You may have noticed that it can be difficult to get a good deep breath in between reps of the front squat. Not everybody has this problem to the same extent, but most everybody would have noticed that the front squat makes breathing a bit restricted. The position of the elbows, combined with the heavy load on the shoulders, restricts the chest. It is easy to simulate this effect right now as you read this: simply raise your arms up over your head and try to take a deep breath into your upper chest. You should notice that the chest wall is restricted and it is close to impossible to take a full breath this way.

Now, many of you should right now be saying, but Eric, dammit, you're not supposed to breathe into your upper chest. Bingo! This means that those trainees who are upper chest breathers will have more difficulty during the front squat than those who are diaphragmatic breathers. For the purpose of this explanation, we will assume two general groups of trainees:

• Habitual upper chest breathers (you breath this way all the time)
• Stress chest breathers (you breathe this was when your are out of breath, anxious, etc.)

Each group, to some extent, must be able to take proper diaphragmatic breaths during the front squat in order to get that precious air. This means each group may need to practice diaphragmatic breathing on a fundamental level. Therefore, the first thing to do to begin solving this problem is to read Paradoxical Versus Diaphragmatic Breathing, see where you stand and follow the steps in the article accordingly.

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Even some of us who a good diaphragmatic breathers during normal, quiet breathing may switch to upper chest breathing when we a exerting ourselves and are out of breath.

During the front squat itself, beyond the trouble getting a good breath between reps, there are a couple of other associated problems. When you front squat, your core is braced. Now, your core "braces" automatically in response to you loading a heavy bar on your shoulders and trying to maintain equilibrium. Also, you probably would have used an "abdominal brace" which is the conscious act of tightening the core muscles to get ready for a heavy lift, which would serve to reinforce the natural contraction that is already happening intermittently as you hold the bar, because you are about to initiate a rep. What some people may find is that they are unable to maintain this core brace while breathing, which may lead to breath holding, either consciously or unconsciously. If you are a chest breather you will notice that this actually perturbs you and causes your upper body to actually move posteriorly and anteriorly. just slightly, but enough to cause further perturbation down the chain so that it is harder to maintain your front squat setup.

Also, some who do breathe correctly into through the diaphragm may find that they have a hard time maintaining a brace while using diaphragmatic breathing. In other words, they cannot maintain and abdominal brace without holding their breath. If you have this problem, and you have also been told that you have to suck in a big breath and hold it in order to brace the core, then you'll have a hard time ever learning to breath freely during front squats.

All that breath holding, both during the lift itself and in between when you don't know you're doing it, can end up making you dizzy, subject to exertional headaches, or even brief but dangerous blackouts. Now, you know me, I am no fear monger. These things are possible, not likely. One thing is clear, though, if you can't breathe you are going to be missing an essential ingredient in your lifting, so that's enough reason to solve this problem. However, if you are subject to dizzy spells or exertional headaches, the ability to take diaphragmatic breaths without feeling like you need to dump the bar can help you a great deal. Many lifters take a series of short panting breaths between reps of a very heavy lift, and although some of them do it for no reason other than to get ready to take an even bigger breath, others due it to "clear the cobwebs" for lack of a better phrase. Breaths like this may help to regulate elevating blood pressure between repetitions of a lift.

The Front Squat Breathing Drill

The first thing to do, as mentioned above, is to learn about proper diaphragmatic breathing and then to learn to do it. Depending on the depth of your problem with chest breathing, this may take a long while or just a couple of days or weeks. There is no point in engaging in a breathing drill that uses diaphragmatic breathing if you have never taken a diaphragmatic breath! You have a more fundamental problem and it is quite important that you fix it, as the article will explain: Fix Your Upper Chest Breathing.

Once you have become somewhat "adept" at correct breathing, you can begin to use the front squat breathing drill. The first part uses a concept invented by Stuart McGill, which he calls developing and "athletic diaphragm." For this purpose, he tells us to get ourselves good and out of breath, in some way, and then do front planks for time. The front planks force you to brace your core, through co-contraction of the abdominal, back, and glute muscles and being out of breath forces you to have to breathe while maintaining that core brace. For McGill, the purpose of this was not heavy lifting, but dynamic and multi-directional athletic movements that require core activation while continually breathing. As you can see, certain lifts cause similar needs, as they force us to maintain an activated core while still being able to catch our breath, and the front squat makes breathing more difficult for chest breathers.

So, the front planks are very useful for this, and I use them in this drill, but while they make diaphragmatic breathing more likely to be the breathing pattern used, they do not absolutely force you not to breathe correctly. This makes the front planks a good fit for those who are already habitual diaphragmatic breathers and just need to learn to maintain a core brace while breathing but not as useful for those that are having trouble during the front squat because they are chest breathers. Remember, you should have already learned about diaphragmatic breathing before starting this drill, but I do not expect you to be a master and do it under periods of stress.

For that reason, I have also included supine or 'glute' bridges. Bridges actually force you to breathe through the abdomen much better than planks. You will find, although you may have never noticed, that they restrict the chest in a similar way to the front squat. Once you combine that with being short of breath, it is a good trainer and reinforcer for maintaining correct breathing under stress. Still, the bridge does not require the core to be braced as vigorously as the front plank, so we use both. The bridge comes first, to remind us, activate, and reinforce proper breathing, and the front plank comes second to train it more effectively. So the first phase of this drill should last for several weeks, as long as you need it to feel thoroughly masterful of breathing in this way. Here are the steps, although they are so simple, listing them out is probably overkill.

So this is Phase One:

1. Do some kind of vigorous movement to get out of breath. You want to be panting and needing to "catch your breath." Hint: Larger muscles groups used through a large ROM will work quicker than something like the treadmill. Do body weight squats or something like that for ver quick repetitions. It is really your choice though, as long as get the job done.

2. As soon as you are out of breath, get into a supine bridge position and hold it for 15 to 30 seconds.

3. If you need to, get out of breath again.

4. Do another supine bridge, hold for 15 to 30 seconds.

5. If you need to, get out of breath again.

6. Get into a front plank position. If you are very tired you can do it on your elbows. Hold for 15 to 30 seconds.

7. Repeat. (I shouldn't have to tell you to get out of breath again if you need to, right.)

Continue phase one for at least three weeks or as long as you feel you need to. Then go to phase two. Phase two will involve Heavy Barbell Walkouts. A walkout is nothing more than loading a heavy bar on your shoulders and "walking out" as if you are about to do squats, but instead you only stand there with the bar for a while, forcing you to maintain position (it's a core thing).

This is phase two:

1. Set up the squat rack for a front squat and load the bar with your about ten pounds below your current heaviest working weight, or UP TO 10 to 20 lbs beyond it, if you are comfortable supporting it. Remember, you are going to be compromised and having trouble catching your breath, so act accordingly.

2. Get out of breath, just like in phase one.

3. Load the bar onto your shoulders in a front squat position and perform a front squat walkout. Hold for 15 to 30 seconds. You should be forced to catch your breath by breathing through your belly instead of your chest while also needed to maintain enough core brace to keep steady.

4. Put the bar back on the rack (I can't believe I wrote that out).

5. Rest a little then get out of breath again and repeat steps two and three.

6. Repeat step four.

As you move along, you can load the bar heavier and heavier. Normally you should always be able to do a heavy bar walkout with a heavier weight than you actually squat with but you do not normally do aerobics and get all panty before a walkout, so tread carefully and build up when you feel comfortable with it. Continue practice should make breathing during front squats second nature to you.

Breathing for Overhead Press (Military Press)

The same breathing difficulties are common during overhead press, if not even even more. More intrathoracic pressure is created during the press. The drill is used in the same way for the press as the beginning position for the press is similar to the front squat. See comments below for further explanation.

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by EricT

Why? I've always wondered about this? Are you such an Adonis but at the same time so weak that you need to work your butt off so that you can become as strong as you look? Even pro bodybuilders are pretty darn strong compared to the average Joe. But let's just stick with the average Joe, not the pro. Let me ask again, why would you want to get strong without adding any muscle?

I wonder this because at least once a month I see a new article explaining how to do this. Why is this concept so popular? Is it because:

You Don't Want to Get Bulky

Well, that won't happen. I know that you may have read articles that tell you that doing strength training will turn you into Arnold faster than Arnold himself became Arnold with bodybuilding, but those articles are, pardon me, full of crap. It will take years of dedicated strength training for you to get all huge. And as I have pointed out again and again, those big old bulky strength dudes who you THINK got their quasi-bodybuilder look from pure strength training, have likely done their fair share of work in bodybuilding parameters, as well as plenty of biceps curls and chest flyes. If you don't want to get bulky you will not, unless you are a muscle gaining freak, what is typically referred to as an "easy-gainer".

You Think Big Muscles will Slow you Down

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See point one, above. Nope. High force strength training increases speed. Even if you don't train for speed it increases rate of force production. Strength training has become a very important part of athlete's training for speed. Likely you will read that high repetition bodybuilding training will bloat you with big "empty" muscles, decrease your ROM, and slow you down. Well, Flash, if you are so concerned about speed, why are you into bodybuilding? Stick to strength training and you can have your speed and eat it..I mean you can have your speed and your muscular strength. Obviously, those training for speed should have most of their training dedicated to that skill.

You Want Dense Muscles, Not Big Ones

I take it you've been reading Pavel. This goal, nowadays, seems to be the most popular one. To bad it is utterly meaningless. Muscle density is not a clearly defined concept. Some people think that muscle density is something similar to muscle tone, or tonus. I.E. it is how hard your muscles are and is related to…

Wait a minute. Let's start from the beginning. Some think that the word tone refers to the shape and definition of muscles. This is the origin of "toning exercise" and toning routines. This is an incorrect usage of the word tone.

More correctly, the term muscle tone or "tonus" refers to the tension in the muscles. You can think of it as a state of partial contraction (very slight) in which the muscles are kept, kinda like the muscle is always "ready for action." More specifically, it refers to the slight tension that can always be felt in a relaxed muscle, which is called the muscle's resting tone. Strength trainees, athletes, and active individuals will tend to have increased resting tone. That is the technical explanation.

Problem is, even within this technical arena, it's used differently by different experts and authors (common problem), so that some people may only consider tone by looking at the muscle's resistance to passive stretch and others might only press the muscle (palpation) to test its tone, which is a way of judging its stiffness and consistency. These two different methods do not measure the same property but are both looking for "tone". Different pathological states may change these features relative to one another, making tone an ambiguous term.

Not only does tone lack an exact definition (or true understanding), other words related to it are also ambiguous, like firmness, stiffness, elasticity, and tension. Then comes in muscle density. It goes like this: "I want to have strong and hard muscles without being big. Therefore I want dense and toned muscles." It seems like to get dense and toned muscles you have to go for the same ambiguous firmness, stiffness, etc. to get these two different features. The guys in lab coats cannot even decide on what exactly they mean, but you can?

Density could refer to the actual density of an individual muscle fiber, which for mammalian muscles is about 1.056 g/cm³. You cannot change that.

Or it could refer to the intramuscular fat content or how closely packed together the myofibrules are. If intramuscular fat is decreased or the density of myofibrillar packing is increased, this should theoretically serve to increase muscle tension capacity. When you engage in strength training, these things happen. You don't do resistance training to have these things happen, you do it to increase the strength (tension generating capability) of the muscles. These changes in the muscle, and many others, are part of the explanation of how muscles get stronger. They are a couple of features, among several, that are side effects of the strength training process. The goal of isolating this one component of the results of strength training through a special kind of strength training simply means that you are capping off just how strong you are willing to get.

Why? Because these changes are part of the initial stages of strength training! They happen early on, along with neural change and simply help explain why there can be such a profound increase in muscular strength in the early stages of training without apparent changes in muscle mass. Eventually, to keep getting stronger, morphological changes become more and more important. You "only" want to have toned and dense, but small muscles, then you only want to get so much stronger, and no more. Period. That is easy. Strength train a little, and then maintain. There is no magic recipe, really.

I cannot imagine a more silly and boring goal than "decreasing my intramuscular fat, increasing myofibrillar and resting tone." If that is your goal, then happy training. If it seems I'm engaging in a bit of hyperbole, perhaps I am. But specific measurable goals are fairly important in training. If I have correctly translated the "tone and density" hoopla into it's actual components, then I'll leave it up to you to determine whether these are goals within themselves or simply a couple of components of the outcome of increasing muscular strength.

Strength training is a fairly specific activity. Its goal is to increase the absolute force producing potential of our body. But I have to tell you, when someone starts telling people they should be careful, they don't want to get too bulky! Better train for tone! Increase density! Do body weight only training!…Some of us get a little perturbed. Because these people are implying that developing large strong muscles through strength training is a walk in the park. They are acting as if this happens because we accidentally trained too heavy and too hard. No. It takes years and years of "backbreaking" work to get "big, strong, and muscular" let alone huge and bulky. Many people who do dedicated strength training, past noticing that they seem in shape and "look strong" you would not think of as huge and bulky. It just doesn't work like that. You have to want to get huge and bulky to get truly huge and bulky.

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by EricT

Training for maximal strength is essentially training to exert maximum muscular force. So what is force? The easiest way to think of a force is as a simple push or pull. When you push or pull on a barbell or other implement you are exerting a force. The pull of the Earth's gravity on an object is a force. Friction is a force. To be more precise, then, a force is something that causes or tends to cause a change in the motion or the shape of an object.

When you attempt to deadlift a heavy barbell you are exerting a pulling force on the barbell. That force has a magnitude, a direction, and a point of application. By applying the force you are attempting to change the state of motion of the barbell. If your force is too weak, the barbell will not move. There is a greater force acting against your effort. In this case it is the weight of the barbell or the inertia of the barbell. The weight is the downward force of the Earth's gravity acting on the weight, which is proportional to its mass. The inertia of the object is it's tendency to maintain its state of motion, whether moving or not. Inertia is easy to understand. The more massive an object is the more it tends to maintain its present state of motion. A 300 lb barbell has a lot of inertia. Now imagine a 300 lb linebacker running at you full-tilt. To stop him, you'd have to overcome his inertia. In either case, you must change the state of motion the object or body.

The failure to move a heavy weighted implement, such as our barbell, is a source of confusion for strength trainees. This is because the application of force is thought of as the actual result of the force or more specifically, its effect. Most strength training articles concerning force simply relate the classic Newtonian law F = ma which translates to force equals mass times acceleration where m is the mass of an object in grams or kilograms, and a is the amount of change in velocity in meters per second squared, i.e. acceleration. However although this is usually reported as the absolute definition of force it is really a relationship or a means to measure the effect of force which is the resultant acceleration of an object. This is great for physics and mechanical laws but for defining force it makes force itself a mere abstraction that grows out of the change of an object's velocity. This view of force, despite it's precision, doesn't really help us train for strength as the effort we exert against a weight is NOT an abstraction.

Even if your barbell does not move your application of force to it creates a tendency for it to move. If a friend also grabbed on to lend a hand, the barbell might move. The absolute force being applied to the bar increases. Our goal, then, in training for maximal strength is to increase our ability to exert muscular force, plain and simple. Force is probably mentioned on GUS more than any other strength related word. For further reading see the many other pages concerning force or forces.

Some Technical Notes, Just for Fun

• The symbol for force is F.

• The pound is a unit of force. However, the SI unit¹ of force is the Newton, named after Isaac Newton and abbreviated as N.

• A newton of force is the force required to accelerate a 1 kg mass 1 m/s/s which is written in mathematical terms as: 1.0 N = (1.0 kg)(1.0 m/s/s). One newton equals 0.225 lb of force and one pound equals 4.448 N.

• Force must be considered in terms of it's point of application, its direction or "line of action", and whether is pushes or pulls. Since a force has magnitude (size) and direction it is a type of vector. A vector is represented by an arrow on a free body diagram. The length of the arrow represents the size of the vector, the orientation represents direction, and one end of the arrow represents its point of application. Other vector quantities are weight, pressure and torque.

• For the purposes of strength training we are not concerned with a force that deforms, or changes the shape, of another object. Instead, we are concerned with forces that either start, stop, speed up, slow down, or change the direction of an object. Since deformation is ignored or assumed not to occur this is called rigid-body mechanics.

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by EricT

Raise your hand if you have recently read a news or magazine article, on the web or elsewhere, explaining the results of one study and making concrete conclusions based on that one study. Yep, all of you. I figured as much.

A study in Australia revealed that young women fight off colds better than young men. Case closed. Not. First of all, "a study in Australia" is not an appropriate reference. No reference, no credibility. Second of all, there is no way that ONE study could possible "reveal" conclusively that young women have colds that go away quicker than young men.

I know that you probably don't care about a study that says young women have shorter colds. But what if the study reveals something you'd like to believe? What then? I know it is tough to not cling to any little tidbit that confirms our favored reality. Trust me, I do. For instance, you know those toning shoes? Sketchers Shape-Ups, Reebox EasyTone, MBT…you've seen the ads. There was one study from The American Council on Exercise which suggested that, low and behold, those shoes don't do any of the things they claim to do, such as activate the calves and hamstrings better and burn more calories. The study 1 by Porcori, et al. was divided into two trials, with 12 females each, one group for muscle activation and one for caloric expenditure. I have very little doubt that these shoes are complete and utter crap. But one study of 12 just ain't enough for me to go around saying we have conclusive proof. I'd say we have a good indication, but you won't see a front page banner on GUS proclaiming this NEW STUDY!

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And let's be fair here. Concerning the referenced study, the author of the related article 2 on the Ace Website complains that the studies performed by the manufacturers of these shoes are not peer-reviewed, failing to see the irony in the fact that neither is the Ace study, having not been published in a peer-reviewed journal! Something is amiss, is it not? In fact, according to an article by Denise Mann 3 the Skechers company president actually called out the study based on this fact. Man, you've got a problem when the company guilty of BS in-house "studies" proving their products effectiveness actually call you out on your study not being peer-reviewed. Could Ace be biased as an organization? Sure, it's possible. Should we take Ace funded studies as seriously as other studies funded by independent sources? Maybe not. After all, Ace is about producing fitness professionals who make a living helping people get fit. Still, this does not mean that the study is completely bogus. It's just not enough and questionable, as all studies are. And before you ask, Mann is pretty good at reporting on these things and yes, she actually references her articles.

