals should focus on calming your body using such skills as stretching, moving around, so as not to get tight, light massage or deep, controlled breathing.

When mental (cognitive) anxiety tends to be excessive, your goal should be to calm the mind—effective skills include using positive self-talk, focusing on process goals (as opposed to outcome goals), distracting oneself so as not to think about being worried and reminding oneself of past successes to build confidence."

The problem here is the idea that there is a such thing as bodily anxiety and that this is what somatic anxiety is. The body can be physiologically activated by anxiety but ALL anxiety is MENTAL. Somatic anxiety is not the bodily manifestations of anxiety, as the author states, but is one PERCEPTION of those manifestations.

Let me explain it in simple terms. If a bear is chasing you through the woods you will experience what is called state anxiety which is made up of two components, cognitive and somatic anxiety.

Cognitive state anxiety is the mental component of anxiety and is caused by negative expectations about success or about negative self-evaluation.¹. This is the "thinking" part of anxiety in which we engage in negative self-talk about the chances of failure or success and we fear the consequences of failure.

Somatic state anxiety is the physiological and affective elements of the anxiety experience that develops directly from autonomic arousal.² This is our "bodily experience" of the physiological changes brought about by anxiety.

The fallacy here is viewing what goes on in the body as somehow separate from the mind. When we attempt to relax the body through massage or deep breathing our purpose is to relax the mind. When we use techniques to relax the mind, our purpose is to relax the body. In other words, a relaxed mind means a relaxed body and vice versa. One cannot exist in the other. You can't be completely chilled and tense at the same time!

Now, putting one and two above together we come to another problem. Are we really that accurate when it comes to our self-report of our anxiety experience? What if we have high TRAIT anxiety? What if we are habitually tense? The psychological changes that accompany a high anxiety state can make our perceptions of physiological change quite inaccurate. We may be quite unaware of just how tense our muscles are, how fast our heart is beating, etc. and so on. If you are like most other people in the modern world you are experiencing a certain degree of inappropriate muscle tension right now and are not even aware of it.

Right now, then, at this moment, your "anxiety experience" may not be all that "in tune". It is unrealistic, then, to think one can use hindsight to find the 'perfect storm' of arousal in some far in the past moment. Especially since for those of us that are actually out there DOING it, such moments come in an endless stream and blend together.

And the recipe fits only the competitive athlete who probably has a few stand out moments to draw on, both good and bad. Even then only a relative few are likely to stick out, giving a poor sampling from which to draw data. And even if you could remember the Goldilocks moment, you couldn't just snap your fingers and recreate it.

All the techniques talked about above are about achieving a certain degree of momentary relaxation. The reason so many fail at achieving this is because they have never learned to master FULL relaxation.

If you want to be able to control your level of arousal on short notice the first step, therefore, is to first learn to turn the arousal knob down to one. We experience EVERYTHING relative to something else. It is how we categorize the world. As I pointed out in the earlier articles about muscular tension, for instance, the moment you truly recognize what excess tension feels like, is the moment it goes away. Or comes back. Think of it like finally getting a nice new mattress after sleeping on an old lumpy one for years. Suddenly the old mattress seems even worse.

One thing that the article does get right is the difference between being outcome focused and performance focused (task versus outcome orientation). But this is not a switch many people can just turn on and off at will. If you are focusing on the uncertain outcome of an event or a task such as lifting a heavy weight and try to tell yourself "focus on the task" you will simply be concentrating on NOT concentration on the outcome. This is not how one achieves flow, which is the purpose of all these many articles in the Getting in the Zone series.

The "easy" cases that just become outcome focused now and again because of a particularly important event or moment are just that…the easy cases. The hard cases are ALWAYS outcome oriented. Even so there is more going on in an athletes mind than just the uncertainty of winning or losing. There are past injuries and current, chronic ones. There is performance anxiety and there is the real world anxiety that follows the athlete onto the field as well.

I think that there is too much focus on perfecting the state of arousal. A perfect solution isn't needed. A working solution is needed that can be slowly improved upon.

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by EricT

Does the history of food energy units suggest a solution to "Calorie confusion"?

by James L Hargrove

Department of Foods and Nutrition, University of Georgia, Athens, GA, 30602-0001, USA

Nutrition Journal 2007

The Calorie and It's Context

The Calorie (kcal) of present U.S. food labels is similar to the original French definition of 1825. The original published source (now available on the internet) defined the Calorie as the quantity of heat needed to raise the temperature of 1 kg of water from 0 to 1°C. The Calorie originated in studies concerning fuel efficiency for the steam engine and had entered dictionaries by 1840. It was the only energy unit in English dictionaries available to W.O. Atwater in 1887 for his popular articles on food and tables of food composition. Therefore, the Calorie became the preferred unit of potential energy in nutrition science and dietetics, but was displaced when the joule, g-calorie and kcal were introduced.