None of this means that I won't think you are silly for spending over 100 bucks on any of these shoes. I don't need studies, most of the time, to tell me when a fitness product is not worth the material it's made from. But I'll need to wait for some confirming evidence before I start referencing research to support my opinion. Right now, it's just an opinion backed up by one small study, which may have it's flaws, including it's lack of scholarly publication. If you want to know, you go read it; I actually referenced it! Boy was that tough! I want to get back on track.

From my perspective there are two problems. One is that news and magazine articles routinely fail to properly reference the research they mention. Studies absolutely must be properly listed, with a link, complete journal citation, or both. If you cannot easily go find the study and read it yourself, the article's validity is suspect. Many times, you will find, even once you search out the study in question, the conclusions of the study's authors are not anything like the conclusions of the magazine article. This happens constantly, in fact. Not just in big publications but all over the web. Usually, people look for articles that seem at a glance to support what they already believe, and have no regard for what the study's authors actually conclude!

The other problem, from my perspective, is that it is nothing more than content baiting. The public is being led to believe that huge discoveries are being made in the realm of fitness and health almost on a daily basis. Single small studies are used for no other purpose than to support a provocative headline to draw you, the reader, in. These news and magazine outfits do not care if what they report is accurate and they surely do not care if it makes a difference in your fitness pursuit. If they did, they would research the articles much more widely. The typical formula for these articles goes like this:

1. Vague reference to some study, usually only with a place named, like Austrailia, or the last name of one of the researchers

2. Vaguely related quote by an expert in the same field, usually someone who has a vested interest in confirming the conclusions of the said study

I would love to be able to have a subject for an article every time someone does a study related, in some way, to fitness. Then, all I'd have to do is check Pubmed every day looking for something juicy and write some half-ass post on it. I'd have a website filled with content and provocative headlines. I wouldn't even need to stick strictly to fitness. What about a "recent study" that shows that pregnat women who eat chocolate have healthier babies who with better temperaments. What do you think the response to that would be? Yippee, I can eat chocolate! Like a pregnant woman needs and excuse, anyway. 4

Even when it comes to reading and analyzing single studies, though, there is a particular skill and expertize required, which the average journalist does NOT posses. There are, however, many good scientific blogs related to fitness that do a much better job. So, all you need to do is skip the big headline at the top of the Google pile and look for some blog entries by people like, say, Bryan Chung, who, it just so happens, weighed in on the barefoot shoe thing recently. You know, Vibram FiveFinger shoes and all of that. Just so happens there is a study from Ace on the barefoot shoes as well, according to this article. 5

Self Plagiarism, Salami Slicing, and Publish or Perish

It is good to be aware of emerging research but don't let the horse get ahead of the cart. It takes a while for enough data to be gathered to make meaningful conclusions. Before I leave you I want to give you one more thing to watch out for, in regards to scientific research published in peer reviewed journals. It's a "dirty little secret" if you will.

The unethical and damaging practice I am talking about is sometimes referred to as "self-plagiarism". Let's say I write what is essentially the same article, with the same thesis and conclusion, and publish with different wording in several different places. Is this a big deal? Nah. These are just informal articles and if I were to follow this practice it would just be for the purpose of fitting the article to a particular audience I was aiming towards. Plus, if I had a "parent" article I would most likely acknowledge this article in some way.

But what if a scientific researcher does this? Well then it is a very damaging and, to me, quite unethical practice. The major problem is using some data, or other part of an earlier study or paper in a new paper without cross-referencing it, to make it appear as the data, study sample, etc. is completely new and original to the study or paper in question. This absolutely puts a wrench in the whole kit-n-caboodle we call science. And it is done constantly. Most studies I find, in fact, are published in several different journals with no reference made to ever being published before. The question is, is it done deceptively? Well, if no mention is made of how parts of one paper overlap with another, it is always deceptive! If we think something is new, when it is not, it completely skews our evidence base, making it hard to make informed decisions.

Usually, once an article has been published in a peer-reviewed journal, it is not acceptable to re-publish it, and this could be considered copyright infringement.

Many times, you will see the same name pop up again and again in regards to a specific scientific claim and it will seem like said person is just publishing reams of research in regards to this claim. When you see this happen, consider that this person may be doing another form of self-plagiarism called salami slicing. This is when a researcher takes what is essentially one large study, that could be reported in one paper and slices it up into smaller chunks which he scatters all over the place, mostly to increase the author's number of publications. This makes the importance of the work seem greater than it actually is..call it a shotgun effect.

Don't blame it entirely on the researchers, though. Not many want to increase their publication count just for the sake of it! It's publish or perish and, according to Nature Materials: "Much of the problem arises not from an inherent desire among researchers to maximize their publication count, but from the conditions that are set by funding and appointment bodies, which determine what gets funded and who gets tenure. In the 'publish or perish' climate that has evolved over recent decades, overemphasis on the size of an individual's (and, increasingly, entire research group's) publication record as a means of quantifying their research output inevitably rewards quantity over quality. Moreover, this has the effect of abdicating responsibility for such assessment to the journals in which they publish — a responsibility that is neither appropriate nor desired." 6, ((bibicite cicutto))

The explosion of researchers and journals is huge enough without the above practices adding to the pile. I mentioned the term "peer-reviewed' a couple of times in this post but it has started to become a joke since there are just too many papers appearing on a daily basis for most of them to be peer-reviewed.

You can bet that your average fitness article citing some research study (while not actually citing it) is completely oblivious to these problems.

by EricT

Instead of listing out twenty tips in an obviously deceitful display of "yeah right you gullible fool," all I really need to say is this: Pick twenty random things from around your house that can be smeared on a burn, poured on a burn, etc. And you have your twenty home remedy tips.

Soy sauce. Mustard. Vinegar. Hey, take some chewing tobacco, chew it up real good, and spit it on your burns. I swear, it works wonders. My grandmother used to swear on it for bee stings, too. The point is it doesn't matter what I say, there is someone who will believe it.

Okay, so many people swear by using soy sauce for burns. Especially if you believe the comments in reply to articles on "The People's Pharmacy," those purveyors of crap science for the gullible and easily duped. But what you may not realize is that I can pretty much pick something out of my refrigerator or pantry and write a little article on how it works for burns and be guaranteed that some people will try it and find that it "works." And if I put it on the right kind of website, say one that speaks out against "bad science" (oh, the irony), Big Pharma, and the guvment, I can probably get plenty of testimonials, in the form of comments in response to my little home remedy article. We are losing the battle against irrational thought, that's all there is to it. But I do hope the tide turns soon.

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So does soy sauce do anything for a burn? How should I know? I have no physiological or other basis for believing it should work. I've never seen any type of study done on soy sauces for treating burns. Why? Can you imagine writing out a grant request for your big honking study on soy sauce for healing burns? No. So there is not a good well controlled study or a bad one. They don't exist. But according to some people's "home experiments," soy sauce works. It kills the pain and speeds the healing.

Okay. What does that tell us? It tells us nothing. Nothing, folks! Mustard works the same way, according to "home experiments." Can you imagine smearing such an irritant on a burn? Well people will do some very silly things. What do mustard and soy sauce have in common? Rhetorical question. What can we say about the anecdotal evidence concerning soy sauce and burns? A lot. The first thing, of course, is the fact that it is anecdotal evidence in the first place. But beyond that what about the people who report these experiences? Are they lying? Well, not exactly, or at least not always. Anecdotal reports do not have to be untrue, as far as the basic facts are concerned. They are just unreliable as a source of evidence to support a claim. In this case, the anecdotal experiences of some people who have used soy sauce to treat minor burns cannot be relied upon as a source of scientific evidence to support the claim that soy sauce helps minor burns.

And yet something must be going on, right? I mean, if a couple of people say that they used soy sauce on their burn and the pain went away, and they are not lying, then soy sauce must do something for burns. Nope. It does not follow. Seems like it follows, I know. So just why aren't these personal experiences a valid representation of the effectiveness of soy sauce as a burn remedy?

Well the main reason, in my opinion, which is really the elephant in the room, has to do with what is called a "causal inference." Causal inference is something I have mentioned again and again, in many different contexts, because so many trainees make them without knowing how very difficult they are to make!

The Oh So Inaccurate Causal Inference

Okay, so causal inference works like this: You're taking a tray of cookies out of the oven and your finger accidentally touches the hot baking sheet. For you hardcore bodybuilder types lets say it's a piping hot tray of homemade protein bars. Ouch! You run to the sink to run some cold water on your burned finger and while you're doing that you remember reading that soy sauce was just the thing to relieve the pain of a burn and make it heal fast. Matter of fact, it is apparently miraculous in its burn relieving properties! So you get out the Kikoman, pour a little in a saucer and just sort of soak your finger in it for a while.

Next thing you know, your finger doesn't really hurt at all. What's more, no blister forms and the next day, besides a little redness in the area, the burn seems to be pretty much taken care of. The soy sauce worked and as far as you're concerned you have proven it by a medical experiment. Well, before you rush out and buy Medicine for Dummies and hang out your shingle, you might want to read on.

First, since we're talking about causal inference in the context of your little experiment we will ignore the obvious: Your experiment sucked. There was only one subject, there was no control. You are not a trained scientist and know nothing at all about setting up valid research studies. Let's ignore that and just say that you have made a causal inference about your lack of pain and the use of soy sauce.

Before I lay doubts on your reasoning skills let me say that when it comes to causal inference, us humans are particularly adept. We can draw quick conclusions about why someone does a certain thing or a particular event happens and stand a very good chance of being right on the money. We don't even have to realize that we are making such a conclusion.

For instance, if you are taking your new puppy out for a walk and just as you open the front door there is a huge crack of thunder, your puppy may then associate the door with the noise, and thus become frightened of the door, at least for a little while. A dog does not rationalize or understand that it is making an inference. Door equals noise is probably the extent of his understanding. On the other hand, your four year old child, although he may initially associate the door with the thunder may quickly realize that he has heard thunder on other occasions when the door was not being opened and that he has seen the door opened many times without an accompanying clap of thunder. Or, if he does not realize these things, he may discover them later and consider that this new evidence lays doubt on his impression that the door caused the thunder. Regardless of how he comes to the conclusion that his initial impression was wrong, however, he will gather and process information regarding the incident and thus come to some conclusion. This we do constantly, even on a daily basis, whether we are scientists or not. The more experience we gain in the world, the more accurately and quick come our inferences.

So let's compare thunder to minor skin burns. What happens when lightning strikes? Thunder follows. We know this. It's not chance. You can lay a bet on it. Even if you don't see the lightning, but hear the thunder, you can attribute it to lightning and be darned confident in your assessment of the situation. So what happens when you burn your finger on a tray of cookies?

Well, let's see. It hurts. And unless there is something neurologically wrong, you snatch your hand away as quickly as possible. What else? How long does it keep hurting? Does it turn red? Does it blister? Does your finger fall off? How long does it take to heal?

You're getting the point, I know. Burns are variable. You cannot make many accurate predictions about a 'burn' in general until you see the severity of the burn. And there can be a broad difference between two MINOR burns depending on the temperature of the object giving the burn, the time of contact, and the speed of your response…such as how quick you run cold water over it.

So I want you to think back. You do a lot of cooking, right? How many times have you burned yourself in the last year? Hurry up, I'm waiting. Three times? Ten times? More? You don't know, do you? You don't remember exactly. You may be thinking, BS, Eric, I remember. About five times.

I'll bet you're wrong in your guess. I don't think there is much chance you remember every little burn you got. Because they are little. They stopped hurting within a half hour at most..maybe just a dull pain left at most and you forgot all about them. They just weren't dramatic enough or significant enough to make a lasting impression. You remember the blisters. The big ones. The dramatic ones. But not every one.

Some burns are just not a big deal and they pass away quietly..becoming a "non event." Some burns form a blister and take a few weeks to fully heal. Some are even worse. But when you burn your finger and reach for the soy sauce, you do not take any of that into account when you make your causal inference. You do not take into account that this ONE instance of the pain going away quickly does not give you enough data to make an accurate inference, based on the "natural history" of a burn. You quickly connect soy sauce to burn healer. I guarantee that if you mapped out your burns for a year (not burning yourself on purpose of course) and used soy sauce on half of them and nothing but a cold water rinse on the other half you would find that the same thing happens to both sets. Some burns are minor and the pain goes away quickly. And some burns last. Regardless of soy sauce. What's more, I think you'd find this to be true even if your monitoring system wasn't very good.

So, what I want you, the reader, to realize, is that the way we think causes us to accept such claims and to rationalize the validity of those claims even though our own personal evidence is so flimsy. We do not need a bunch of high-brow talk of statistics and studies to understand that we just don't know as much as we think we know, much of the time.

So Do We Need a Soy Sauce Burn Study? NO! Absolutely not. Because there is absolutely no reason to think that soy sauce has any efficacy for burns and research dollars would be better spent on things that have at least a modicum of physiological basis. I do have my mind open to the possibility that there is a basis for the efficacy of soy sauce, and other things, for burn treatment, and that it may turn out to be a working treatment. But that does not mean I keep my mind so open I completely misplace it.

In case you actually came to this article looking for information on treating minor burns, please see How To Treat Minor Burns: Basic First Aid.

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by EricT

Most people probably first heard of propofol when reports of Michael Jackson’s untimely death broke. As the shocking circumstances were unraveled and revealed, an unusual drug was reported to be responsible. Propofol became a household word, well, almost, anyway. But, for those who work in healthcare and especially, anesthesiologists, use of this drug really is an everyday occurrence. In fact, most anesthesiologists will probably use this medication in one manner or another on almost every patient.

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Propofol falls under the category of a sedative-hypnotic drug. That means that anesthesiologists and other qualified physicians use it to achieve various states of sedation for patients in a hospital or appropriate surgical setting. Like many anesthetic medications, it is not entirely clear how propofol exerts its effects.

Propofol administration always occurs through an intravenous line into a vein, to reach the central circulation and quickly affect the brain. When given slowly or in small doses, sedation without loss of consciousness is possible. Usually, an infusion pump will be employed to maintain constant and consistent dosing of the medication. Since propofol does not have pain-relieving qualities of its own, intravenous pain medications are often used in conjunction with propofol for short, minimally or moderately uncomfortable procedures.

Most often, propofol acts as an induction agent for general anesthesia. General anesthesia, by definition, results in a state of unconsciousness. Propofol, to induce general anesthesia would be given in a larger, single dose pushed slowly from a syringe into the IV line. The dose is calculated based on a person’s weight and is adjusted based on coexisting medical conditions. Anesthesiologists are specifically trained to understand that propofol affects all body systems and thus, has side effects that must be anticipated. Complications result if the drug is not properly used.

Propofol will predictably cause a drop in blood pressure, heart rate and breathing. For this reason, monitoring of vital signs must absolutely be done continuously while propofol is in use and until its effects are cleared from the body. The more and faster the medication is given and the unhealthier a patient is, the more drastic and rapid these changes in vital signs occur. It takes years of training to be able to predict and successfully manage the severity of these side effects. Medications should always be immediately available to treat drops in blood pressure. In addition, there is no specific reversal agent for propofol, so if complications occur, the practitioner should be skilled at supporting the patients breathing until the drug wears off. This requires not only oxygen, but also other equipment and skills to open the airway and maintain respiration. If breathing has stopped completely, which it will with a large enough dose of propofol, mask-assisted delivery of oxygen or even the placement of a breathing tube and assistance from a ventilator should be available until spontaneous respiration returns. The time it will take for this to occur depends on the dose of the drug, the specific metabolism of the patient, other drugs given with the propofol and other factors.

Anyone who is not skilled in these techniques should not be using propofol, even in a hospital setting. It is not approved as a sleep aid nor should it be used in a private residence with inadequate monitoring and rescue equipment. It is a useful and safe medication only when used in the proper setting by appropriately trained professionals.

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by EricT

By Ground Up Strength

The various scientific names of the body's 600 to 650 or so muscles,¹ at first, appear to be a bewildering hodgepodge of Greek and Latin. You may think that anatomists were just picking mysterious words out of an ancient hat in order to confuse you. That is not true at all, however. Although in some cases the methods used to name muscles are not very effective, the names of muscles are based on a naming system and, believe it or not, there is order and logic in how the muscles are identified. The more you are exposed to the study of skeletal muscles, the more you will begin to recognize the underlying structure. Often, knowing the meaning of the words will help you understand what muscle is being referred to just by its name. Sometimes, though, even knowing the meanings of the words will not help and all you can do is memorize them.

Still, being familiar with the meanings and the underlying system of naming is better than relying on rote memorization alone, because even though you won't always be able to find a muscle by its name, you will at least know what muscles are NOT being referred to. Knowing the structure of muscle naming can also help you decipher the function, location, and other information about muscles form their names alone.

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Muscles May Be Named According to Any of These Characteristics

1. Where is the muscle located? This may refer to a body part, to the origin and insertion of a muscle.
2. What is its basic shape? What does it look like?
3. What is its function? Does it extend a joint or flex it?
4. How many origins does it have ("heads", parts or divisions)?
5. What is the muscle's origin and insertion?
6. What is the muscle orientation relative to the midline of the body? Or, in other words, what direction do the muscle's fibers run in? Are they straight (rectus), or perhaps oblique (slanted)?