This article will explain the context in which Nicolas Clément-Desormes defined the original Calorie and the depth of his collaboration with Sadi Carnot. It will review the history of other energy units and show how the original Calorie was usurped during the period of international standardization. As a result, no form of the Calorie is recognized as an SI unit. It is untenable to continue to use the same word for different thermal units (g-calorie and kg-calorie) and to use different words for the same unit (Calorie and kcal). The only valid use of the Calorie is in common speech and public nutrition education. To avoid ongoing confusion, scientists should complete the transition to the joule and cease using kcal in any context.

Introduction

The purposes of this article are 1) to note that the first known published definition of the Calorie from 1825 is available on the internet; 2) to suggest why W.O. Atwater selected the Caloriea (modern kcal or 4.186 kJ) as a unit of potential energy for nutritional education and the first database of food composition; 3) to note the important connection between the man who defined the Calorie and Sadi Carnot; 4) to review the origin of other energy units; and 5) to explain how the kcal recently supplanted the Calorie even though both units had been obsolete since 1948. The article will conclude with a suggestion about how to eliminate the confusion that was caused because different scientific committees introduced disparate definitions for the same word.

The dilemma of calorie confusion

Nutrition scientists, dietitians and clinical nutritionists face a dilemma that other scientists do not. Ever since the adoption of the international system (SI) of scientific units in the 1950's, the joule has been the only defined SI unit of energy. Neither the g-calorie nor the kcal is an SI unit. However, unlike other scientists, nutritionists are involved in public education concerning energy balance, and the U.S. lay public has been familiar with the Calorie for over 100 years. Indeed, the Calorie on U.S. food labels is one of the few tools available for public education about energy balance. At present, it is not helpful to ask lay people to set aside this tool and instead learn metric prefixes and SI terminology. An interesting but little known aspect of this situation is that the Calorie predated the joule by more than 60 years, and the original definition was almost exactly the same as presently found on U.S. food labels. One purpose of this article is to explain the priority of the Calorie relative to other energy units, and how it was displaced by the joule and kcal.

A second question that should be addressed is whether there is only one way to do away with the ambiguity imposed by using Calories, g-calories, and kcal in different contexts. This problem has even found its way into U.S. federal code. For example, in Title 21, section 104.20, part d of the Code of Federal Regulations[1], the following statements are made regarding food fortification (italics added):

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Definitions of energy units

Before discussing the history of the energy units that are commonly used in nutrition, it is useful to provide their present definitions:

Joule

The joule (J) is the only unit of energy defined in the SI system. It is the work done by a force of 1 newton (N) moving an object 1 meter in the direction of the force, and has base units of kg m2 s-2. These units can be derived as the work of lifting a mass (kg) a distance (m) against gravitational acceleration at sea level (9.806 m s-2). Because the work of lifting 1 kg by 1 m equals 9.8 J, 1 J is the work done in lifting 0.102 kg by 1 m. Alternatively, it is the work required to move an electric charge of 1 coulomb through an electrical potential difference of 1 volt. It can also be defined as the work done to produce power of 1 watt continuously for 1 second (1 W-s). Note that these definitions are stated in terms of work but none relates directly to heat or potential energy.

calorie

The "small calorie" or "g-calorie" is defined as the amount of heat required to raise the temperature of 1 g of water by 1°C with a temperature change from 14.5 to 15.5°C. The current US Dietary Reference Intakes define 1 cal as 4.186 J [2]. Some texts use the thermochemical calorie, 4.184 J.

Calorie

The Calorie was originally defined as the amount of heat required to raise the temperature of 1 kg of water from 0 to 1°C at 1 atmosphere of pressure. When used to express potential energy on food labels, it is defined as 4.186 kJ and is identical to a kcal.
kilocalorie

When the m-kg-s system was adopted in the 1930's, the cal was defined as a thermal unit in the cm-g-s system and 1 kcal was defined as 1000 cal in the m-kg-s system. All forms of the calorie were deemed obsolete in science after the SI system was adopted in the 1950's.

It is worthwhile to note that the Calorie (or kcal) has consistently been used to indicate the potential energy in foods (or the chemical energy stored in human tissues), whereas the primary use of the joule is as a unit of work or of energy in general.

Why did W.O. Atwater choose the Calorie?

The U.S. public began using the Calorie only after W.O. Atwater introduced it as an energy unit for foods in 1887. His series of 5 articles on food constituents was published in a popular periodical called Century magazine and was addressed to the educated lay public. Because his article on food energy (The Potential Energy of Food [3]) is a milestone in nutritional science but is out of print, a facsimile has been appended to the present manuscript [See Additional file 1]. As shown in Fig. 1, Atwater not only defined the Calorie in terms of heating 1 kg of water, he also indicated that it was the amount of potential energy required to perform about 1.53 foot-tons of physical work at perfect efficiency. The modern equivalent is 426.6 kg-m at 1 g (4,186 J). On a following page, he noted that the mechanical efficiency of machines was about 8% but that of humans and animals was about 20–30%. In short, the central point of his article was to explain the need to provide sufficient potential or chemical energy from food to support manual labor.

Additional file 1: The Potential Energy of Food. A facsimile of the following historical article: Atwater, W.O. The Potential Energy of Food. The Chemistry and Economy of Food. III. Century 1887; 34:397–405. Format: PDF Size: 1.6MB Download file

This file can be viewed with: Adobe Acrobat Reader

Figure 1: W.O. Atwater introduced the Calorie to US audiences in an 1887 article in Century magazine. Note that he defined the Calorie as potential energy needed to support a given amount of physical work against gravity, which he calculated as foot-tons.

As will be shown below, the Calorie was the only named energy unit that existed in English dictionaries of the time (Figs. 2 and 3). The joule had been proposed as an electrical unit in 1882, but had not entered the lexicon, and the small or g-calorie was not defined in dictionaries (it was used in some scientific papers, however). This record can be verified by consulting the Oxford English Dictionary [4], which identifies word origins. As a scientist, however, Atwater was certainly aware of the g-calorie and may have known that a commission of the British Association for Advancement of Science was discussing alternative units. The reason that he chose the Calorie lay in his purpose of educating the public about rational food choices.

Figure 2: Timeline comparing use of the Calorie (kg basis or kcal), g-cal, kcal and joule. MKS, m-kg-s system of units; CGS, cm-g-s system of units. First known usage of the Calorie in German was by Mayer in 1845 [29]. First known occurrence in English was when Adolphe Ganot's physics text [6] was translated in 1863.

Figure 3: Top, the calorie as defined in the 1883 Imperial Dictionary [7]. Bottom, the original published definition of the calorie as described in Le Producteur (1825) [19].

In the sense of being a unit of heat, the word calorie did not enter the English language until the 1860's [5]. Earlier editions of Webster's dictionary defined calorie as "a principle of fire or heat." This usage suggests that before calorie became a heat unit, it might have been an alternative for, or confused with, caloric (calorique), which entered English usage in about 1891 (OED). Usage changed when Adolphe Ganot's French physics text was translated into English in 1863[6]. The Calorie then entered the English vocabulary with the same definition that French physicists used. Thus, the 1883 edition of the English Imperial Dictionary [7] defined the calorie as "the quantity of heat necessary to raise the temperature of a kilogramme of water one degree Centigrade" (Fig. 3). Ganot specified that the initial temperature was 0°C (implicitly assuming a pressure of 1 atmosphere).

In the 19th century, a large portion of most workers' income was spent on food for family members and livestock. When asked to write his articles in Century magazine, Atwater had just returned from post-doctoral studies in Karl Voit's laboratory where he also worked with Max Rubner[8]. In non-English speaking countries, the g-calorie was the customary unit of calorimetry because most scientists believed that Favre and Silbermann [3] had invented the calorie and defined it in that sense. After the relationship between heat and work was established, many workers alternatively used the kg-m or ft-lb as units, or else defined unnamed "heat units" in reference to changes in water temperature. Even 20th century histories and biographies mistakenly credit Favre with naming the calorie[9,10]. Voit and Rubner used the g-calorie or the German term for unnamed "heat units." Although it seems puzzling that Atwater would have switched from the g-calorie to the Calorie, there is probably a simple reason.

The Century Company published both Century magazine and W.D. Whitney's comprehensive Century Dictionary (later, the New Century Dictionary). It would have been natural for Atwater's editor to verify that the Calorie was defined in the dictionary that was published by his own firm. In that dictionary, the Calorie was defined as the heat needed to raise the temperature of 1 kg of water from 0 to 1° centigrade. There was no entry for a g-calorie or a joule. As an educator, Atwater would have realized that the g-calorie was too small because over 2 million units would be needed per day. Moreover, the lay public was not familiar with metric prefixes and it would have been unnecessarily complex to add the kilo-prefix. The Calorie was already defined based on the heat capacity of 1 kg of water.

However, in the 1870's, French chemist Marcellin Berthelot had observed that there were two definitions for the same word. He decided to define the lower-case calorie as a g-calorie and use the capitalized Calorie to refer to the kg-calorie[11]. Later dictionaries adopted this custom and began referring to "small" and "large" calories. In contrast, the kilocalorie was not introduced as a heat unit until 1894–1908[12,13]. Therefore, when Atwater's series on nutrition was published, the energy units available were the large Calorie, the small calorie, or work units of kg-m and ft-lb. He chose the Calorie (with equivalent ft-tons) and the public quickly accepted the new word. Moreover, because food energy was expressed as Calories in subsequent food tables [14,15], nutrition science likewise adopted this unit for energy. The happy state in which American nutrition scientists, educators, and the public used one definition lasted from 1887 until about 1970. The question of origins then becomes why early French dictionaries and physicists such as Ganot[6] had defined the Calorie in terms of heating a kg of water, rather than the small or g-calorie that was used by Favre and Silvermann [16]. How did the Calorie enter the French lexicon?