Each of these basic characteristics are "coded" with root words used to form the larger name. Many times, as well, a muscles name must be based on its relationship to another similar or paired muscle. Let's look at some of the basic words used to describe muscles:

Words That Refer to Muscle Size

• Maximus: largest (gluteus maximus is the largest muscle of the buttock)
• Minimus: smallest (gluteus minimus is the smallest muscle of the buttock)
• Medius: intermediate in size, do not confuse with medialis (gluteus medius is the the intermediate sized muscle of the three buttock muscles)
• Major: larger (pectoralis major is the larger muscle of the chest)
• Minor: smaller (pectoralis minor is the smaller muscle of the chest)
• Brevis: shortest (peroneus or fibularis brevis is the shortest of the peroneal muscles)
• Longus: longest (peroneus or fibularis longus is the longest of the peroneal muscles)
• Vastus: great or huge (used for two muscles of the thigh: vastus lateralis and medialis)

Words that Refer to Muscle Shape

• Deltoid: triangular (e.g. deltoid muscle of the shoulder)
• Rhomboid: diamond shaped (e.g. rhomboideus minor and major muscles, collectively the "rhomboids")
• Quadratus: square or four-sided (e.g. quadratus lumborum or quadratus femoris)
• Trapezius: trapazoidal shaped (e.g. trapezius muscle)
• Serratus: serrated or saw-toothed (e.g. seratus anterior)
• Teres: round or cylindrical shaped (e.g. pronator teres)
• Platysma: flat (e.g. platysma muscle of neck)

Words that Refer to Body Parts or Regions (Location)

• Pectoral: chest (two muscles, pectoralis major and minor)
• Brachii: arm (biceps brachii)
• Carpus: wrist (flexor carpi radialis and ulnaris)
• Palmaris: palm of the hand (e.g. palmaris longus)
• Digiti: finger or toe, singular (extensor digiti minimi)
• Digitorum (finger or toes, plural (flexor digitorum profundus)
• Indicis: index finger (extensor indicis)
• Hallucis: great or big toe (abductor hallucis)
• Femoris: thigh (rectus femoris)
• Gluteus: gluteal or buttock region (three muscles, gluteus maximum, minimum, and medius)
• Tibialis: lower leg or shin bone (tibia) (tibialis anterior and posterior)
• Peroneus: fibula, sometimes fibularis is used (peroneus longus)
• Spina, Spinalis: spine (erector spinae, spinalis cervicis and capitis)
• Spinatus: spine of the scapula (infraspinatus and supraspinatus)
• Pollicis: thumb (adductor and opponens pollicis)
• Oculi: eye (orbicularis oculi)
• Oris: mouth (depressor anguli oris)
• Labii: Lips (levator labii superioris)
• Capitis: head (splenius capitis)
• Cervicis: neck (semispialis cervicis)
• Thoracis: thorax (spinalis thoracis)
• Abdominis: abdomen (rectus abdominus)
• Lumborum: lower back or lumbar (quadratus lumborum)
• Scapularis: scapula or shoulder blade (e.g. levator scapulae)
• Costals: ribs (intercostals or internal intercostal muscles meaning "muscles between the ribs")

Words that Refer To Relative Location

• Lateralis: located to the side or laterally (vastus lateralis)
• Medialis: located toward the middle or midline (vastus medialis)
• Anterior: toward the front or anterior surface (tibialis anterior or serratus anterior)
• Posterior: toward the rear or posterior surface (tibialis posterior)
• Superior or Superficialis: superficial or toward the surface (flexor digitorum superficialis and obliquus capitis superior)
• Inferior: underneath or away from the surface (Obliquus capitis inferior)
• Profundus: located deep (flexor digitorum profundus)
• Supra: above or over (supraspinatus)
• Infra: below or beneath (infraspinatus)
• Sub: below or under (subscapularis)
• Internal: inner (internal oblique)
• Inter: between (intercostals)
• Dorsi: of the back (latissimus dorsi)

Words that Refer to Muscle Fiber Direction

Note that some writers confound fiber direction terms with shape terms, so that rectus, which refers to fibers that run up and down, straight and parallel with the midline, are called "straight" muscles in terms of shape. However, fiber direction does not necessarily denote the overall profile of a muscle, only the orientation of the fibers.

• Rectus: straight, or "erect", specifically meaning parallel to the midline (rectus femoris meaning "straight muscle of the thigh")
• Transversus: transverse or perpendicular to the midline (transversus abdominis or transverse abdominis)
• Oblique: slanted or diagonal to the midline (external oblique)
• Orbicularis, Sphincter: a name given to ringlike muscles that encircle and orifice and that may form a constricting passage (lower esophageal sphincter and orbicularis oris and anal sphincter)

Words that Refer to Number of Origins or Heads

The suffix "-ceps" means heads. A head is a major division of a muscle that has its own tendon.

• Biceps: two heads (biceps brachii which means "two headed muscle of arm" and biceps femoris which means "two headed muscle of the thigh")
• Triceps three heads (triceps brachii which means "three headed muscle of arm")
• Quadriceps: four heads (quadriceps femoris which means "four headed muscle of the thigh", commonly called the quadriceps)

Words that Refer to Actions

Since the various muscle joint actions are so common, muscles that use action terms in their names usually also give other clues as to their appearance or location.

• Flexor: flexes joint, or brings two ends closer together, decreases joint angle (flexor carpi radialus)
• Extensor: extends joint or bring two ends further apart, increase joint angle (extensor carpi radialus)²
• Levator: elevates a structure or part (levator scapulae)
• Depressor: depresses a structure or part (depressor anguli oris)
• Adductor: adducts or moves a part toward the midline
• Abductor: abducts or moves a part away from the midline³
• Pronator: pronates or turns the hand or forearm downward or backward (pronator quadratus and pronator teres muscle)
• Supinator: supinates or turns the hand or forearm upward or forward (supinator muscle)⁴
• Rotator: rotates one structure relative to another (rotatores spinae)
• Opponens: Refers to thumb actions only and named for the action of opposition, which is when the tip of the thumb is brought into contact with other fingers (opponens pollicis)

Some special action words used for certain muscles:

• Sartorius Muscle: Derived from the muscles activity when crossing the legs and named after the Latin word for tailer, sartor. Tailors used to sit on the floor cross-legged to do their work, before sewing machines were invented. Other explanations are also put forth, such as the cross-legged pedaling action of old sewing machines, which enlarged the muscle in tailors, and the muscles location along the "inseam."
• Buccinator: Derived from the muscles action in compressing the cheeks, which occurs when pursing the lips and blowing forcefully, as when playing the trumpet. The word buccinator means "trumpet player" so the buccinator is the "trumpet player muscle."
• Risorius: Derived from this facial muscle's action in producing the facial expression associated with laughter, which is risor in Latin. The actual expression of the muscle is more appropriately described as a grimace. 2
• Masseter: Derived from the muscles major action in chewing, coming from the Greek masētēr, meaning "a chewer."

Words that Refer to Origins and Insertions

It is not necessary to name every possible origin and insertion for each muscle. Only a relatively few muscles are named by these terms. Below are some examples, giving the muscle name and the words for the individual attachments that form the name. The first part of the name always refers to the origin and the second part to the insertion, which are joined together to form a compound word.

• Sternocleidomastoid: Sterno and cleido for its origin, the sternum and clavicle; and mastoid for its insertion, the mastoid process.
• Brachioradialis: Brachio for its origin on the upper arm and radialis for its insertion on the radius of the forearm.
• Genioglossus: Genio for its origin on the chin or "geneion" and glossus for its insertion on the tongue (glossus).
• Sternohyoid: Sterno for its origin on the sternum and hyoid for its insertion at the hyoid bone.
• Coracobrachialis: Coraco for its origin on the corocoid process of the scapula and brachialis for its insertion on the humerus of the upper arm.

As can be seen by the various terms and methods used to name muscles, it is by far a perfect system. Unfortunately, throughout the many years spent describing and naming the body's muscles, anatomists failed to stick to one method. Although there is indeed structure, some parts of the structure is more scientific than others. For instance, there is nothing particularly scientific in calling a muscle "deltoid" because it is shaped like a triangle. Likewise, although a word like "femoris" would seem very precise, there are many muscles associated with the femoris, or "thigh bone" and therefore a name like "quadratus femoris" means only "a square-shaped muscle of the thigh bone," which still requires us to memorize the muscle rather than to be able to guess it's precise location and function by its name. This muscle, after all, could be located on the anterior or the posterior part of the thigh and could be a hip muscle or a knee muscle. Although gluteus maximus sounds sufficiently scientific to most laypeople, calling a muscle "a large buttock muscle" is hardly scientific.

It would seem, then, that those names giving location and action are best, and these would be termed physiological names. Well, for those studying only human anatomy and human muscles, this may be the case, but for comparative anatomy and to describe the same muscles in different animals, it is a mess, as not all muscles necessarily share the same exact function in all animals. As stated above, perhaps the best system is a morphological one, which uses the origin and insertion of a muscle for its name, at least for purposes of comparative anatomy. Still, for students of human kinesiology and physical training, comparative anatomy is, at best, a side-line. Therefore, more descriptive names are more useful and most of us should be thankful that the morphological system never really caught on, although anatomists may grapple with the incongruities.

There will always be some memorization involved in learning the names, functions, and locations of the muscles. There is just no way around it. Yes, you may know that the brachialis has something to do with the arm, because of the "brachi" in the word, but that's all you know. How is it different than the brachioradialis or the coracobrachialis?

After studying the terms above, you should start to see patterns emerging. As you move down the lists, you should start to recognize the terms previously encountered in the muscle examples given, so that, as you learn, the names start to make more and more sense. This is especially the case in the more descriptive names. Fortunately, the other, badly named muscles, such as the deltoid and trapezius muscles, are the more familiar muscles to laypeople, and most shouldn't have much trouble with these bad apples. Learn all the terms in this article, and even with no memorization of the individual muscles you will know a great deal more than most people about the muscles of your body.

Clearing Up Some Anatomical Confusion

As you read this article and study the lists, you may wonder about the terms arm, forearm, leg, and thigh. How are you supposed to know what arm means. Does he mean my upper arm or my lower arm (forearm)?

When it comes to anatomy, we rely on certain foregone assumptions. That is, anatomists rely on these assumptions while everyone else is confused by them. When this article refers to the "arm" as in "brachii" it means the upper part of the arm. Why? Because in anatomical terms arm means upper arm and forearm means lower arm. For the legs, it's the opposite. The word leg, in anatomical terms, means the lower leg and the word thigh means the upper leg. So your arm is actually only the portion of that appendage from your elbow to your shoulder and your leg is only the part of that appendage from your knee down.

Example of Specific Muscles and How They Were Named

The following is a list of specific muscle name explanations, with images, that should assist you in your study. When possible, further explanation to the relevant anatomy is given. These muscles are listed in no particular order, they are just examples!

Infraspinatus

The infraspinatus is named for its position relative to the spine of the scapula. "Spinatus" refers to the scapular spine and "infra" means that the muscle is situated below it.

The image above has the spine of the scapula labeled. I have also labeled the suprapinatus fossa, for reference. The scapular spine separates the infraspinatus and supraspinatus fossa on the posterior surface of the scapula. Note that the scapular spine ends on the acromion process, where the clavicle joins, forming the acromioclavicular joint. See that the muscles is situated "below" the spine.

Extensor Carpi Ulnaris

The extensor carpi ulnaris, as you should immediately know if you've been paying attention, is an extensor of the wrist (carpus).

The muscle inserts onto the ulna bone of the forearm. However, the name is not simply an indication of where the muscle inserts. It actually inserts onto the base of the fifth metacarpal (proximal part of the little finger). Instead, the "ulnaris" in the name describes it's relationship to the bone and it's role in movement. Here, we have an extensor of the wrist on the ulnar side which means it is an ulnar extensor of the wrist. Without opposition from other flexors and extensors on the radius, the extensor carpi ulnaris, together with the flexor carpi unlaris, would tend to cause wrist adduction or "ulnar flexion" rather than pure wrist extension. As it is, the muscle is active in both wrist extension and wrist adduction.

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Unless otherwise noted, all images on this page used under license. Images by LifeART (and/or) MediClip image copyright 2010. Wolters Kluwer Health, Inc.- Lippincott Williams & Wilkins. All rights reserved. Images not for reuse.

by EricT

This post is meant to discuss three basic propositions about training the deadlift. The first concerns a statement that we frequently read or hear concerning the development of supporting grip strength for deadlifts: Deadlifting is all you need to train your grip for deadlifts. I'm going to explain to you why this false assumption is made and how it is not true for everyone. The second has to do with the correct way to grip the bar. I am not sure that many people even know there is a correct method to grip the bar that results in a more secure grip and more protection against ripping the skin, and ripping off calluses. The third concerns calluses themselves. So here goes.

The Deadlift is All You Need for Supporting Grip Strength

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Now, it should be a bit self-explanatory. Do you really expect your grip, controlled by small muscles, to progress right in line with much larger and coordinated muscles like your thighs, hips, and back? Do you expect the strength in your hands to progress in a way that corresponds with the strength in your entire body? A bit naive, don't you think? So why do people say it so much?

Assuming they are not being defensive about their own lackluster grip strength, it's probably because they have never pulled above 300 to 325. It could be a little less or a little more. You see, an average male, with average grip strength can pretty much support at least 300 on the bar. Yep. Average grip strength is much stronger than you thought, I'll bet. Hey, you may be below that. Nobody falls perfectly at the top of the graph. That's not the point. The point is, a guy who worked his deadlift up from 150 to say, 325, may think that the deadlift has been training his grip and so think that this means that "all you need for grip strength is the deadlift." What he didn't realize is that his grip just hasn't been that challenged yet. If anything, he trained and built up endurance, but not necessarily absolute gripping strength. At some point he will have to augment his grip with alternated or hook grip; or use straps; or do some grip training on the side to keep his grip in line with the weight on the bar. Probably he will have to do both. That is, he will have to use an augmented grip or straps and yet still need to do dedicated grip training.

Proper Way to Grip the Bar

Most articles and explanation get this wrong. Dead wrong. Good one right? There are two opposite viewpoints: One says you should "grip the bar with the palm." That confuses most trainees. How the heck do I grip with my palm? I use my fingers to grip things. Well, you are correct, sir. You can't grip anything "with your palm," as such. What people mean by this is that you should seat the bar in the palm of your hand first, between the thumb and forefinger, and then wrap the fingers around. This will bunch and pinch the skin at the base of the metacarpophalangeals (base of fingers), pulling at the calluses if they are there and/or causing them to develop as ridges which are more easily torn off in the future. They may also press on the underlying tissue and bone while lifting, causing pain.

The second viewpoint says you should "grip with your fingers." As if there was any other way. But what they mean is that you should hook the bar with your fingers and then squeeze it in, thus allowing the bar to pull at the skin at the base of the fingers, which results in ripped calluses for some lifters, some of the time. Wrong again. This results in a less than secure grip and may actually cause large calluses to develop in places that are more uncomfortable, such as the proximal interphalangeal joints of the fingers.

The best way to grip the bar is actually what comes out of these two incorrect instructions. That is, those who give the first two methods are just repeating something they heard without understanding the steps involved and you will see how it can be misconstrued as "grip with your palm" or "with your fingers." So here is how to do it:

1. Seat the bar on the part of your palm just underneath base of your fingers, the place where the biggest calluses tend to form. Press the skin against the bar firmly.

2. Maintain this contact with the bar while pushing your hand forward, away from you, so that the skin under your fingers is dragged slightly backwards, toward the base of your palm. This will cause your hand to start to bend around the bar.

3. Keep pushing forward, maintaining pressure, and bring the palm of your hand onto the bar by placing the webbing between the thumb and index finger around the bar. So now, you are "palming" the bar. Your fingers should have naturally wrapped around the bar and your thumb should come to rest near, or over, your index finger, depending on your inclination.

4. Rotate the bar away from you until your wrist is straight.

Although I wrote this out in steps, it's all done at the same time. If you can use it, gym chalk will help a great deal. Chalk does more than just provide more friction for you grip, it helps to facilitate getting a better grip in the first place. Although there are only subtle differences between this and the way most people would "naturally" grip the bar, the skin under the fingers is not snagged nearly as much. You may have a slight bit of discomfort in your hand, as you may be palming the bar correctly for the first time. Your hand will relax more over time and this should feel normal to you with practice.

Obviously, we are assuming that you do not think that the 'correct' way to grip the bar is to use a hook grip. The hook grip is an augmented grip and is not something most lifters would turn to right off the bat so this post assumes that you are gripping the bar according to most people's natural inclination, which would be in a "power grip" where the thumb comes around the bar to buttress the grip. Using the method above for an alternated grip, is a bit more tricky, but the steps are the same.

Whether to use the hook grip to augment your grip, when needed, or to use an alternated grip is up to you to decide. This article, Hook Grip Versus Alternated Grip For Deadlifts, contains the most thorough breakdown of the the issue that you will find, whether in a book or on the internet, and it gives my conclusion as to the best course of action.

Myths and Facts about Calluses from Deadlifting

Myth: You must care for you calluses or they will tear off. You must shave them down with an emory board or some other implement regularly. You must keep your hands moisturized, etc.

The reality is that some people have their calluses over-grow and feel very uncomfortable when lifting. They may also have them frequently rip off during deadlifting, severely impacting their training ability until the skin heels. And other people rarely think about their calluses except to be thankful they are there to protect their skin..and to display as a badge of lifting honor. So, remember that this is a case of 'speak for yourself.' It is difficult to be sure why some people have problematic calluses and some don't. Part of it is incorrectly gripping the bar, so hopefully we've got that sorted out. But the rest of it we may be able to tease out by understanding a bit more about callus formation.

Calluses are caused by the same thing that blisters are caused by: repeated mechanical trauma to the skin in the form of pressure and friction resulting in a heat buildup. If the trauma comes too often and is too severe, a blister will form. A blister is a raised separation of the dermal and epidermal skin layers. These raised skin sacs (vesicles) are filled with a clear or serous fluid. They form to act as a sort of padding to protect the underlying tissue from further damage.

Although many experts write about how to get rid of calluses or care for them, most athletes would rather have a callus form than a blister. Well, when the mechanical trauma is repeated, but not for too long or too severely, a callus will likely form instead of a blister. So, a callus can be thought of as a more permanent and positive adaptation to the stress on the tissues. They are usually asymptomatic except for pain caused by large calluses pressing on underlying or adjacent tissues. Sometimes calluses are problematic but this can usually be prevented. For instance, over-large calluses on the feet in painful areas are usually caused by poor fitting shoes. The moral, if there is one, is that even good things can sometimes come with a cost.

If you develop overly large calluses on your hands from lifting, and this causes pain, you can gently file them down with a file or pumice stone. But if your calluses don't give you any problems, by all means, leave them alone. Calluses are actually toughened areas of skin and they don't just automatically rip off every time a breeze blows, which is what some lifters seem to think. They are, however, more susceptible to tears because the area of skin that forms the callus is thicker and less elastic than the surrounding skin, moving as a unit. When tears happen, it is not the callus, of course that is tearing, but this large unit being pulled away from the surrounding skin. It is more likely that heightened activity or friction (perhaps because of frequent failing of grip) causes a blister to form underneath the callus. Yes, a blister can form under a callus. This weakens the integrity of the callus, making it prone to being torn. So, trim and manage your calluses as you need to, but don't try to get rid of them. You need their protection, otherwise, you'd end up with blisters.

Comments

General References

Shultz, Sandra J., Peggy A. Houglum, and David H. Perrin. Examination of Musculoskeletal Injuries. Champaign, IL: Human Kinetics, 2010. 642.