Coinage of the Calorie as a unit of heat

Although some authors have suggested that Lavoisier named the calorie [17], Ziegler notes that the word was never used in his original publications[18]. The first known published definition of the calorie (1825) occurred in a Parisian journal called Le Producteur. Journal de l'Industrie, des Sciences et des Beaux-Arts [19]. (The quotation may be found on the Gallica Internet site [20] by doing a title search for Le Producteur and then entering 583 in the search box, Aller Page.)b A portion of that page is reproduced in Fig. 3, which comes from a very detailed series of anonymous articles that describe a course on industrial chemistry given annually by Professor Nicolas Clément-Desormesc. Much of the course discussed the theory by which steam engines convert heat into useful work, and a unit of heat was required. The first step in calculating fuel efficiency was to define how much energy is contained in fuels. Therefore, in discussing calorimetry, Clément provided a definition that was recorded by an anonymous auditor, translated as:

Clément and Carnot calculate a mechanical equivalent of heat

Nicolas Clément was a noted professor and industrial chemist[24] with many interests besides the theory of heat. He had trained at the École Polytechnique with Charles Desormes, who was an assistant in the laboratory of Guyton de Morveau, a renowned chemist and colleague of Lavoisier, Berthollet, and Forcroy[25]. From 1801–1819, Clément and Desormes published numerous papers on topics such as the composition of carbon monoxide, proof that iodine is an element, a value for absolute zero, and a value for the ratio of the specific heats of gases at constant pressure and constant volume that is called ? [24]. The value of ? is important because it provided a means of calculating the mechanical equivalent of heat (Joule's coefficient) [26].

From 1812–1819, Clément and Desormes conducted studies on the nature of heat and derived an algebraic method for calculating the mechanical power that can be obtained from steam. Clément read the paper to the Académie des Sciences in August, 1819, more than 20 years before Mayer or Joule took up this subject. Parts of the manuscript were published in the Bulletin de la Societe' d'Encouragement in 1819 and later donated to the Royal Society of London[27]. The method for calculating mechanical power was sometimes called the Law of Clément-Desormes. Fox[21,28] and Lervig[22] state that two key concepts in the paper were the conservation of heat (calorique) and adiabatic (rather than isothermal) expansion of steam vapor.

The record shows that Clément not only defined the Calorie but also could calculate the amount of work that could be obtained from steam. Clément taught his students that the energy content of charcoal was 7050 Calories (kcal) per kg, and that 650 Calories was required to convert 1 kg of water to steam. One kg of water vapor could do work as it expanded from 1 L to 1700 L. Clément assumed conservation of energy (or calorique) and employed engineering units for work (Dynamie) equivalent to lifting 1000 kg to a height of 1 m. Clément noted that steam engines of the day could obtain about 300,000–400,000 kg-m of work from 1 kg of charcoal. Without considering efficiency, this would give a value of less than 57 kg-m/kcal. This is about 13% of the theoretical maximum, but Clément probably did not have a way of calculating absolute thermodynamic efficiency. One of Clément's important contributions was to show that higher operating temperatures and pressures permitted greater efficiencies.

Around 1819, Clément was introduced to Sadi Carnot and gave him a copy of his paper on the motive power of steam. Carnot clearly thought that Clément's approach was not fully satisfactory, and derived an alternative equation with 3 parts that correspond to a production phase, expansion, and release of spent steam. Carnot later gave his colleague an unpublished manuscript, "Recherche d'une formule propre à représenter la puissance motrice de la vapeur d'eau." One equation for motive power, F, was written as follows[28].

N equals 48.2, and is the ratio P*V/367 where P is the pressure of a 10.4 m column of water and V is 1700 L (the volume of 1 kg of steam). P, p', t and t', respectively, are the vapor pressures and temperatures at the beginning and end of the cycle of operation. Carnot gave an example with p = 760 mm Hg, p' = 9.47 mm Hg, t = 100°C and t' = 10°C. He reported a value of 66,278.5 kg-m but rounded the number to 66,000 because he regarded it as imprecise. Fox[28] states that the correct value of F under these conditions is 66,734.8. By dividing this work by the number of Calories required to heat the kg of water to form steam, the result is 66278/650 = 102 kg-m/Cal.

The maximum amount of work that can be obtained from a perfectly efficient machine using 650 Calories of fuel is found by multiplying the number of Calories times Joule's coefficient, 427 kg-m/kcal. The answer is 277,550 kg-m. This indicates that Carnot's equation gave an answer that represents 23.8% efficiency. Probably, the calculated maximum is not equal to the ideal because perfect efficiency is only obtained if the condenser is operating at absolute zero. William Thompson (Lord Kelvin) later calculated Carnot cycle efficiency from the equation,

Where η is efficiency, To is operating temperature, and Tc is condenser temperature (K). At the temperatures stated, efficiency equals 23.5%. This correction would yield a mechanical equivalent of heat equal to 422 kg-m/kcal, which is very close to the modern value. The manuscript that Carnot provided to Clément does not discuss what later became known as Joule's coefficient or the mechanical equivalent of heat. However, Carnot did write a note to himself ([28], p. 191) that "the production of one unit of motive power requires the destruction of 2.70 units of heat." This indicates that he had calculated that 1 Calorie was equivalent to 370 kg-m of work (1000/2.7). This was the same value that Mayer later found, presumably because both men calculated the equivalence using the gas law (the logic is explained in[26], pp. 107–9). Mayer is also the first man known to have used the Calorie in a German publication[29], and he recommended using the kg-m as a common unit of work and energy

The recovered manuscripts demonstrate that the man who invented the Calorie was thinking deeply about heat. He not only defined a Calorie and used it in his calculations, but understood that the energy in fuels was related quantitatively to the amount of work that could be obtained from a heat engine. Clément and Desormes had developed an algebraic method of calculating how much work could be obtained from a steam engine as a function of the temperature and pressure of the piston and the condenser. Carnot solved the same problem using integral calculus and gave Clément a copy of his formula as well as his paper describing what is now called the Carnot cycle. Evidence suggests that Carnot knew that a "mechanical equivalent of heat" existed, but there is no record that he told Clément how to calculate the theoretical maximum. It is stunning that work of this prescience was not published and remained unknown to anyone who had not taken Clément's course. Through his influence on other chemists and engineers, it seems very likely that Nicolas Clément was indirectly responsible for the Calorie entering the French lexicon [30]. However, with no publication other than dictionaries to cite, the origin of the Calorie was unknown to Atwater and other scientists who later used the term.

Caloric equivalent of work by humans and animals

Whereas Clément was interested in obtaining maximum work from a given amount of fuel in industrial settings, Atwater's nutritional studies were motivated by a desire to provide nutritious yet inexpensive food for people who were accustomed to physical work. In explaining the Calorie, he indicated that the heat unit was equivalent to about 1.53 foot-tons mechanical energy (Fig. 1). He also noted that human mechanical efficiency was about 20%. Let us derive the modern "mechanical equivalent" in relation to kJ and kcal.

The work (J, with base units of kg m2 s-2) done in lifting a mass (m) of 1 kg by a height (h) of 1 m against gravity (g) is:

W = m*h*g = 1 kg*1 m*9.806 m s-2 = 9.806 J(3)

1 kJ = 102 kg-m (at 1 g)(4)

1 kcal = 102 kg-m/kJ*4.186 kJ/kcal = 427 kg-m(5)

The kg-m unit employs the kg as force (like the English or US pound) rather than mass because it assumes that the mass is being acted on by gravitation at sea level. If one converts 427 kg-m to US units, it is equivalent to about 3100 ft-lb or 1.55 ft-tons. These considerations lead to a very simple way of estimating the energy needed to climb. If stated in units that are relevant in nutrition (kJ), it is:

Where W is kJ of energy, m is mass (kg), h is height (m), 10-3 converts J to kJ, e is efficiency (unitless, a value between 0.2 and 0.3), and 102 is the mechanical equivalent (kg-m/kJ) (Eq. 4). If one prefers to express energy as kcal, the mechanical equivalent is 427 kg-m/kcal (Eq. 5). Eq. 6 may appear unfamiliar, but it is the original form of the energy balance equation that relates the potential energy in food to the expenditure of mechanical energy that the food will support. The equation implies that one who consumes 1 kcal must perform work equal to some fraction of 427 kg-m to remain in energy balance. For example, how high a mountain would a 70 kg person need to ascend to eliminate the energy in 1 pound (0.454 kg) of fat? If one assumes the fat contains 3500 kcal of energy and that efficiency is 20%, the answer is about 4,270 m (14,000 feet, similar to Mt. Rainier). This relationship was self-evident to Atwater but has been lost from modern nutrition texts.