Arndt, Kenneth A., and Jeffrey T. S. Hsu. Manual of Dermatologic Therapeutics. Philadelphia: Lippincott Williams & Wilkins, 2007. 46-48.

by EricT

By Ground Up Strength

The extensor digitorum¹ muscle gets its name from the Greek and Latin ex which means "out of", and the Latin tendere, which means "to stretch". So an extensor is a muscle that stretches out or straightens out a joint. The word digitorum is from Latin, indicating the digits or fingers. Communis is Latin for "common" and it refers to a muscle which has several branches or structures.1

The extensor digitorum muscle, also called the extensor digitorum communis, is an extrinsic hand muscle. Located in the posterior forearm, it is thicker at its proximal end and flattens out as it reaches the wrist. It may be the most apparent of all the forearm hand muscles as it is responsible for most of the shape of the dorsal (extensor) surface of the forearm and you can clearly see it's tendons when you extend all four fingers. This may tell you it's function, which is, in fact to extend the fingers, and it is the only muscle capable of extending all four.

Along with several other muscles it is part of the "extensor compartment" of the forearm. These other muscles are the extensor indicis, extensor digiti minimi, exensor pollicis longus, and extensor pollicis brevis. It also extends the wrist and is sometimes reported to weakly flex the elbow 2, 3 See also intrinsic hand muscles.

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The Extensor Digitorum

Beginning at the distal humerus, the extensor digitorum runs down the dorsal surface of the forearm between the extensor carpi radialis brevis and the extensor carpi ulnaris muscles, which all arise from a common tendon. The muscle then gives way to four tendons on the four fingers. These tendons are united by a oblique bands over the back of the hand so that individual movement of the fingers by the muscle is limited, but not eliminated. The individual parts of the muscle are capable of producing independent finger extension, with the middle and ring extensors being the most symptomatic for trigger points. The tendons on the index and little fingers are commonly joined by thicker tendons from the extensor indicis and the digiti minimi muscles. 4

The action of the extensor digitorum in finger extension is significant and the muscle can be overworked by frequent forceful gripping or repetitive actions of the fingers. Strength trainees engaging in dedicated grip strength training, especially high volume repetitive training, can certainly overload this muscle as any powerful flexion of the fingers requires great activity of the antagonistic extensors, especially since, without them, strong flexion of the fingers while closing the grip would also cause the wrist to bend (flex). Trigger points in the extensor digitorum can cause pain in the forearm, hand, and fingers. 4

Extensor Digitorum Origin, Insertion, and Action

Origin: The common extensor origin which is a smooth area on the anterior distal aspect of the lateral epicondyle of the humerus. It's tendon is fused together with the tendons of the extensor carpi radialis brevis, the extensor digiti minimi, and the extensor carpi ulnaris. There are also attachments arising from the adjacent intermuscular septa and from the fascia of the forearm muscles which neighbor. 2, 5

The Extensor Tendons

Insertion: Four separate tendons form a myotendinous junction around one-third of the way up the distal forearm (2/3 of the way down the proximal forearm). Initially somewhat attached, the tendons separate at the extensor retinaculum and form complex attachments at base of the distal phalanx and middle phalanx of each finger, with attachments on the proximal phalanges also being possible (The tendons and the extensor mechanism they are a part of have many possible variations and are highly complex).

Locating the Extensor Digitorum

Actions: Extension of the four fingers, primarily at the metacarpophalangeal joints. Also some extension of the proximal interphalangeal joints, assisting the interossei and lumbricals. Some seperation (adduction) of the fingers. Wrist extension. 2,1

Extensor Digitorum Trigger Points Referred Pain, Symptoms, and Causes

Pain derived from trigger points in the extensor digitroum could be mistaken for arthritis pain in the fingers or even Tennis elbow because of symptoms at the elbow. Sore and "tender" fingers and aching forearms are also possible, even without actual pain in the joints. Overuse of the fingers in forceful activities such as with pianists, mechanics, carpenters, typists, etc. are likely to cause overload and trigger points in the ED muscle. Overuse of the grip, as in inappropriate grip strength training, are likely also to cause TrP's in the muscle. Although it would be easy to surmise that maximal grip crushing grip training, as with heavy duty hand grippers, would be the most likely to cause this, it is just as likely to be caused by light grippers used with high repetitions, or other types of grip training done with too much volume or frequency. Also, any kind of repetitive gripping or twisting motion of the hand may be responsible.

Typing on a computer keyboard causes the finger extensors to be active almost constantly since they must keep the fingers extended over the keyboard between keystrokes. Mouse clicking, likewise, presents the same problem.

A weak grip and painful and/or stiff fingers can be due to extensor digitorum trigger points. The pain is exacerbated when trying to grip any object strongly and upon such activities as shaking hands. Trigger points in this muscle radiate pain down the dorsal forearm, to the back of the hand, and into back of the fingers (dorsally). The pain does not reach the end of the fingers, but may reach as far as the proximal interphalageal joint. Symptoms will appear in the finger which corresponds to the involved area of the muscle, being the middle or ring finger extensor. The image below shows the approximate point that trigger points develop in the muscle.

Extensor Digitorum Trigger Point Locations

Trigger points in the middle finger appear most often. Pain from this extensor TrP radiates down the dorsal forearm and sends concentrated pain to the middle finger. Trigger points in the middle extensor are also capable of occasionally referring pain to the frontal or "volar" part of the wrist² The image below shows the referred pain pattern of this TrP.

Middle Finger Extensor TrP Referred
Pain Pattern

TrP's in the ring finger extensor send pain down the dorsal forearm, crossing the back of the hand, and concentrating pain into the ring finger. The TrP's in this part of the muscle may also send pain upwards, toward the outer elbow at the lateral epicondoyle region so that symptoms similar to the pain of so-called "tennis elbow" is experienced. This condition, called lateral epicondylitis is actually due to pathology in the common extensor tendons rather than problems in the muscle bellies, whether due to TrP's or otherwise. However, in addition to the ring extensor of the extensor digitorum, other forearm muscle trigger points, such as the brachioradialis, supinator, and extensor carpi radialis longus, and brevis can send pain to lateral region of the epicondoyle.³

Since lateral epicondylitis, although initially causing pain only in the lateral elbow eventually tends to spread pain down the arm, pain that is actually being referred from the extensor digitorum or other forearm muscle trigger points can easily be misdiagnosed as lateral epicondylitis, even though no pathology is present in this region. 4,6 The image below shows the referred pain pattern of the ring finger extensor TrP.

Ring Finger Extensor TrP Referred
Pain Pattern

Extensor Digitorum Trigger Point Treatment

Using the images above to locate the approximate areas of the trigger points, you should easily be able to palpate the muscle and find the area that elicit a response, which will typically be close to the surface where the taut band can be felt. Those with well developed forearms will be able to see the muscle working when wiggling or extending the fingers. Others can palpate the muscle two or three inches down from the elbow on the outer surface of the forearm and feel the muscle jumping when working the fingers. Once you locate the trigger points they can be treated with a number of simple devices. The fingers of the opposite hand can of course be used but a hard device that can exert deeper and firmer pressure will work best.

A tennis ball can be used against a wall but a small hard rubber bouncy ball, about 1.5 inches in diameter, like the kind sold in party supply or dollar stores, will work even better. Place the ball between a smooth wall and the affected forearm so that the back of your hand is facing the wall and your forearm is horizontal. Using the wall as a rolling surface, roll the ball along the muscle, starting at the middle of the forearm and ending at the elbow. Lean your body weight against the ball to increase pressure as needed. Concentrate the strokes on the most tender areas that house the trigger points.

A firm hand-held roller massage ball works well. Use a roller massage ball in the same manner except hold the support base of the ball in the opposite hand and rest the arm to be massaged comfortable against your stomach so that you can easily access the outer forearm with the ball and apply good pressure.

A Knobble [self-massage tool] will work well held in the hand, and can be used to work a deeper and smaller area. There are many other hand-held self massage devices that can be used, such as the Jacknobber and the Indexknobber. Use these in a manner similar to the roller ball.

You can perform multiple sessions throughout the day, but keep them to around a minute or two in length. 7

Extensor Indices Muscle

While you're treating the extensor digitorum muscle, go ahead and look for trigger points in the extensor indicis muscle, which are likely to be present. Both the EDC and the EI are usually considered together in trigger point treatment. Trigger points in this muscle sends pain to the radial side of the back of the hand (closer to the index finger). Feel for this muscle on the back of the forearm about three inches from the wrist. It is located between the radius and ulna bones, as shown in the image below. A contraction can be elicited by extending the index finger. 4, 7

Extensor Indicis Muscle

The wall method will probably not work well for this muscle. The Knobble is the better tool for the job. 7 The image below shows the extensor indicis trigger point and referred pain pattern.

Extensor Indicis Trigger
Point and Referred Pain Pattern

Other Associated Trigger Points

Although it is possible for trigger points in the extensor digitorum finger extensors to develp alone, it is also likely that they will develop as part of the above-mentioned "tennis elbow" associated symptoms, which is characterized by trigger points in the supinator, brachioradialis, and extensor carpi radialis longus muscles. Refer to Simons and Travell's Myofascial Pain and Dysfunction: the Trigger Point Manual, Volume One: The Upper Extremities for more complete information. 4

Unless otherwise noted, all images on this page used under license. Images by LifeART (and/or) MediClip image copyright 2010. Wolters Kluwer Health, Inc.- Lippincott Williams & Wilkins. All rights reserved. Images not for reuse..

This page contains affiliate links to Amazon.com. We have not been compelled in any way to place links to particular products and have received no compensation for doing so. We receive a very small commission only if you buy a product after clicking on one of these affiliate links.

by EricT

By Ground Up Strength

The following is a simple guide to the many different kinds of simple sugars found in prepared and processed foods. All of these sugars contain about the same carbohydrates and deliver the same amount of calories, and so are essentially equivalent, to white table sugar. To begin, the basic monosaccharides and dissaccharides important in nutrition are briefly discussed.

The Monosaccharides

Monosaccharides are the simplest form of carbohydrates. They cannot be reduced in size by hydrolosis and so are sometimes called "simple sugars". However, in common usage the term simple sugar usually also includes disaccharides, discussed below, which are two monosaccharides bonded together.

The three main monosaccharides important in human nutrition are glucose, fructose, and galactose. Glucose, a 6-carbon atom, is by far the most abundant monosaccacharide in nature and the most important nutritionally. Fructose is another monosaccharide found in fruits, flower nectar, honey, and the sap of trees. It is a good deal sweeter than glucose. The third simple sugar is galactose, which is a component of "milk sugar", a disaccharide called lactose. Glucose, fructose, and galactose are all classified as a triose, referring to the number of carbon atoms in their saccharide unit (tri- means "three" and -ose means "sugar).

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Disaccharides

Disaccharides are the most abundant form of the ogliosaccharides, which consist of short chains of monosaccharide units joined by covalent bonds.

Sucrose, which is the disaccharide in white table sugar, is the most important nutritionally, comprising at least a third of the carbohydrate intake in an average diet. It is what most of us are thinking of when we say the word "sugar." and contains equal amounts of bonded glucose and fructose (ß-D-fructofuronasyl-α-D-glucopyronoside). Sucrose contains 5 grams of carbohydrate per teaspoon, delivering about 20 kilocalories.

Lactose, also discussed below and mentioned above is the principal carbohydrate of milk, composed of equal parts glucose and galactose. The third disaccharide is maltose. Maltose, or "malt sugar" is two glucose units linked together. It is produced anytime starch breaks down.

How Is Sugar Made?

White table sugar¹, which, as discussed, is produced from sugar cane or sugar beets. Sugar cane. which is actually a tropical grass², started being used as a source of sugar thousands of years ago in India, where it was mentioned in writings during the period of 1400-1000 B.C. Although no one knows for sure, it is generally excepted that the plant originally got its start in New Guinea. Modern sugar cane is actually a hybrid of several species of the genus Saccarum.

Sugar beets, which are white rather than red, are another viable sugar crop. They are a much more recent crop for this purpose, having only been introduced as a means for extracting sugar in 1794. Most of the world's sugar comes from sugar cane, however.

Harvested and Cut Sugar Cane
Image by Rufino Uribe via Wikimedia

How Are Sugar Cane and Sugar Beets Refined?

After the sugar cane is harvested, it is washed and then shredded by giant steel rollers, which crush and squeeze the juice from the cane. Water is then sprayed on the crushed plants to get more juice to seep out. Harvested sugar beets are washed, sliced and soaked in vats of hot water to extract the sugar.

The juice from either plant is then heated in evaporation tanks so that it is concentrated into a thick syrup called molasses. Sugar crystals are induced to form so that they can be separated from the molasses by centrifuge. After the "raw" sugar crystals are obtained, the sugar is further processed according to the end product being produced, such as white, turbinado, powdered, or brown sugar.

Harvested Sugar Beets
Image by Hans Hillewaert via Wikimedia

Types of Sugars

The sugars below may give a little less or a little more than these 20 calories but as a consumer you have know way of calculating the difference and even if you could, it would make no difference to your overall diet. Therefore, consider all of them to be the same as white granulated sugar on a teaspoon to teaspoon basis.

Although most of the sugars mentioned below are produced from sugar cane or sugar beets, there are some other sugars mentioned as well because they are sometimes used, or have been used, as ingredients in food manufacturing.

• Brown Sugar: processed white cane sugar to which molasses has been added. It contains varying amounts of sucrose, caramel, and molasses, which are impurities that are originally removed during the refinement of table sugar. Brown sugar can be anywhere from 85 to 95% pure sucrose, depending on how much molasses is added, which is what determines the difference between "light brown sugar" and "dark brown sugar" we are familiar with. Yes, it's a fair guess to say that light brown sugar contains a bit more sucrose than dark brown sugar. But not enough less to make a difference in the diet!

• Concentrated Fruit Juice: Used as a sweetener in processed foods, this is a concentrated sugar made from dehydrated and deflavored fruit juice. This sweetener is often used to sweeten products so that they can claim to be "all fruit" or "pure fruit."

• Confectioner's Sugar: Finely powdered granulated white sucrose sugar. Most confectioner's sugar for home use has some corn starch, wheat flour, or calcium phosphate added to keep it free flowing. Also known as icing sugar or frosting sugar.

• Corn Syrup: A syrup, synonymous with glucose syrup , made from maize (corn) via either acid or enzyme hydrolysis. This syrup contains glucose and varying levels of polysaccharides, maltodextrins, etc. It can be hydrolyzed to various degrees up to the point of producing pure dextrose (glucose). Corn syrup comes in various strengths (sweetness) which are determined by the amount of hydrolysis and come in "dextrose equivalents" (DE): 24, 36, and 42 DE. The higher the DE the thinner and sweeter the syrup is. The lower the DE the thicker and more starch-like. Corn syrup is one of several types of "starch hydrolysates" that are popular in the food manufacturing industry.

• High Fructose Corn Syrup (HFCS): Produced from corn syrup (glucose syrup), some of the glucose is isomerized to fructose by the enzyme glucose isomerase. Although it is possible for HFCS to be contain up to 90% fructose, the most common product used contains around 42% fructose, as this most closely resembles sucrose. HFCS is less expensive and sweeter than white sucrose sugar, and so is a popular sweetener of beverages such as soda. In other instances, such as baking, many criteria determine what type of corn syrup, or sweetener will be used.

• Honey: A sweet syrup produced from the nectar of flowers by bees as a food source for the hive. Honey is always a mixture of glucose, fructose, a small amount of sucrose, and moisture, with some other sugars and impurities. Composition will vary depending on the flowers the bees used to produce the honey. A typical batch consists of around 40% fructose and 35% glucose, and 1 to 2% sucrose. Other sugars may include isomaltose, turanose, trehalose, erlose, maltotriose, melecitose, and raffinose, but these are present in only trace amounts of less than one percent. The rest is moisture, minerals, vitamins, beeswax, ash impurities in varying amounts, some enzymes, and aromatic volatile oils, which contribute to the unique flavor. The fructose in honey is sometimes referred to as levulose by the honey industry.

• Invert Sugar: A thin liquid solution of glucose and fructose produced by adding an acid³ to a solution of sucrose (sucrose dissolved in water). The acid hydrolyzes the sucrose, causing it to break down into d-glucose and d-fructose. Sweeter than white granulated sugar, it resists crystallization, making it ideal for professional candy makers who use it to give candy a smooth, melt-in-the-mouth, texture.

• Lactose: Lactose is a natural disaccharide of glucose and galactose. It is the primary carbohydrate found in milk. Lactose is about 1/5 to 1/6 as sweet as sucrose, meaning it barely tastes sweet at all. It is highly prone to crystallization. The food industry uses lactose, separated from milk, as a browning agent in baked goods and to improve the water holding capacity of processed meats like ham. It is also used in the making of candies and frozen deserts (beside the natural lactose already found in the milk used to make ice cream, etc.). As an "added" sugar, it does not contribute much to the diet but as a natural sugar it is found abundantly.

• Maltose: Maltose occurs naturally whenever a starch molecule is broken down, whether by a plant to use it's stored starches as fuel, when seeds are germinating, or when starches are being digested in the intestinal tract. Maltose, is used in fermented beverages (beer), breakfast cereals, and some infant formulas.

The maltose used in making beer comes from malt or malt extract, which is a mix of broken down starches consisting mainly of maltose. Usually made from barley or wheat, cereal grains are allowed to sprout which causes the enzymatic breakdown (hydrolysis) of the starch to maltose.

Perhaps the most famous occurrence of maltose in a prepared food is Post's "Grape Nuts" cereal, which was made from wheat and malted barley. C.W. post is said to have mistaken the maltose for glucose (dextrose) which was commonly called "grape sugar" by manufactures at the time, hence the name Grape Nuts.

• Maple Sugar: Produced by boiling maple syrup until most of its water evaporates and the sugar crystallizes. This sugar, like maple syrup, is almost entirely sucrose with only small amounts of free glucose and fructose. It also naturally contains invert sugars. Maple sugar is not commonly used today.

• Molasses: Of all the "sugars" molasses can easily lay claim to being the most nutritious. Molasses is what is left over after the sucrose crystals are removed from the concentrated sugar cane (or beet) juice. It is boiled repeatedly in order to crystallize as much of the sugar as possible, until no more sucrose can be extracted. This repeated boiling makes the molasses become darker and darker. The darkness determines the grade, with Blackstrap molasses being the darkest and most bitter.