Advent of the g-calorie

From 1824 to 1851, several well-known dictionaries and physics texts defined the Calorie in terms of heating 1 kg of water[6,18,31]. Despite this, the definition must not have been widely known among chemists. Favre and Silbermann published a series of studies on heats of oxidation of acids and bases, and in 1852 [16] used the calorie as a heat unit based on a mass of 1 gram. Whereas Clément never published his definition outside of Le Producteur, Favre and Silbermann published extensively in prominent chemical journals and their work was well known in the field of chemical calorimetry. Perhaps because there was no way to cite Clément's work, most scientists assumed that Favre had invented the unit and that it was defined as a g-calorie. Nonetheless, the large Calorie was still the only unit defined in dictionaries and physics texts.

Because of the dual origins of the calorie, by the 1860's, the same word was being employed in reference to g-calories and kg-calories, but no one had applied metric prefixes to the units. Finally in 1879, the chemist, Marcellin Berthelot, differentiated the two units by capitalizing the large or kg-calorie and noting that it equaled 1000 of the smaller g-calories [11]. Prior to that time, the calorie was most often written with lower case units, but because the word is a noun, it was capitalized when written in German. Certainly, Berthelot knew the metric prefixes and it is unclear why he did not apply them to solve the problem. A timeline of these events is shown in Fig. 2.

Karl Voit was a prominent German physiologist who developed one of the first laboratories that could evaluate food energy and human energy usage. He certainly would have known of Mayer's work on the caloric equivalence of physical labor, but did not adopt the kg-calorie as a standard. Instead, Voit began using the g-calorie in lectures on human calorimetry in 1866, and stated that daily metabolism of one male subject was 2.25 to 2.4 × 106 g-calories, depending on prior diet[32], p. 35. The most likely reason for this choice of energy units was that students of calorimetry knew about Favre and Silbermann's work but not Clément's. By 1883–85, Voit's student, Max Rubner, had published papers using the g-calorie to define heats of combustion for food and heat produced in respiration studies [33-35]. In the same period, Henneberg and Stohmann were using calorimetry for proximate analysis of livestock feeds at the Weende Experiment Station [36].

Debut of the kilocalorie

It is not known what source Raymond used when he named the kilocalorie in his 1894 textbook of medical physiology[13], but the unit was not in general use. He may simply have decided to avoid confusion between g-calories and kg-calories by using accepted metric prefixes. Even in 1903, English dictionaries still defined the calorie relative to a kg of water and there was no definition of a kcal. The kilocalorie was not introduced in an indexed scientific publication until after Armsby proposed a new energy unit to be called a Therm in 1907[37]. In response, A.T. Jones wrote a letter to the editor of Science noting that Armsby's new name was unnecessary, and reminded readers of the convention of using metric prefixes. Jones specifically stated that if one accepted the g-calorie as a unit in the cm-g-s system, then the next larger energy unit should be called a kilocalorie[12]. In 1909, a "kilocalory" was introduced in a supplement to the New Century Dictionary. The kcal began to enter other dictionaries after the m-kg-s system was introduced in the period between 1918–1935[38,39]. The OED notes that by 1923, European physics texts were employing the kilocalorie as a unit of heat and that the unit was known to German law. In 1927, the New Century Dictionary still defined the "calory" as the heat needed to raise the temperature of 1 kg of water by 1°C, but noted that a "small calory" based on heating 1 g of water was also used. Beginning in about 1935, the kilocalorie began appearing in English dictionaries and the period of "calorie confusion" set in.

Origin of the cm-g-s system and the joule

The base units in the original metric system were the meter, the kilogram and the second. Admittedly, the way the units are named suggests that the g is the base unit and the kg is a derived unit. However, the metric system was originally intended for commerce and the kg was based on the weight (not mass) of 1 liter of water at 0°C. Energy was not considered to be an item of commerce, and no units of energy were suggested by any official organization until the First Law of Thermodynamics was understood. A commission was established by the British Association for Advancement of Science after 1862 to define precise electrical units. The members of the commission were primarily British physicists and engineers; no member of the committee had a background related to nutrition. They introduced the cm-g-s system in 1873 and named the dyne and the erg as units of force and work[40]. They then departed from the rule of naming units with Greek or Latin roots and decided to honor important scientists such as Ampere, Ohm, Volta and their colleagues, Watt and Joule. The OED states that the joule was proposed by Siemens in 1882 and the British Association adopted it for the cm-g-s system in 1888[41].

The joule was originally an electrical unit, but the committee realized that the same unit could be used for heat, work, and any other form of energy. By 1896, the committee had decided that a g-calorie could be considered a secondary unit of energy[41,42]. The committee noted that there was no agreement concerning what temperature of water should be selected as a basis for defining the calorie. It seems evident that no committee member thought to check the definition of calorie in the Imperial Dictionary[7], nor did anyone observe that it would have been satisfactory to leave the unit at 0°C and make corrections based on tables of the specific heat of water as a function of temperature [43]. It would also have been feasible to base the Calorie on the molar heat of benzoic acid, as was normal practice in calorimetric studies [26].