The amount of sucrose in molasses differs, depending on whether sugar cane or sugar beets was used. Sugar cane molasses contains about 30 to 40% sucrose, some glucose, fructose, and invert sugar. Sugar beet molasses contains about 60% sucrose. Other components are inorganic salts, organic acids including amino acids, hemicellulose and pectin fiber, waxes, and ash.

• Raw Sugar: The term "raw sugar" as for as the consumer is concerned, should be considered a marketing joke, as there is no standard definition as to what kind of sugar can be called "raw". If one wanted to be particular, the word "raw" would mean that virtually no refining of the sugar had taken place. But this also begs the question of what is "sugar" and what is simply "dried cane juice". However, most experts would tend to consider raw sugar to sugar that is extracted from sugar cane juice but not refined any further. That is, not washed or decolored. True raw sugar contains dirt, insect parts, yeast, molds, and many other contaminants. As a result, the FDA banned its sale to the public.

However, there are some products sold as "raw sugar" to consumers, such as "Sugar in the Raw". These products labelled as raw sugar could be anything but raw sugars typically are a cruder stage of the sugar production process, before "white sugar" is completely refined. In the United States, such sugar is called turbinado sugar after the centrifuge in which it is spun. In the U.K. it is called demerara sugar. This sugar has been centrifuged and some of the impurities removed but it retains a light brown, amber color due to the leftover molasses content. It is not truly "raw" however, it is simply partially refined, with larger crystal size.

Turbinado Sugar
Image by Leena via Wikipedia

Sugar Alcohols

Sugar alcohols, which are also known as polyols are used in food labelled "sugar free" and are often referred to as nutritive sweeteners. Chemically, they are saccharide derivatives in which a ketone or aldehyde group has been replaced by a hydroxyl group. These are naturally present, in small amounts, in some fruits and vegetables but they are produced commercially by hydrogenating mono, di, or polysaccharides. They have become popular as a sugar alternative because they are sweet and possess similar properties but deliver less energy, about 1 to 2.5 less calories per gram, than sugar. They are absorbed more slowly and less completely by the intestines.

However, this incomplete and slow digestion leads to sugar alcohols being fermented by the intestinal flora. If consumed in excess, they can cause gastrointestinal upset in some people, leading to flatulence, diarrhea, bloating, and other symptoms.

The advantage, in terms of calorie reduction, would appear to be small. Also, there is the problem of the tendency for people to take in more energy from foods that appear to have less calories because of "sugar free" or other reduced macronutrient labeling. Sugar alcohols do have less of an impact on dental carries (cavities) however, because bacteria in the mouth metabolize them much more slowly. This makes them particularly suited to chewing gums, breath mints, or any product that remains in the mouth for long periods.

The sugar alcohols approved for use in the U.S. include erythritol, isomalt, lactitol, maltitol, mannitol, sorbitol, and polyglycitols (hydrogenated starch hydrolysates)⁴. These products are not intensely sweet like many artificial sweeteners, the non-nutritive sweeteners like saccharin, aspartame, and sucrolose, which are also called intense sweeteners. In fact, some of the sugar alcohols are only about half as sweet as sucrose, while others are about as sweet, but no sweeter.

Demerara Sugar
Image by Glane23 via Wikimedia

Why Does Brown Sugar Become a Hard Lump?

When molasses is mixed back into white sugar, the molasses forms a film around the sugar crystals. As long as the molasses is moist, the brown sugar will be soft. But if the moisture is allowed to evaporate out of the molasses, it becomes something like a glue, causing all the sugar to stick together in a hard mass. To keep this from happening, brown sugar must be stored in an airtight container like a sealed plastic bag or tightly sealed glass jar. It may help to store it in the refrigerator.

A moist paper towel over the hard sugar will soften it back up, as the sugar draws the water in. This takes about 12 hours, however. You can also pop hardened brown sugar in the microwave for 10 to 15 seconds to soften it, but this is only temporary so the sugar must be used immediately. If your making chocolate chip cookies, make sure not to mix eggs into piping hot sugar!

What About Botulism in Honey?

The risk of botulism poisoning from honey consumption is a frequent concern. It is true that botulism spores (Clostridium botulism) may be present in honey. For this reason honey should never be given to children under the age of one year, as their intestines are not yet able to handle botulism spores, which may colonize the infants intestines and produce botulism poisoning. In healthy older children and adults, there is little risk.

One survey in 1978, which examined honey from 32 U.S. states, estimated that the maximum amount of botulism contamination in honey was around 8 to 28 spores per kilogram of honey. Other surveys in different parts of the world found no contamination in some countries but contamination with different strains in others. The level of contamination worldwide, when randomly examined, tends to be very low, as little as 1 - 10 spores per kg. and for this reason honey should absolutely not be given to children under the age of one year. However, the levels of contamination associated with infant botulism are much, much higher, on the order of 10⁴ spores per kilogram. These samples also tend to be limited to C. botulism, rather than A. or B. botulism, which may suggest that these high levels of contamination are not a random but normal incidence but the result of contamination from and outside source or the the result of botulism amplification in the beehive for some reason.

What is Molasses Used For?

Sugar cane molasses is used to make rum. Rum can actually be made by distilling fermented sugar cane juice or molasses. Cane juice is preferred in the West Indies but most Rum is distilled from molasses, which is generally considered to be the best base. To make rum, a "mash" is started using molasses that has been diluted until it contains the desired concentration of sugar. This mash is then fermented by yeast. It is possible to simply allow the yeasts that are naturally present in the environment to ferment the sugar in vats that are open to the air but most distillers prefer at least some control, understandably so, over the specific type of yeast that is allowed to ferment their mash, short of absolute laboratory precision, which would undoubtedly take some of the art out of the production of Rum. So yeast is added to the mash and the conditions are controlled to allow those yeasts to ferment, producing ethanol alcohol and carbon dioxide as by-products.

If one were making beer, which used a "wort" instead of a mash, after fermenting is done, all that would be left would be to separate the liquid "beer" from the solid precipitates (including dead yeast), carbonate, either naturally by further fermentation in the bottle, or artificially (as large production beers must use), allow the beer to age, and then it is ready to drink. So in essence, the making of beers, like Ales or Lagers, and the making of liquors such a Rum or Whiskey, starts out much the same, although using different base ingredients to start.

However, Rum is a "distillate," which means that the alcohol within the fermented mixture is extracted and collected separately by distillation. To do this, the fermented liquid is heated in a sealed vessel to around 175 degrees Fahrenheit, which evaporates the alcohols from the liquid, which are run through pipes and allowed to recondense back into a liquid state to be collected. This is a "raw spirit," which contains between 70% to 95% alcohol. It can be sold as is, and is sold this way in certain places, such as the Carribean. But most Rum is first aged and then may be blended with spices or fruits. Afterwards, the distillery blends different batches of Rum together until the taste desired is achieved. If this step was skipped, every batch of Rum a certain distillery produced would taste different. Blending the Rums allows expert tasters to reproduce the same flavors in every batch of Rum that is put into bottles. Most rum is then diluted with water so that it contains 40 to 50% alcohol by volume. Molasses can also be used to produce ethanol alcohol for fuel.

Molasses is also used to produce baker's yeast (Saccaromyces cerevisiae), or feed yeast (a high protein feed supplement). The darker molasses grades, such as Blackstrap, is used in animal feeds for livestock (Blackstrap is also available for home use). It can also be used as a crop fertilizer, for which it has advantages and disadvantages.

Molasses is used widely in baking cookies, cakes, and breads and some people like to add molasses to sweet potato or pumpkin pie. It is also used sometimes used in toffees and caramels, and included in barbeque sauces and baked beans.

What's the Difference Between Molasses, Treacle, and Golden Syrup?

There seems to be a lot of debate about the difference between molasses, treacle and a product called "golden syrup." Apparently, this debate is not new but has been going on since the 1800's. Nobody today seems to really know the difference, but many claim there is one.

Today, treacle seems to be a generic word for any syrup made in the process of refining sugar cane. However, in older texts treacle is said to refer to the waste drained from the sugar molds after the sugar was removed from the molasses, or to a more clarified molasses product.

Treacle can range from light to dark but in common parlance treacle usually refers to the light syrup that results from the first boiling, which is also called light treacle or golden syrup. However, golden syrup sometimes refers to a treacle that has been further refined by reboiling and filtration through charcoal. There is also a version of this which was "invented" and sold by a Scotsman name Lyle Abam, a product which is still sold today. This has created some confusion about the origin of golden syrup.

Much darker syrups resulting from the second boiling, are called either just treacle or dark treacle by the British, which Americans call molasses. The product of a third boiling is called Blackstrap by the British and Americans alike.

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by EricT

In my post Homeopathy Is Not a Drug and Other Babbles I had quite a rant, albeit a very informative one, about some idiotic things a NaturalHealth.com article said about homeopathy and about homeopathy quackery in general. If you read that you will be more in flow with what is to follow. Cuz I'm not done!

Much of that post concerned chemicals. The food faddist or the homeopathic zealot, when he hears the word chemical, cries "POISON!" Yet, chemicals are what our food is made of and the term toxic chemical, taken by itself is meaningless.

In my response to a reader of Jamie Hale's article Organic Food: The Real Story I had quite a lot to say about the idea of toxins. The reader tried to draw some vague distinction between "natural toxins" and "toxins developed in the last 100 years":

"There is one very important point that must be considered when speaking of ANY toxins, whether natural toxins we can expect to find in organic foods or "synthetic" toxins.

But before I bring up that point I'd like to talk about the word toxin itself. It's always a good idea to define our terms. Colloquially, we use the word toxin to describe any bad chemical that gets into your body and interacts with the body's cells in a negative way, causing damage. A poison could be thought up as a very bad toxin that does a great deal of damage very quickly or kills you outright very quickly. So lets assume by the word toxin we mean chemicals that cause slow damage.

Most people are probably not aware that in biology a toxin is a bit more specific. That is, they are damaging chemicals or poisons that are produced IN NATURE BY BIOLOGICAL MEANS.

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Even in the case of insecticides like DDT, which the article mentioned, we are still talking about organic chemicals. DDT for instance, is an organochloride. So even though we talk about these things being synthesized or isolated they are still produced via chemical reactions involving organic compounds that…happen in nature. We just ramp it up and produce chemicals in large quantities that only happen very rarely "by themselves". There are many examples of these types of toxins.

The biological toxins that plants produce to defend themselves or for whatever reason and the organic pollutants that we "produce" and then introduce into the environment artificially…they are all NATURAL."

So, what is an example of a natural chemical found in plants that we are all familiar with? Salicylic acid is a very good example. A chemical called salicin is found in abundance in the willow tree. That is used to make salycylic acid, what we all know as aspirin. 1 It is an analgesic, good for pain. It is good to fight inflammation, as a non-steroidal anti-inflammatory (NSAID). It can reduce fevers, as an antipyretic. It is a prophylactic measure against heart attack and stroke for those at risk. It is the active ingredient in many anti-acne skin-care products and an antiseptic in some toothpastes. It's a pretty useful chemical. When I was growing up, baby aspirin was a pretty regular thing for aches, pains, and headaches. That was before we were aware of how toxic aspirin is to children.

In children, aspirin is associated with Reye's syndrome. It is a condition of acute encephalopathy and fatty change in the viscera. Although the syndrome has been recognized since 1963, it took a while for it to be associated with aspirin. In 1980, 556 children with Reye's syndrome were reported. After 1987, when aspirin was identified as a culprit, very few cases have been identified. 2

If you take enough salicylic acid, it will be toxic to you as well. As I painstakingly pointed out in the first post linked here, it is all about the dose. As I also pointed out, anything, if you were able to consume enough of it, could become a poison. This was recognized as long as 500 years ago by a guy by the unwieldy name of Theophrastus Phillipus Auroleus Bombastus von Hohenheim, aka Paracelsus, who said: "Alle Dinge sind Gift und nichts ist ohne Gift; allein die Dosis macht, dass ein Ding kein Gift ist." Yes, we have Latin in this blog. That means, basically, that everything is a poison and nothing is a poison and only the dose makes a thing a poison or a remedy. Or, like I said earlier, the word toxin, taken by itself, is meaningless. Today, we usually sum that quote up as "The dose makes the poison." Tell a homeopathic zealot, a "natural food" snake oil artist, or other assorted crank that and he may want to kill you for it, just as Paracelsus's enemies were rumored to have done to him! 3

Salicylic acid is found in varying quantities in all fruits, vegetables, herbs and spices. It plays an important role in how plants protect themselves from pathogenic infection. 4 According to Hayat, et al., it is a phenolic derivative plant hormone that is distributed in a wide variety of plant species. It is involved in plant growth, thermogenesis, flower induction, uptake of ions, ethylene biosynthesis¹, stomatal movement, reversal of ABA effect on leaf abscission, enhancement of chlorophyll and carotenoid pigments, photosynthetic rate, and more. 6

Plants make salicylic acid, in particular after exposure to a pathogen, and use it as a key regulator of SAR and expression of defense genes. In fact, as early as the 1930's a phenomenon called systemic acquired resistance (SAR) has been known whereby spraying salicylic acid on plant crops "snaps them to attention and puts their defenses on high-alert against future attacks." 7 Clearly this chemical is a bit important to plants, as are a great many other chemicals that plants produce. Lots of these chemicals could be harmful in large enough doses. And many of them could be helpful at the right dose as well.

So we understand that the plant foods we eat contain chemicals that could be toxic. But rarely does a plant food contain enough of any one chemical to be toxic. The plants that do contain such large amounts…we do not eat. For instance, we do not eat willow, we use it as a medicine. Willow then is a "herbal" rather than a food plant. Even though it contains some of the same nutrients as the plants we do eat (which may also be called herbs sometimes but let's avoid that semantic quagmire). Certain plant nutrients, therefore, when functioning in large doses as a drug can be considered pharmacologic agents. Single plants that we eat rarely, if at all, contain a large enough dose of such pharmacologic agents to have an impact on disease treatment or even prevention that falls beyond the physiologic functions of the specific nutrients.

Salicylic acid (SA) has no important nutritional role for humans. In fact, it interferes with the transport and excretion of certain nutrients, such as folate, thiamin, vitamins C and K. 8 Obviously it has a other effects. As became apparent in the earlier post, there is an interesting dose-dependent paradox involved. One medicinal use of the chemical is as an antipyretic (fever reducer). At low doses it is an effective agent for this. As I stated earlier it is highly toxic at large enough doses. In fact, one of it's effects at high doses is the opposite of it's fever reducing effect at low doses. It raises body temperature to dangerous levels, called hyperpyrexia.

There is evidence that suggests that consumption of fruit and vegetables has a protective role in the development of chronic degenerative diseases such as cardiovascular disease (CVD) and cancer. We know that aspirin therapy, with SA being the major metabolite, is used as a prophylactic in those at risk for heart attack and stroke. There is some evidence that chronic low-dose aspirin therapy may be a helpful preventative against cholorectal cancer, as well. Is it reasonable to ask, therefore, whether the SA in fruits and vegetables plays a role in the protective nature of these foods? Could it be that chronic consumption of these foods means that we take in very low does of SA but enough to raise circulating levels to the point where it contributes to this protection, similar to how aspirin therapy does? Yes. This is a reasonable question that has in fact been asked. 4

However, it is important to know the difference between what science asks and what we should take as food being medicine. If you've wondered what the point of this expansive essay on SA is, you've now encountered it. See, while there are many nutritional reasons to eat lots of fruit and vegetables, a reasonable one is not so you can get your salicylic acid! If SA plays a part in the protective nature of FV consumption, no scientist would tell you to abandon the aspirin therapy that your doctor prescribed for you. FV consumption would simply be seen as a potentially helpful adjunct to that therapy. And of course there are a great many other interesting chemicals that may be important such as ellagic acid and other phenolic phytochemicals. Right now there are still as many questions as answer about these compounds.

Certainly it is true that some nutrients, even vitamins, can have physiologic effects beyond their functional role in the body. High dose niacin (nicotinic acid), for instance is used as a cholesterol lowering agent. Using niacin this way is no longer using it for nutrition. We do not "use" or "take" nutrients, after all. Using niacin this way is using it as a drug. The doses go well beyond the amount of the vitamin needed for biological functions. The amounts used for cholesterol lowering, in fact, must far exceed the requirements of nutrition and the recommended daily amounts. This comes with clear-cut dangers and such therapy must be monitored. Yet, I can assure you that you will find many "nutrition experts" to tell you that some supplementary Niacin in your diet is "all you need to lower your cholesterol." We must be aware that a nutrient to be used as a pharmocologic agent is no longer being used as a mere dietary supplement!5

Conduct a search such as "salicylic acid in human nutrition" and you will doubtless get many "nutrition" articles telling you about all the SA in fruits and vegetables and hinting that this will have some effect on your health that makes it worth your while to eat those fruits and vegetables. A "medicinal" affect will be implied. Here we get to the gist. There is a difference between information about nutrition and information about alternative medicine, or mainstream medicine. If a certain food chemical featured in a "nutrition" article is not an actual nutrient, then you are not looking at a nutrition article. Most likely, unless you are reading a good scientific journal, you are looking at an alternative medicine article.

The problem is that, at present, most nutrition information is, in fact, actually alternative medicine information. Chemicals like SA are the fodder for these articles. This is dangerous and irresponsible, to say the least. A person who replaced his aspirin therapy with large amounts of fruit and vegetables because some silly article suggested to him that it's the same difference could be putting themselves at grave risk. The act of trying to cure disease by a careful manipulation of the foods we eat is NOT nutrition. It is fallacy, at best, and as Shwartz and Swhartz point out in "An apple a day: the myths, misconceptions, and truths about the foods we eat," we must view it with skepticism.

On the cover of that book is the picture of an apple that is labeled with some of the apples constituents. Among these are vitamin C, water, sugar, polyphenols, acetone, and formaldehyde. The book goes on to explain that one apple contains over 300 different compounds. Are we getting the idea here?