The units of the cm-g-s system were too small for many scientists, and it seems that the use of metric prefixes to define different scales was not an automatic standard. To accommodate a larger scale, the m-kg-s system was proposed around 1918[38]. Therefore, prior to the development of the Systém International des Unites, the m-kg-s system and cm-g-s system co-existed (Fig. 2). In 1935, the International Electrotechnical Commission adopted the m-kg-s system. It accepted the g-calorie as a thermal unit in the cm-g-s system and the kcal for the m-kg-s system[39].

The Bureau International des Poids et Mesures (BIPM) was established in 1875 to reach consensus on basic metric units. During the 1930's, the BIPM convened the Consultative Committee on Thermometry (CCT) to clarify standards of heat. The committee was led by W.H. Keesom, who summarized a proposition that the calorie should equal 1/860 watt-hours or 3600/860 joules (4.186 J)[44]. From then on, any secondary thermal unit was to be defined relative to the joule rather than to the heating of water at any temperature. The 1948 General Conference also recommended discarding the calorie because it could not be derived directly from basic units. In 1954 the SI base units were adopted, and in 1970, the Committee on Nomenclature of the American Institute of Nutrition advised that the kilocalorie should be replaced by the kilojoule (kJ) in scientific publications[45,46].

From 1935 forward, most scientists probably believed that the g-calorie had been a base unit in the original metric system. Clément's definition had been entirely forgotten, and no one seems to have objected that the Calorie had been defined differently in dictionaries for 50–100 years. It did not matter to the physicists and electrical engineers that ordinary people who used food tables had never heard of the joule. Nutrition scientists may have noted Kennelly's article on the m-kg-s system[39], but the Calorie had been the nutritional unit of potential energy since the first food tables were published[3,8,14] and no one was in a rush to change.

The transition from Calories to kcal in nutrition

By the time the kcal became a recognized unit, the venerable Calorie had been in the U.S. English lexicon for over 50 years. Because the Calorie was adopted as a unit to express the physiological fuel values of foods in USDA Farmers' Bulletins[14,15], the unit made its way into articles and books that dealt with weight reduction. For example, Dr. Lulu Hunt Peters' popular "Diet and Health with Key to the Calories" specifically cited Farmers' Bulletin 142 as a source of information [47]. Because of similar precedents, nutrition-related publications worldwide employed the Calorie as the sole energy unit until about 1960. This usage became dominant when the U.S. Recommended Dietary Allowances (RDA) began to employ the Calorie from 1943 until 1956[48]. The Calorie was also used in handbooks for clinical dietitians and medical practitioners[49]. Ironically, as S.I. units developed after 1948, it was recommended that all forms of the calorie be abandoned. Beginning in 1960, papers published in nutrition and dietetics sometimes noted that the Calorie was the same as the kcal, and the same point was made in the 1964 U.S. RDA. By 1968, the kcal had replaced the Calorie as the unit of choice in the RDA, and between 1964–1970, most nutrition journals made the transition. It is ironic that by 1954, the physicists and engineers who had instigated the change had abandoned calories in favor of the joule. To the extent that the kcal was ever an "official" unit, its reign only lasted from 1935 to 1948! Nevertheless, editorial style guides for essentially all international journals in the life sciences accepted the g-calorie as a base unit and allowed the kcal to be employed to express larger quantities of energy.

The outcome of the attempt to become more sophisticated about energy units was that a word that was understood by scientists and the public alike from 1887 until about 1960 was abandoned by the professionals. From 1970 on, all nutrition texts had to change from Calories to kcal, although some protests were made. The chapter on energy in Goodhart and Shils' 1980 Modern Nutrition in Health and Disease [50] defined the Calorie, the kcal and the joule but complained, "Personally, I am happy with calories." One can easily verify the late transition from Calories to kcal by checking back issues of AJCN, the Journal of Nutrition and any nutrition textbooks published before 1975. This history is probably unknown to any scientist who earned a doctorate after that year.

Summary

History shows that the Calorie of food labels has priority over other energy units, dating to at least 1824. Scientists of the time were using calorimeters in a discipline called calorimetry, and it was quite natural to adopt a heat unit with the same Latin root. Existing manuscripts show that the unit was initially defined in Clément's course on industrial chemistry [22] and a published description of the course [19], and not in a publication that was recognized by scientific bodies. One lesson that any scientist would draw from this history is that it is essential to publish ideas and definitions in peer-reviewed journals. Although Nicolas Clément did not do this, his influence was sufficient that the word gained a dictionary definition by the 1840's. The Calorie was defined in engineering publications during the 1820's, and it is inexcusable that later workers failed to note these sources [30].