Clearly, trying to cure a disease by close manipulation of thousands of compounds, of which even the lowly apple has 300, is a bit silly. Yet a healthy diet can certainly play a role in preventing disease. However, we must go on what we know and consider the net diet, not individual compounds whose properties are just now beginning to be unraveled. Most of the quack nutrition articles I have been mentioning tend to focus on one or two "superfoods" which are miracles of prevention by virtue of one antioxidant or another. Most of these articles tend to ignore the fact that a hundred other fruits or vegetables rather than the one they focused on could have contained much higher levels of anti-oxidants. As I've pointed out in the past, picking the best food is not such a clear cut proposition.

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by EricT

By Ground Up Strength

Sea salt is often touted as a more healthful alternative to ordinary table salt. Many food products are now proclaiming the use of sea salt on their labels and health food stores have long promoted it's healthful benefits. Although some of today's food advertising concerning sea salt is in regards to it's giving a better flavor to the food products there is no doubt an additional incentive to take advantage of the public's perception of sea salt as more nutritious and health giving.

Ordinary table salt, the salt such as Morton's which we are all familiar with, is sodium chloride (NaCl) and is commonly derived from halite (rock salt). Salt has long been of great importance, not only to provide sodium in our diets and flavor to our dishes, but also for food preservation and chemical production. In fact, table salt only accounts for about one percent of all the salt used and the rest is used to produce chloride, de-ice roads in winter, agriculture, food processing, and various other manufacturing processes. A great amount of salt is used in the dairy industry, for tanning leathers, fertilizer, caustic soda and soda ash.

Salt can also be mined by the evaporation of sea water. For instance, around the coast, sea water can be pumped into shallow ponds which are allowed to evaporate so that the salt crystallizes on the floor of the pond to be collected later. Alternatively it can be taken from natural inland "brine springs" which occur where rock salt is close to the surface and water moving through the ground dissolves the salt and forms brine streams. It is also mined, as mentioned, from underground deposits as rock salt, which accounts for about one third of salt production in the United States. These halite deposits come from the seas of long ago (millions of years) which have dried up and left their salt behind in huge amounts. Besides evaporation of sea water and rock salt, lake brines, and the salt crust from dry lake beds make up the rest of salt production.

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The Uyuni Salt Flats in Bolivia
image by Ricampelo via wikimedia

All Salt is Sea Salt

When sea water evaporates a brine of sodium chloride (NaCl) forms, most of the other minerals precipitate out, and the salt crystals fall to the bottom of the solution. Although some additional trace minerals may be left in sea salt products, such as magnesium and iodide, there is no additional health benefit and the compositions of most salt sold for human consumption is close enough to identical to be called identical. As well, table salt has long been fortified with iodide so any iodide in sea salt products cannot be considered to be significant.

As you may have gathered, all salt can correctly be called "sea salt" since all salt, at one point, came from the sea. And, in fact, many of the products, sold as sea salt in your grocery store may well be the same exact salt that is sold as "salt" under another brand name. It may well have been supplied by the same company, coming from the same place. Morton salt, which most people are familiar with, comes mostly from land bound salt mining, except in California, where it is sea salt, sold as the same product. Morton does not label salt that comes from the land as sea salt, as some other brands do. But as stated, all salt is technically sea salt. 3

A 1992 article in Vegetarian Times magazine by Sally Cullen, "Salient Points About Salt", reports that a senior lab technician for Cargil, Inc., a major salt producer, supplies salt to both natural-food companies and grocery stores. The only difference in the salts supplied, according to the technician, is the type of anti-caking additive used. The "natural" salts use magnesium carbonate and the grocery store salts use silica aluminate. Each company simply put's its own brand name on the product. According to the same article, Hain brand sea salt and Safeway house brand salt are the same salt, from the same producer, evaporating pans, and bin. 3

The consumer needs to be aware that unless a sea salt product is known to come from a particular location and the salt from this location is known to possess certain attributes, such as trace minerals or other deposits, which give it a unique flavor in cooking, there is no need to pay more for a product sold as "Sea Salt".

It is frequently reported that sea salt is "less refined" than ordinary salt and while this is sometimes true it is not always the case. In the U.S. all salt sold for human consumption must contain at least 97.5 percent sodium chloride, whether labeled sea salt or not. It must be free from heavy metal contaminants as well. This, essentially, means that all salts sold in the U.S. MUST be refined to some extent. A few different trace minerals may be present, here or there, depending on the salt's origin, and these may contribute to flavor. But there is no significant nutritional difference whatsoever. Do not rely on sea salt as a way to ensure consumption of trace minerals. This would contribute nothing measurable except excess sodium, at best. Table salt contains around 21,00 to 23,00 milligrams of sodium per teaspoon, depending on the brand and degree of refinement.

The flavors and odors from a particular salt may be important to cooks, and various sea salts can make a difference in this regard. Some salts have other minerals added to them as well, such as Hawaiian sea salt which has Alaea, a volcanic red clay high in iron oxide, added to it. 4

Some other sea salts are Black salt, Kala Namak, or Sanchal, from India, which has a pink gray color and a sulfurous odor. Sel Gris from France, also called Celtic salt or Grey salt, which is gray to light purple because of it's clay content. Other salts may be more or less refined depending and have slightly different flavor depending on the region they come from. See this overview of different salts for more information.

Don't believe the claims you may read about the "healthful" benefits of sea salt versus "unnatural" table salt. These claims are imaginary and based on nothing but the typical concept that anything that sounds more natural must be better for you. Choose your salt based on it's properties for your dishes, nothing else.

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by EricT

By Ground Up Strength

The splenius muscles are broad and thin, getting their name from the Greek word splenium, meaning bandage. Capitus comes from the Latin word for head, caput which refers to the origin of the splenius capitus on the mastoid process and adjacent occipital bone of the skull, underneath the sternocleidomastoid. Cervicus derives from the Latin word cervix which pertains to the neck, referring to the splenius cervicus having its origin on the cervical spine. 1,2

The splenius muscles make up one layer of four layers of posterior cervical muscles. The most superficial of these layers are the upper trapezius muscles, which form an inverted V at the back of the neck. The splenius muscles are just underneath the upper trapezius at their upper insertion and deep to the rhomboids at their lower origin. These flat and thin muscles form a regular V shape, unlike all the other layers, which form inverted V's except for the vertically oriented semispinalis capitis, which the splenii overlies. The splenius cervicis is more vertical than the capitis and moves around the neck superolaterally.

Origin

• Splenius cervicis: originates at the spinous processes of the third though sixth thoracic vertebra.
• Splenius capitis: originates from the lower half of the spinous processes of the seventh cervical vertebra and the upper three or four thoracic vertebra.

Insertion

• Spenius cervicis: inserts on the transverse processes of the first three cervical vertebrae. The splenius capitis inserts on the mastoid process and the occipital bone.

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Action of the Splenius Muscles

When both sides of the splenius muscles contract together, extension of the neck occurs. When one side contracts alone rotation and lateral flexion to the ipsilateral (same) side occurs.

Figure 1: The Splenius Muscles

Splenius Trigger Point Causes and Symptoms

Trigger points in these muscles are one of the many causes of headache of myogenic origin. TrP's in the splenius capitis and cervicis muscles can be caused by sudden direct trauma, often as a result of whiplash injury. Any postural stress that holds the head in an extended and rotated position for a long period of time can also lead to trigger points in these muscles. A cold draft on these muscles, especially if already fatigued, can also help activate Trp's, especially when the muscles are already fatigued. Sleeping on a pillow underneath the neck and upper back, so that the neck is extended, can also be a problem.

During strength training, performing pullups, lat pulldowns, or similar exercises while looking up with the head cocked forward, chin projected and neck extended may be likely to irritate these muscles.

Splenius Capitis Trigger Points

The main symptom of trigger points in the splenius capitis is referred pain at the top of the head, close to the crown or vertex. See figure 2 below for trigger point locations and referred pain pattern.

Figure 2: Splenius Capitis Trigger Points and Referred Pain Pattern

Splenius Cervicis Trigger Points

The primary symptom of TrP's in the splenius cervicis is pain in angle of the neck, head and especially the eye. The pain is often reported to seem to shoot through the head to the back of the eye but may also be present in a band around the side of the head leading to the eye. A feeling of pressure in the eye may also be involved. Splenius cervicis trigger points, in addition to causing pain around the orbit of the eye, may blur the vision.

Splenius cervicis TrP's can also be a cause of stiff neck, which limits rotation of the head, along with the levator scapulae. Splenius involvement alone will cause less stiffness then levator scapulae involvement alone, which is the main "stiff neck" muscle. When both muscles are involved, rotation of the head may be completely restricted due to pain. When stiffness remains after treatment of levator scapulae TrP's it is likely due to leftover TrP's in the splenius cervicis. The sternocleidomastoid and upper trapezius can also be associated with stiff neck. See figure 3 below for trigger points and referred pain patterns.

Figure 3: Splenius Cervicis Trigger Points and Referred Pain Pattern

Main Symptoms Summarized

• Pain inside the head leading to the eye
• Pain at the top of the head
• Pain at the angle of the neck
• Neck Stiffness and pain upon rotation
• Blurry vision

Associated Satellite Trigger Points

It is highly unlikely that trigger points will occur in the splenius muscles alone. Associated trigger points should be expected in the levator scapula and any of the posterior cervical muscles such as the semispinalis capitis and cervicis; and the multifidi.

TrP's in the splenius capitis may give rise to satellite trigger points in the temporalis and semispinalis (which may also be caused by upper trapezius TrP). Trigger points in both the splenius muscles may be spawned from TrP's in the upper trapezius. 2, 5

Self-Treatment of Splenius Muscle Trigger Points

The splenius muscles are difficult to palpate due to their being located beneath other muscles. However, the muscles in this area are thin so some success can be had by massaging the cervical muscle area in general. A thera cane, knobble, or tennis ball can be used but the fingers may still be the best tool to get in deep to the splenius muscles. Treatment by a qualified professional with trigger point experience may be best in the case of whiplash injury due to a rear-end car collision or intractable problems with this area such as severe stiffness and pain that cannot be solved by self-treatment.

To self massage the splenius muscles it is best to lie on your back so that the neck is relaxed. Using the arm opposite of the side you intend to treat, bring your hand around the back of your neck, feel for the mastoid process behind and below the ear and the occipital protuberance and spine of the cervical vertebrae below it. The groove-like area between these two features is where you want to begin massaging. Dig your fingers into the fibers close to the mastoid process while rotating your head and flexing it slightly to the opposite side. Rub along the orientation of the fibers or use cross strokes. You may need to use your other hand to lend support to the working fingers. Alternatively, you may want to use the non-working, same-side hand to help position the head.

Work your way down, along the spine in this groove which is known as the lamina or laminar groove, feeling for the very tight and painful areas. A hook like motion, that simultaneously presses and stretches the muscle, can also be employed. Your neck should feel more fluid and free to rotate and bend after a good massage of this area. Again, professional treatment is always recommended and it is best to use self-treatment as an adjunct to the services of a therapist. These muscles are difficult to completely palpate and spray and stretch or dry needling may be needed in some instances. 2,4

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Unless otherwise noted, all images on this page used under license. Images by LifeART (and/or) MediClip image copyright 2010. Wolters Kluwer Health, Inc.- Lippincott Williams & Wilkins. All rights reserved. Images not for reuse.

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by EricT

Bench press, bench press, bench press. I'm amazed at how many bench press warriors I come across. No, I'm not talking about the guys who just love to bench press and like to see those numbers go up, but they try to keep their training balanced. I'm talking about people who only train upper body and actually consider bench press (and curls) to be a good measure of "strength".

Now, I have said on numerous occasions that strength has many different definitions for many different people. But diplomacy can turn into hypocrisy after a while. There has to be at least some bench marks (pardon the pun). Some objective measures that we can always turn to to say…that there is strong. Well, one very general benchmark of mine is that having bodily strength should help keep you healthy and injury free. I do NOT mean in the currently fashionable "corrective exercise" way. I don't even really mean the functional fitness way since the best way to function is to do the thing you wish to function well at, with other training being supportive to that goal. No, I mean, if you take the trouble to get strong then you should be able to do activities that require muscular strength without blowing out your back or pulling something.

To be more blunt and more specific, if you want to claim to me you train for strength, then you should at least be able to help your buddy move his furniture without "straining yourself". No, no, I don't mean you're superman and can block bullets with your eyeballs. I mean you are at least moderately prepared for a good days physical labor. Which is an accomplishment in itself this day and age! Can I get an amen?

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So somebody made a comment to me the other day that is pretty much the epitome of the bench press warrior and a classic example of how people misunderstand the mechanics of carrying heavy stuff.

"I can curl my weight, and bench twice it… I could care a less how my legs look. I have no need in real life to be able to leg press massive amounts of weight…I'm fine if my legs can carry the weight my arms can lift".

Now the day I say anything about leg press and how a guy's legs look is, well, not a warm day in hell, if you catch my drift. But who among you thinks that carrying stuff is all about your arms and legs? There are not many reasonably healthy people with arms that can support more than their legs can carry. This in itself is hardly a "goal".

Most of us strength people, when we talk about "lower body work" it is a term of convenience. We aren't really "working the quads and hams". We know that our legs are rarely a limiting factor in getting a weight up. Rarely. Not never but rarely. But what about everyday people and so on and so on and scooby dooby dooby?

We usually think of our body in one of two ways: either as a collection of parts or as "all of a piece". Which version we choose tends to depend on what task we are involved in. For instance, for a bodybuilder, the body suddenly becomes a collection of parts. For a dancer, it is suddenly all of a piece.

Biomechanics, however, sees the body as a system composed of various segments. I don't need to tell you that those segments are all connected. So…yeah, there are parts in between the legs and arms. And those parts are part of the system that is carrying the heavy thing around.

Any system has something called a center of gravity (CG or COG). Although gravity of course acts downwards on all of the body's segments it's effect is as if all that downward force were concentrated at a single point. There are more technical definitions than that, but trust me, unless you already know about such things, they will not help you understand this any better. The important thing to know is that a body weight is balanced in all directions around this point.

The CG of an object determines it's behavior because it is as if all of it's masses concentrate at that area. when you pick up or carry something very heavy that center of gravity is altered slightly. The body must be able to stabilize itself to be able to support the weight without tipping over. To be stable means to maintain the center of gravity over the base of support. So this entails the trunk being able to alter and maintain an adjustment in a position that allows the the center of gravity to be "re-balanced".

You carry a box full of books you lean back slightly. Now you understand why. The muscular system that does this is the so-called "core" musculature. It doesn't matter how much you can curl or bench press if you cannot stabilize the load. It is not about having big legs. Or leg pressing a lot…which most anybody can do, really. The other day I was carrying a huge window air conditioner. The weight of one of those is very off center. The side where the compressor is being much heavier than the other side. At first I grabbed it with the heavy side away from my body. Felt like it weighed a ton. Duh. I turned it around. Suddenly it's a peanut.

You see, the heavy side of the A/C being carried forward of my body by about two feet caused my center of gravity to be shifted heavily forward. Actually I should not say "my" center of gravity but the center of gravity of the "system" I was a part of. My body was the stable base for this system and it had to work much harder to balance a load that was carried in front of me. When I turned the A/C around so that the heavy side was against my body, the center of gravity was shifted closer to the base thus making a more stable system. And that's why it was easier to carry. It still weighed the same.

Well all lifting and carrying is dependent upon you being able to stabilize this COG. Lifting weights prepares you for this. And when I say lifting weights I mean lifting heavy things from a standing position so that your stability is actually challenged. You may have heard people say that things like the leg press do not make you strong. Well, now you know why. All that quad strength cannot be expressed in anything resembling a realistic way if you cannot stabilize a heavy load. And if you fail to stabilize a load…you will "fail" to lift it, either through outright failure or through injury. The same thing goes for the bench press.

However although there must be some objective definition of strength, I am not really talking about what strength training, and strength itself, is or is not. I am talking about the attitude that suggests strength resides in one's arms and legs. Remember, we are talking about a whole system of moving parts here. No matter how strong your arms and legs are, their force must be effectively transferred through the rest of that system. So, strength is related to the task at hand.

While strong arms and shoulders from bench pressing help you bench press more, they will not help you carry a heavy window air conditioner. And while strong legs from the leg press will help you leg press more, they will not help you squat more or carry a heavy load around on your shoulders. So here we get to another thing about strength. It is specific. What you should see emerging here is that the best way to get "stronger" at a certain lift is to practice that lift. Everything else related to training for that lift is entirely secondary to that. There is nothing that is essential but the lift itself.

I may be surprising some readers here. We've heard so much about he importance of core stability work, after all. Am I saying that even this is secondary? Yes. I believe wholeheartedly in core stability work. Supposing we are talking about the non-injured trainee, however, core stability is part of the baseline fitness that prepares you to be able to train those heavy lifts. They therefore are a part of maintaining the general physical system that is needed to train aggressively for maximal strength. But the lift is the most important part of training the stability needed to do the lift!

The greatest strength effect of any weight lifting exercise will be towards that exercise itself. It just so happens that certain lifts carry over to helping your buddy move his furniture more than others and if you believe there is such a thing as "real world" strength then basic kinesiology should tell you that those exercises that involve exerting muscular force from a standing position are superior in this regard.

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GUS Member Comments

by EricT

Most people know two things about interset rest periods for strength training: you can rest shorter or you can rest longer. If you rest shorter you are training for endurance and if you rest longer you are training for strength.

That is a fairly simplistic way of viewing it and yet that is just about the level of sophistication that most trainees bring to thinking about rest periods. But wait! It makes sense on some level. To keep things simple, for our purposes we can define strength and endurance in the following way:

• Strength is the ability to produce force by muscular effort.

• Endurance is the ability to sustain that force production a given period of time, whether holding a position or performing many repetitions.

Variously referring to muscular endurance, strength endurance, or muscular strength endurance, other definitions which are a bit less precise are often proposed for muscular endurance. Such as the ability to perform work over a long period of time or the ability to sustain muscular contractions over time. These definitions are great for a general population. They would fit, for instance, the ability of a cashier in a grocery store to continually pick up products, scan them, etc. But this is just doing work so does not fit our needs for strength development. It's easy to understand why…the weight does not get any lighter as you lift it up and down. You have to exert the same amount of force to lift it on the last rep as on the first rep. So we are concerned with sustaining force production.

If you think that a key to developing muscular endurance is doing more work in less time then it is logical to work towards less rest. If you think strength is about maintaining muscular force output over time then it makes sense to rest longer and therefore be able to exert that same level of force for more reps (i.e. more work).

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But of course in reality it takes a little bit of everything, along the way, to keep getting stronger. So, if your only conception of rest is 'shorter for endurance' and 'longer for strength' how do you know how to use rest periods? The answer most of the time is "I'm building mass right now so I rest shorter" and then "I'm emphasizing strength right now so I rest longer". What this really translates to is that you are on the fence! As I've tried to make abundantly clear in most all of my writings, strength training for maximal strength is always about developing absolute force potential. Or, in plain English, it is always about getting stronger!

A bunch of time spent "emphasizing" mass means you are sacrificing force potential. You have to play catch up and "turn" that mass into force. Seems silly to even type out to me but that is how people think about it much of the time…as if it is not crazy to work your ass off to build a muscle that you then have to teach how to work! How you think about rest periods governs how you use them. There are other ways to think about rest periods and instead of using rest periods you can learn to "take advantage of them".

Rest between sets is the same as rest in general, to some extent. It is about recovery. Longer rest periods mean more time to recover and more time to recover means maintaining more strength over the course of a session. If we take longer rest periods and shorten them over time, by whatever means, we can learn to maintain a certain force with less rest. In other words we can "recover" from it quicker. But the downside to that is the point of diminishing returns. There comes a time when you are no longer doing strength training but endurance work..thus the definitions given above.

Let me give a very straight-forward, but extreme, example. If I were to do 400X5x5 reps using 5 minute rest periods I could try to increase my reps and even increase my sets in order to build up endurance. Alternatively, I could do none of that and instead decrease my rest periods over time. I could try to shorten the rest periods until I got to the point I could do the same sets except only using 2.5 minute rest, or less, between sets. This would increase the ability of my muscles to recover quickly and thus increase muscular endurance. After all that effort, however, what have I accomplished? I can "endure" the work better but does this translate to a higher 1RM? Not really. I haven't increased my force potential by very much, if at all. I've increased my endurance.

It should be a given that you cannot increase strength a great deal without increasing the load but many trainees seem to think that an increase in muscular endurance should correspond to a predictable increase in their 1RM. It doesn't.

The above scenario doesn't seem to be worth the trouble and yet I told you before that it does take a little bit of everything. Meaning that along the way you will be using all sorts of different rest periods.

Obviously, for your secondary or assistance exercises you will use shorter rest periods than for your main lifts. Both for time management and relating to the goal of those exercises. Usually, for me that means "gathering volume" (which does mean mass), staying balanced, and putting forth beneficial work towards helping your main lift. But beyond that you will use different amounts of rest even for your big lifts. Since the scenario above failed and we ended up just spinning our wheels in terms of absolute strength, what do we do?

It's Not Endurance But Work Tolerance

At first glance that seems like the same thing. But not quite. Tolerance simply has a much broader meaning than endurance. Endurance is a part of tolerance but not the whole meaning. Let's say you can run three miles in a go. This speaks to your level of endurance for running. But let's say you get terrible cramps afterwards. This speaks to your level of tolerance. So, even though you can endure the running you don't have a lot of capacity to accept it's consequences. You might say, "all things being equal I could run three miles" but all things are not equal and you probably won't be running much until your tolerance for running improves and you are not affected by it by having terrible muscle cramps.

Work tolerance, as opposed to just endurance, means that we can maintain certain levels of work without breaking down. Without sustaining injury for instance. But it also entails our ability to withstand it psychologically. We call that "fortitude". Just like endurance, tolerance is something we have to build up. We can do that by manipulating rest, and thus recovery.

A strength trainee has very little need to be able to lift heavy weights with one minute rest in between. You want to lift the heaviest weight possible. You like to lift things up and put them down. Yeah, yeah. So do I. In order to lift very heavy things, though, you have to be able to lift very heavy things a lot. How's that for technical?

Are you not feeling me? Well, maybe you've been excited when your favorite powerlifter managed to pull some super human weight. You see a guy lift 800 pounds and you go wow, I wish I could do that. What you don't think about is how many times he has lifted, say, 730 to 780 pounds and just how much work that is. To get to that 800 he had to be able to tolerate a lot of heavy pulling without pulling something! I know "corrective exercise" is big right now but if you think rotator cuff exercises are going to get you to an 800 pound deadlift, well you really don't know what work is.

Now if we just wanted to endure we could lift very very light weights for many many reps. This would be classically what we think of as endurance. One might relate this to a marathon. The intensity is very very low and such levels of aerobic work can be sustained for unbelievably long periods of time, especially if fuel is taken on board. But a middle distance runner, or a swimmer, might want to increase his capacity to run near top speed for longer periods of time. This has to do with tolerance.

Example: Lactic Acid Tolerance Training

Lactic acid threshold training was a big thing for a while. The idea was to increase the period of time you could work before reaching the "threshold" upon which time you cannot work for very much longer because of the build up of lactic acid. But then a lot of physiologists explained that there was no real "threshold" and everyone got confused and went back to twiddling their thumbs at Pubmed. For a while though "lactic acid threshold" training was big from bodybuilding to power lifting.

But lactic acid tolerance training is a real thing (sometimes called lactate tolerance). It is mentioned in Periodization Training for Sports by Tudor Bompa in the following passage:

Lactic acid tolerance training increases athletes' ability to tolerate lactic acid buildup…Very high levels of lactic acid can result from high intensity reps of 40 to 50 seconds. Lactic acid tolerance increases as a result of skeletal muscles' removal of lactic acid from the bloodstream. [According to studies] lactate transporters increase in number as a function of high-intensity training…The ability to clear lactic acid from the blood stream and transport it to slow-twitch fibers for energy usage is an adaptive response that delays fatigue and inevitably improves performance." - Bompa1

How do you "delay fatigue"? You manipulate rest and recovery, just like I've been saying. To delay fatigue you manipulate fatigue. You work with it, not against it. The same thing is needed to train for maximal strength but we really do not need to worry about the physiological details to know how to do it.

Bompa goes on to talk about the ability of an athlete to tolerate the pain of acidosis. He means to be able to tolerate "the burn" and that athletes who can tolerate this better can perform longer. Tolerance, not just endurance, see?

Consolidation is about increasing work tolerance for a certain weight range. But it really makes up a large part of what we are doing when strength training.

Working Under Fatigue

We don't need endurance but one thing we do need is the ability to work under conditions of fatigue while still maintaining a high force output. I don't just mean lift a weight up and put it down a bunch of times really fast. I mean do it with a modicum of control and without technical (and dangerous) failure. There is a very simple way to think about it. If you can pull pretty well in the 760 to 780 range while compromised then you will have a much better chance of doing that 800 while NOT compromised.

A great deal of what I do then is to have trainees learn to manipulate fatigue. That is a bit different than the seat-of-the-pants method that has been given the flowery name "Planned Over-reaching". Planned over-reaching is a fancy way of saying "get real tired, rest, and get stronger, I hope." We don't want to just get tired, we want to get tired with style.

Enter the Cluster

You've probably heard of clusters. All sorts of fancy theories are given about how clusters work. Most having to do with the nervous system and "hypoxia" and other jargon of the sort. But clusters, at their basic level, are just a way of manipulating fatigue and recovery. The goal is to lift a certain weight more times than you would normally lift it in one straight set. Clusters involve inserting little mini-rest periods between single reps of a multi-rep set. This way you recover just a little but not as much as you would if you were just to stop and take a full rest period. But why not stop and take a full rest period? You'd be able to continue to exert that force over more reps, right?

Yes, that is true. You could do the same amount of volume or much more but with less density. But the value of clusters is they do this mysterious thing to your nervous system, saturate your muscles with midi-chlorians…then a miracle occurs. No, no! Clusters increase your work tolerance! See? We're getting somewhere here.

Clusters are just one "advanced" thing you can do that helps to increase work tolerance. There are many others. A mistake that is often made, though, is to look at clusters and similar things as a standalone "method". That is almost always how these things are tackled. Clusters are much more useful when they are integrated into a full, and more clever, plan.

A Plan Involving "Speed" Work and Clusters

Man you can't combine speed work with clusters! Well, no, you can't combine them as in doing them at the same time. Wouldn't make sense at all. But you can combine them within the meaning of one building off the other. I am going to list out a plan I just gave someone. I don't usually do this as training is individual and what one person can handle or what they need can be quite stupid for another person to do. But this is a good example of how one might integrate the concepts I've discussed here.

Before I get to it, a few comments about the "speed" component of this plan. First, it is using fairly high percentages of max so it falls into the "strength-speed" spectrum of things. Second, I just call it speed work to differentiate it from percentage based routines. That is, while all trainees may benefit from it some may benefit from it more if they are actually very slow and need work in this area. However, when the weights are lighter, we always lift them with the intention of moving them as fast and as "explosively" as possible. If you want to call it speed that is fine. If you want to call it something else that is fine. I do want to differentiate it from percentage based routines because of one main component. Those types of routines usually rely on some "1RM" established at some point in the past. As I've explained many times in my writings, I do not agree with this approach whatsoever.

So, let's say you have lifted 450 pounds once. Maybe a few weeks ago. But you know you can lift 330 to 440 "any day of the week" so to speak. In that case it would be reasonable for you to choose 440lbs, 435lbs, or 440lbs as your "max" and base your percentages off of that. Being conservative is fine. You do not have to be precise as you will be working up to very high percentages, beyond speed work, and then performing clusters and there will be a great challenge in this. But if you were to choose the 450, that you've only lifted once and haven't been able to match consistently then you will likely be overshooting and be unable to handle the plan. So we want heavy enough but not too heavy.

If you just don't have a clue, however, you should work up to a relative max on the first day. This means that using appropriate warmups and acclimation sets you will work up to one single that is the best you can do that day with very good form. You're not going for a PR here. Just establishing where you are at that moment while showing good performance. It should be challenging but not crazy challenging! This plan assumes you are a very advanced lifter and that you have worked with these kinds of intensities often. You MUST be able to handle high volume with high intensities and this assumes that you are a mature lifter. So, I provide this example as an illustration of where we can take such a concept but I am not recommending that very many trainees undertake this, at least without consultation and supervision. If this constitutes a very abrupt "intensification" of training for you…then you should know better than trying it. To be clear, this is NOT for the recreational lifter!

For those able to pick their max, reasonably as described, you have the option of working up to a heavy double or triple on the first day, before the speed work. This is up to the individual. Some will find that their speed improves from doing this. Some will find it to be too much. It depends on your work tolerance (ding!) and your response to heavy lifts. If you feel unable to do this you can warm up to a weight that is about 10lbs heavier than your target working weight, or you can skip it altogether.

On the second session there should be no heavy sets. Just a proper warmup and straight to the speed work. Likewise with sessions 3 through 5. Here is the first five weeks of this eight week plan with the working sets written out, based on a max of 435 (whether relative or guesstimated) as discussed. They go from strength-speed to strength:

1. 75% = 325 x 2 x 8 to 10 sets (working on technique but fast as possible) 2 minutes or so rest periods
2. 80% = 345 x 2 x 2 x 8 to 10 (lift it like you mean it but still work on technique)
3. 85% = 370 x 2 x 6 to 8 (gettin heavy!)
4. 90% = 390 x 2 x 6 (circa-maximal)
5. 95% = 410 x 2 x 4 (is this guy crazy? Stick with 4 unless you are feeling very good about doing more)

This ends the strength-speed to strength work, covering 5 weeks. Here you have had the opportunity to reestablish some good habits while doing some very aggressive work. For some this may be the most aggressive kind of thing you've ever done. I would encourage you not to do it if you are anxious about it as that is usually a signal one isn't ready. There are other ways to get to this level and you simply need a lot of work with heavy weights prior to this. The rest periods should remain fairly constant throughout this period. This is important. Remember this is all about manipulating rest and recovery, it's not just about lifting weights as heavy as possible.

As hard as the weights may seem to some the real challenge here is attempting to maintain the short rest periods throughout. It would not be reasonable to expect the 2 minutes to be maintained all the way from 75% to 95%. The point is to make a valiant effort to do this, while keeping safety in mind. Do not take unnecessary risks. Week 6 lets you "take a break" by increasing the rest periods but maintaining the weight. In effect you will be repeating the workout of session 5 but allowing much more recovery between sets. This way you have challenged recovery and force potential and then you allow a bit more recovery while maintaining force output.

After that you will take the same sets and reps and turn them into clusters. So in this scenario you will have performed a second workout with 410 X 2 X 4, using longer rest periods, on week six. Now you will insert mini rest periods of 15 to 20 seconds between each rep within a set, hoping this allows you to turn the 2 reps into 4 reps. You will do one "cluster set", rest normally, and then perform another cluster. Etc. You can stop at 3 clusters if you are unable to continue or you can go for the whole enchilada and do 4 clusters:

6. 410 x 2 x 4 (5 to 7 minute rest periods between sets)
7. 410 x (4x1) X 3 to 4 (where the 4x1 is a cluster of 4 reps w/15 to 20 secs. rest between, a normal rest of 5 to 7, and then repeated clusters for up to 4)
8. 410 X (4x2) X 2

As you see all we've really tried to do is increase the reps over a very short additional time and without allowing full recovery between reps. Going from 8 reps to 12 to 16 was hard enough. On week 8 we double up the reps, still using the min rest between doubles. Our recovery is challenged even further and the whole time we have been maintaining the same force output..which is VERY high.

We have manipulated rest and in so doing manipulated fatigue. Remember that I defined endurance as ability to maintain force over time (whether sustained or reps). Well, fatigue could be defined as the inability to maintain force over time (for us at least). Here, we have worked under fatigue conditions while trying to only stave off fatigue a little. In other words we've tried to resist the affects of fatigue just enough to maintain force but not more than enough. "Not more than enough" is a very important component here. By manipulating recovery just enough and so resisting fatigue just enough we have worked on tolerating fatigue and thus we have developed more work tolerance.

To understand this, relate it to the lactic acid tolerance training I described above. If the rest periods used were so long that lactic acid was able to be completely cleared nothing would be accomplished! It's the same here. If we rested long enough to allow complete recovery we would not increase our work tolerance. Our ability to maintain this force in the face of fatigue says a lot about our ability to increase force output. Many will find that their actual max attempts are "easy" compared to this work with already established weight ranges.

You should have noticed that while endurance work usually involves lots of sub-maximal repetitions this used near-maximal weights. What we want then is the simple ability to withstand a lot of near maximal work. Under all sorts of conditions, not just "ideal" ones. One of the failures of "strength training theory" is that most of it uses ideas borrowed from sports that never use maximal muscular effort. The same idea about periodization for a swimmer is recycled for strength training. The problem with this is that it tends to involve ideas about monitoring performance and recovery as if you are in fear for your life if you try to lift a heavy weight when "not properly recovered." We want the opposite. We want to be able to tolerate near maximal work even when things are not ideal. Without risking injury and without compromising recovery to the extent that training is disrupted.

This plan is an extreme example that would not suit many right off the bat so you may wonder why I used such an "advanced" plan to illustrate this. Well, if I give a more basic plan it would be more difficult for you to tell the difference between this and many other ways of training that involved volume or increasing endurance. So this served to better illustrate what we are going for even though being this aggressive will not at first be necessary. The example should help you see how we think about it even if it doesn't suit you personally.

One Last Note, Defining Fatigue

Since the word fatigue is used prominently throughout this article, I think it is important to establish a working definition for it, since fatigue can mean different things to different people. Of course, by fatigue, we mean that things are going on inside your body, on a physiological and chemical level, and these things constitute what scientists might consider fatigue. Also, when you feel the physical affects of your training and other activities, you are tired, sluggish, uncoordinated, etc. that is an outward manifestation and we call that fatigue as well.

Here though, when I talk about manipulating fatigue, I am thinking of fatigue as that component, or "factor" that masks your fitness, which in this instance is your force output ability. This is important because it is different from the classic view that has fatigue as making "inroads" on your recovery ability and which would cause you to model training very differently.

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GUS Member Comments

by EricT

I've talked about the athlete fallacy many times. This fallacy is related to exercise guilt and the feeling that if you are not "going all the way" you are doing something wrong, wasting your time, may as well not bother, etc. and so on.

Also related to this idea, intrinsic to it really, is the idea that you must regularly go to the gym and engage in an exercise program or training plan in order to derive any health benefits from exercise. So, in other words, it takes a few weeks to a month to see any true benefit because that benefit is always from the cumulative results of regular exercise.

This is at least partly true. Of course exercise benefit is cumulative and more benefit, over time, will be seen from regular exercise that is based on some kind of progressive overload (to some extent).

Travis Saunders, who blogs regularly for the PLOS blog Obesity Panacea recently posted an article called 7 Myths About Physical Activity. Now, these were not your typical recycled-from-the-webernet-misinformation-mill myths but some surprising ones..some of which should be seen as quite liberating:

"One of the most amazing things about exercise is that the benefits of a single workout are seen within hours of the workout itself, and last up to 3 days after the workout is completed! For example, a single session of aerobic exercise has been shown to reduce important risk factors for diabetes and heart disease such as triglyceride levels, blood pressure, and insulin resistance, while also increasing HDL-cholesterol (the “good” cholesterol). Of course the benefits of exercise increase over time, but even a single workout can produce measurable improvements in important risk factors." - Saunders1

Saunders suggests reading this review by Paul Thompson, et al. What this review discusses is "acute" versus "chronic" response to exercise. Different responses, such as lower blood pressure and triglycerides/cholesterol may require different exposure times to different intensities of exercise and not everything is known about how much exercise is needed to produce these beneficial effects. It should also be clear, which is pointed out in the paper, that regular exercise over time results in greater exercise capacity and thus a greater acute effect. In other words, the more you work out, the harder and longer you will be able to work out and thus the more benefit you will get from it.

Although this may seem obvious, most people do not think of exercise as something beneficial that gets more beneficial over time. They think of it as requiring a long-term commitment before any benefit can be expected to be derived. This is simply not the case. For example, obese people are often told that they must focus on diet and lose weight before they even bother to exercise. They are essentially told they are "too unhealthy" to exercise. It should be clear that exercise will have immediate benefits for everyone, especially the obese, and that these benefits will simply become greater over time.

There are so many conflicting messages in exercise land. "Doing something is better than doing nothing," is perhaps the message that needs to be heard more often. Doing something regularly would be better. Doing something regularly and with a plan would be best.