Arguably, the Calorie is the energy unit that is best understood by the US public. In contrast, the pedigree of the g-calorie began in 1852, and the kcal in 1894–1908. The joule was developed as an electrical unit and a common unit of energy in the 1880's. After the Calorie was adopted by Atwater in 1887, it was used consistently and without confusion in nutrition science until 1964–70. Oddly, when the kcal was introduced as a nutritional unit beginning with the 1964 U.S. RDA, it had already been superseded because S.I. units had replaced the awkward division into cm-g-s and m-kg-s systems. However, most scientific journals adopted the 1935 proposal to allow the joule, the calorie (former g-calorie) or the kcal and eliminate the Calorie. Current style guides show that this is still the case, even though the kcal of the m-kg-s system and g-calorie of the cm-g-s system are officially obsolete. In contrast to U.S. food labels, European food labels must list kJ and kcal. Both units are also reported in USDA databases.

The history discussed here explains why the Calorie came to be used not only in food databases and on nutrition labels but also in most popular recipe books that include nutrition information. One can easily verify that the Calorie (capitalized or not) is the most common unit of food energy found in recipes and articles on the Internet. It is interesting that there is little confusion of usage in popular culture except after scientists helpfully try to explain that the "proper" term is kcal and that it rightly should be converted to kJ. This leads one to wonder whether the physicists and chemists who multiplied the energy units ever took a lunch break.

The motivation for writing this article was to show why W.O. Atwater chose the Calorie (modern kcal) instead of the g-calorie and to explain more about the contributions of Nicolas Clément-Desormesc, the man who probably invented the calorie. The Calorie has a 140 year pedigree in the English language, and there is a question of whether it can or should be dislodged by academics and policy makers. It is a practical unit that lacks the pretension of metric prefixes. It was coined using good rules of naming because calor means heat. The definition is familiar to anyone who has ever heated water. Moreover, energy needs are easy to calculate because men need about 100 Calories an hour, and women somewhat fewer. None of this is true if kJ are substituted. Most U.S. nutrition educators probably would agree that Dr. Atwater made an excellent choice.

Recommendations

Firstly, educated people including college students should understand that all forms of energy can, in principle, be interconverted according to the First Law of Thermodynamics. Because of this, it is convenient to employ one common energy unit (the joule) that enables scientists and engineers to communicate freely using the SI system. It is true that a number of obsolete energy units such as the erg and the therm have ceased to be used in most areas of science. However, there are still reasons to employ different energy units in special circumstances. Good examples are cases such as the electron volt and hartree in which differences in scale make it cumbersome to employ the joule. The fact that it is preferable to use the joule does not mean that it is always the best choice. One might argue that the Calorie has always been used as a unit of potential energy in food and the equivalent energy in human tissues that can be removed by work, rather than work itself (J).

Secondly, if it be agreed that the joule should be the common unit of energy and work for scientific correspondence, then it would follow that journals should stop permitting the obsolete kcal to be used as an energy unit. With that unit discarded, there would no longer be a need for the small calorie to be used in any context, thereby eliminating the major point of ambiguity with common English usage. Furthermore, nutritional databases could remove the kcal and continue to employ kJ. This action would eliminate the problem of using two words (kilocalorie and Calorie) for the same quantity of heat.

The simplest intermediate course would be to recognize that the Calorie is an accepted English word and include it along with the kJ on food labels and databases. It would no longer be necessary to capitalize the calorie because it would have one meaning: the amount of heat (defined as 4,186 J) required to raise the temperature of 1 kg of water from 14.5 to 15.5°C. These actions would eliminate the confusion caused by having two unnecessary words that scientists introduced and should remove from the vocabulary. After all, starting in about 1970, nutrition scientists grudgingly made the transition from Calories to kcal, but the original plan was to abandon all forms of calorie after a short sunset [45,46] That plan could be completed by simply changing the style guides in major journals. The outcome would be the elimination of "calorie confusion" with scientists retaining their joules and the popular press continuing to employ calories in recipes and diet plans, as they have done for a hundred years.

Abbreviations

OED: Oxford English Dictionary;

BIPM: Bureau International des Poids et Mesures;

SI: Systém International des Unites.

Appendix

a). Calorie will be capitalized when the context refers to the modern kcal (4.186 kJ). The lower-case calorie will be used when the g-calorie (4.186 J) is meant.

b). In addition to Le Producteur, records at Gallica include Favre and Silbermann's article on calorimetry, copies of L.N. Becherelle's Dictionnaire National and Adolphe Ganot's Traite Elementaire de Physiques.

c). Nicolas Clément married Claude Desormes' daughter and adopted his father-in-law's name. Nicolas Clément and Clément-Desormes are the same person. One reason for confusion is that their paper on the determination of ? in the gas law is often referred to as "the experiment of Clément-Desormes". Note that Nicolas Clément did not spell his first name with an h.

Acknowledgements

This research was supported by USDA Hatch project GEO-00602.

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by EricT

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