Many of the messages concerning regular activity and exercise concerns fat loss. To lose weight "move more and eat less," we are told. It is rarely mentioned that "moving more" does not need to result in weight loss to positively impact our health. When it is mentioned this benefit is of the far-off kind. The message is that unless you sit down and analyze everything, consult a professional, make a complicated plan with a long-term goal, you will not be accomplishing anything. The mere process becomes so daunting and life-changing that many are discouraged and fearful. When they do begin, this discouragement and fear causes them to do too much too soon, resulting in fast burn out. The perpetual couch potato, is in large part, created by fear of failure which is due to being healthy seeming as hard to do as quantum physics!

The fitness and nutrition industies feed this failure. In large part this is due to the industry being bent on creating customers rather than performing a service. That is, the fitness and nutrition industry is not as "service oriented" as it could be. As Jamie Hale recently said "The overwhelming majority of people working in the fitness industry are not concerned with your health. They have other interests- making money and helping you look better."2

Too often do people suffer heart attacks or stroke and then start going out for walks or other moderate activity. It seems that nobody needs to be told that "something is better than nothing" after they have already seen the results of their ill-health. Yet, making a difference can be by doing something as simple as deciding to walk down to the store instead of drive to it or to take the stairs instead of the elevator.

The same things are true of resistance exercise and strength training. You do not need to be daunted and overwhelmed by the complexity of strength training to get some immediate and tangible benefits from it. You do not need a complicated long-term plan to get started. As a matter of fact, picking a handful of exercises, let's say body weight exercises, and simply playing around with them, getting a feel and deriving a baseline, can and will be of immediate benefit. Yet, many a trainee, if they were to tell a strength coach they were going to do this, would be admonished for it and told they didn't know what they were doing. You must pick a program and stick to it! I've complained about this before:

""Get off your butt and pick a program" is probably the worst thing I could say to someone who is daunted and intimidated by the overwhelming task of changing their sedentary lifestyle. Now a lot of the trainers and coaches out there may disagree with me. "Overwhelming?", they will say. "You just have to do it. You just have to stop being lazy and do it." These attitudes themselves are a big pet peeve of mine because most terse statements like these require all sorts of qualification to be useful."3

Don't let the loud mouth blow-hards scare you out of exercising and back onto the couch. For everybody that enters a marathon for the sole purpose of breaking out of their sedentary habits there are many more who would find this approach to be disastrous. So what is the message here? It is okay to "just" exercise. At least at first. Pick something you are interested in and like to do and start doing it. Just a little at first. Add to it if you like. As you begin to feel better you will most likely find making a more comprehensive plan of attack easier. You will also have more information to go on. Exercise has health benefits…period.

However, if you want to be able to stick to it, there must be some reward. I do not mean an intangible and hard to imagine award to be patiently cultivated for years to come. I mean some immediate reward. This is the reason that such a strategy can backfire. So, knowing that exercise of any kind can have immediate benefits does not mean we can make exercise a habit and make a lasting change in our life. Acute benefits are, of course, temporary!

As I have always recommended in the past, instead of making it your goal something vague like get moving, start exercising, get in shape, etc. try to think of something you would like to be better at. Set a performance related goal. It can be any number of things. Now, don't set unrealistic goals! Such as "win a marathon". Set easily achieved and personal goals like being able to run a mile, perform 5 pullups in a row, do a set of 10 pushups. Maybe you'd like to be a better swimmer? Hey, perhaps you'd just like to see if you can improve your back pain. You catch my drift. Even though you may start by the seat of your pants once you start to see some results your motivation to both organize your exercise and keep doing it will grow.

The message here is that you do not have to sign over your first-born to the training God's to see benefit from exercise. It is okay to "just do something". The trick is coming at it with an attitude that works.

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Member Comments

by EricT

By Peter Janiszewski, Ph.D.

Originally published in Obesity Panacea, a PLOS Blog

This is a each part of a 5-part series delving into the fascinating and seemingly paradoxical research on people who despite being obese, remain metabolically-healthy.

Is Metabolically Healthy Obesity an Oxymoron?

To date, countless epidemiological studies have shown that as you move from a normal weight (BMI = 18.5-24.9 kg/m2) towards overweight (BMI = 25-29.9kg/m2) and obesity (BMI ≥ 30 kg/m2) the risk of many diseases increases exponentially.

Does this imply that every individual carrying excess weight is guaranteed to develop diabetes, cardiovascular disease, cancer, or some other disease?

Although this belief prevails, the cumulative research suggests the answer to the above question is a resounding “NO!”

It all started in 1965. Two researchers, Albrink and Meigs, were performing a general investigation into the health of factory workers, and noted a rather counter-intuitive result: that “many obese men had normal triglycerides.”

Subsequently, in 1982, Ethan Sims first included the designation of “healthy obese” subtype in his classification of obesity, thereby first identifying a unique subset of obese individuals that appear to be at least partially protected from the development of the metabolic disturbances generally attributed to obesity.

Today it is believed that approximately 25-30% of obese individuals ­remain metabolically healthy (normal blood glucose, blood lipids, blood pressure, and cytokine profile) despite their excess weight. However, despite awareness of the metabolically-health obese phenotype for close to 30 years, there currently exist no established criteria by which to define these individuals. Not surprisingly, there is significant variation in the predicted prevalence of these individuals within the total obese population.

Japanese Sumo Wrestler in 2010 Tournament
image by FourTildes

The defining characteristics of the metabolically healthy obese phenotype, in contrast to obese individuals with metabolic risk, include limited abdominal, particularly visceral fat accumulation, an earlier onset of obesity (<20 years) and high levels of physical activity. Additionally, black obese individuals have a greater tendency of being metabolically-healthy in contrast to white obese.

Japanese sumo wrestlers are often used as a popular example of metabolically healthy obese. They are morbidly obese and yet due to their high level of activity have very little visceral fat accumulation, tons of muscle mass, and a healthy metabolic profile – until they stop training, that is. Once they stop training, their fitness drops significantly, they accumulate excess fat in deleterious locations, and their metabolic profiles deteriorate. Football linemen are also a popular example of metabolically healthy obese, when they are training.

As a important caveat, there are countless other health issues brought on by carrying excess weight that are not always metabolic (i.e. joint problems due to excess load, skin infections, etc.). Thus, it is often argued that despite being metabolically-healthy these individuals may still be far from optimal health.

Nevertheless, it is important to note that excess weight alone doesn’t absolutely guarantee the presence of metabolic disease. There is certainly truth to the notion that there is more to health than the number on one’s bathroom scale. 1,¹

Prospective Risk of Disease

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The cross-sectional research certainly supports the existence of a sub-population of metabolically-health obese individuals; approximately 1 in 3 obese individuals has a healthy metabolic profile. But what about the chances of developing chronic diseases such as diabetes or cardiovascular disease – two common ailments tied to carrying excess weight?

We will look at two separate studies investigating this question.

In the first study, 2902 men and women were subdivided into different groups based on their weight (normal, overweight, and obese) and metabolic status (presence or absence of metabolic syndrome or insulin resistance). While this subdivision is a tad confusing, keep in mind that people with excess weight but lacking the presence of the metabolic syndrome or insulin resistance would be considered to fit the definition of the metabolically-healthy obese.

These individuals were prospectively followed for up to 11 years to see who would develop type-2 diabetes or cardiovascular disease.

And what say the results?

Over the follow-up period, 141 subjects (~5% of population) developed type-2 diabetes, and 252 experienced their first cardiovascular event (~9% of population).

In terms of risk for developing cardiovascular disease, overweight or obese subjects without the metabolic syndrome or insulin resistance, that is, metabolically healthy obese, were at NO higher risk in comparison to their equally healthy, but normal weight individuals.

Similar story in terms of type-2 diabetes risk; overweight or obese subjects without metabolic syndrome and overweight, insulin-sensitive subjects were not at increased risk for diabetes in comparison to healthy, normal weight individuals.

The authors of this study provide the following conclusion [emphasis added]:

“[…] in the absence of metabolic abnormalities, obesity itself did not increase risk for cardiovascular disease and was a relatively weak risk factor for incident diabetes.”

A similar conclusion was reached by Canadian researchers following a group of 1824 healthy men for a duration of 13 years.

Again, the subjects in this study were divided into 3 categories of body weight (normal weight, overweight, and obesity) and also on the presence of the metabolic syndrome.

During the follow-up period, 284 of the men developed cardiovascular disease.

Once again, the obese men who despite their excess weight had a relatively healthy metabolic profile (metabolically healthy obese) did not show any greater risk for developing cardiovascular disease in comparison to healthy, lean men.

The authors of this study, concluded the following:

“The results of this prospective population-based study indicate that the risk of ischemic heart disease associated with a high body mass index depended entirely on whether features of insulin resistance syndrome were simultaneously present.”

So, not only may 1 in 3 obese individuals have a healthy metabolic profile, but, in fact, their future risk of developing diabetes and cardiovascular disease may be equal to that of healthy, lean individuals.

But is there more to health than the level of triglycerides in one’s blood, or their risk of diabetes or cardiovascular disease? And if we consider other, potentially more telling outcomes – such as mortality – will metabolically-healthy obese individuals still be considered healthy?2,²

Obese, but Metabolically Healthy: Lower Risk of Mortality?

We just found out that out that diabetes and cardiovascular disease risk among metabolically healthy obese individuals is no greater than that of healthy lean individuals. Therefore, I pose the following question:

Is there more to health than the level of triglycerides in one’s blood, or their risk of diabetes or cardiovascular disease? And if we consider other, potentially more telling outcomes – such as mortality – will metabolically-healthy obese individuals still be considered healthy?

This question brings us to today’s post in which we discuss a landmark study published in the journal Diabetes Care, which was conducted by friends and colleagues of ours: Dr. Jennifer Kuk and Dr. Christopher Ardern. But rather than personally writing about the study, I figured I’d interview Dr. Kuk and get the details of their findings directly from the primary author.

OP: If you were to sum up the main findings of your study to a non-scientist at a dinner party, what would you say?

Dr. Kuk: I’d say that “My study shows that individuals who are obese and do not have common diabetes and heart disease risk factors die at the same rate as those who do. This means being overweight alone puts you at higher risk for dying, even though you do not high blood pressure, high cholesterol or high blood sugar. This highlights the negative health impact of body weight alone”.

OP: Why do you think the prevalence of metabolically-healthy obesity in your study was so much lower than previously reported in others (6% vs 20-30%)?

Dr. Kuk: The prevalence was lower in our study as compared to others simply because we used a more strict definition of metabolically normal. Other studies used insulin resistance or the metabolic syndrome (3+ risk factors) alone, but we defined ‘metabolically healthy’ as the absence of insulin resistance or any metabolic syndrome criteria. We felt this would be a more accurate definition of ‘metabolically healthy’ as each of the metabolic syndrome criteria are associated with morbidity and mortality alone.

OP: How do you reconcile the findings from the current study with those of prior studies suggesting that metabolically-health obese individuals are at no greater risk for developing type-2 diabetes or cardiovascular disease than normal weight individuals?

Dr. Kuk: Although I don’t know which studies you are referring to exactly, but in our study, 80% of the deaths in the metabolically-healthy obese were due to cancer and ‘other’ causes. Other causes are likely traumatic injuries, which highlights an important point. Obese individuals are less likely to survive a trauma as compared to normal weight individuals despite similar injuries. This is related to longer transport times due to their higher body weight, and difficulty assessing and treating the injuries due to their increased size. Further, they are less likely to see their physicians regularly, which may be in part why cancer is generally diagnosed in obese individuals at later stages. Thus, this study fits in line with the idea that these individuals are not more likely to develop these metabolic diseases, but still die from other causes.

OP: Recently, Drs. Sharma and Kushner proposed a new staging system for obesity treatment suggesting that obese individuals without established metabolic risk should be counseled to maintain current weight, rather than lose weight (Read about this on Dr. Sharma’s Obesity Notes blog). Do the results of your study agree or disagree with these recommendations?

Dr. Kuk: One can examine this question from a theoretical or practical standpoint. From a theoretical stand, weight loss improves metabolic factors, functionality and several psychological and social factors, and thus it would be intuitive to recommend that all obese lose weight. However, from a practical perspective it may be unethical to recommend an individual who is not presenting with overt disease to try to lose weight as most individuals fail to maintain their weight loss over the long term. Repeatedly failed attempts to maintain weight loss has been shown to elevate one’s risk for diabetes, cardiovascular and cancer for a given BMI. In other words, it may be better to recommend maintenance of weight rather than prescribing weight loss, knowing that they are likely to fail and be worse off because of it. Though we did not examine this issue, Sharma and Kushner’s staging system examines non-metabolic consequences as well, and it is reasonable to assume that these are equally important to examine as they are also important aspects of health, and inclusions of these factors may alter the associations observed.

OP: Are metabolically-healthy obese individuals actually healthy?

Dr. Kuk: I think that whether metabolically-healthy obese are actually healthy is dependent upon the accuracy of the definition. As we see that obese without cardiovascular disease or diabetes risk factors are at elevated cancer risk implies that our definition of metabolically healthy is not capturing cancer metabolic risk factors. Similarly, risk for trauma events may also reflect aspects of health that may or may not be captured by metabolic risk factors, but are crucial aspects of health. For example, musculoskeletal fitness would be a predictor of risk of falling or functionality.

Thus, if we used a more encompassing definition, we would likely see that these metabolically-healthy obese may be at lower risk for mortality and are healthy. However, as our definition only identified 6% metabolically healthy obese, I would suspect that an all encompassing definition for healthy obese would be a very minuscule proportion of the population.

OP: Thanks very much Dr. Kuk!

So, despite a healthy metabolic profile, no greater risk of diabetes or cardiovascular disease, metabolically-health obese individuals may still be at greater risk of dying early.

Maybe, they’re not so healthy after all.

This work would certainly suggest that all obese individuals – even those with a healthy metabolic profile – should attempt to lose weight. But what if losing weight actually makes these, otherwise healthy, but obese individuals less healthy? 2,³

Obese, but metabolically healthy: Is weight loss detrimental?

While countless epidemiological studies have shown that as you move from a normal weight (BMI = 18.5-24.9 kg/m2) towards overweight (BMI = 25-29.9kg/m2) and obesity (BMI ≥ 30kg/m2) the risk of many diseases increases exponentially, it is also true that approximately 25% of obese individuals ­are metabolically healthy despite their excess weight. These individuals are also at no greater risk of chronic diseases such as diabetes and cardiovascular disease than their lean counterparts. However, as we learned yesterday, despite being metabolically-healthy obese individuals may still be at greater risk of mortality.

This latter point would indicate that despite suggestions to the contrary, all obese individuals, regardless of their metabolic status should be counseled to lose some weight.

But should they? What if weight-loss among otherwise healthy obese individuals actually makes them unhealthy?

According to a paradoxical study by Karelis and colleagues, otherwise healthy obese women who lose weight via dieting may actually WORSEN their metabolic profile.

In the study, a sample of obese women were divided into either metabolically healthy (20 women) or metabolically at-risk (24 women) based on their level of insulin sensitivity (a marker of diabetes risk – the more insulin sensitive, the better) as measured using the euglycemic-hyperinsulinemic clamp procedure. These women then underwent 6 months of a medically supervised dietary weight loss program consisting of approximately 500-800 calorie reduction in daily food intake.

After the intervention all women lost a significant amount of body weight (approximately 6-7%).

More interestingly, however, while the metabolically at-risk obese women showed a 26% increase in their level of insulin sensitivity, the insulin sensitivity of the metabolically healthy obese women actually deteriorated by 13%!

In other words, by losing weight those obese women who were originally metabolically healthy may have actually increased their risk of diabetes.

This finding is very unexpected, and as of yet has not been corroborated by another study. Nevertheless, it does raise the very intriguing possibility that weight-loss among otherwise healthy obese women may not only unnecessary but, in fact, counter-productive.

This finding falls broadly in line with a recommendation paper by Drs. Arya Sharma and Robert Kushner published in the International Journal of Obesity earlier this year. In that paper the authors proposed a novel obesity classification system which not only assesses weight, but also health complications of excess weight. Germane to the above discussion, Sharma and Kushner recommend that among obese individuals who have “no apparent obesity-related risk-factors” the goal of patient management should be to simply avoid further weight gain, or maintain current weight, rather than to induce weight loss. (To read Dr. Sharma’s full discussion of the new classification system please visit his blog here.)

In essence, the idea that healthy obese individuals may not have much to benefit from weight loss, metabolically speaking, is not that surprising – they are healthy to begin with! However, whether weight-loss may actually be ill-advised for healthy obese individuals needs to be investigated by future studies – until a counter-intuitive finding such as this one is corroborated, many remain doubtful (including me). For example, it remains unknown whether exercise-induced weight loss among healthy obese individuals could also result in metabolic detriment (doubtful). Additionally, we have currently no idea if the above finding also holds true among men. 4,⁴

Obese, but Metabolically Healthy: Is Weight Loss Beneficial?

So what have we learned thus far?

1. About a third of obese individuals fail to exhibit the metabolic complications commonly attributed to excess weight.

2. These same individuals also seem to be at the same relative risk of diabetes and cardiovascular disease as equally healthy, but lean individuals.

3. Nevertheless, despite being metabolically healthy, some evidence suggests that excess weight may put such obese individuals at risk for early mortality due to other, non-metabolic, factors.

4. This latter point would imply that all obese individuals should be encouraged to lose weight, despite their metabolic health. This, in fact, is in line with guidelines developed by leading health authorities which currently recommend weight reduction as the primary treatment strategy for all obese patients, regardless of metabolic health. However, as we learned yesterday, weight loss via caloric restriction among metabolically healthy obese may actually result in a deterioration in insulin sensitivity, thereby increasing risk of developing type-2 diabetes.

Now, as most of you know, when a completely counter-intuitive finding like this comes along, where even the study authors fail to come up with a plausible mechanism, it is up to other researchers to follow up with additional research to either corroborate or refute this original finding.

Because I am personally drawn to paradoxical and counterintuitive findings in science, I was very intrigued by the findings of Karelis and colleagues and decided to follow up their study, but include a few variations:

a) Since the study of Karelis et al. only used female subjects, we wanted to ensure this wasn’t due to a gender effect and thus included both men and women.

b) Additionally, to test the possibility that their finding was driven only by modality of weight loss (caloric restriction, in their case) we employed a number of weight loss interventions (diet alone, exercise alone, and the combination of diet and exercise).

c) Finally, while the original study only looked at insulin sensitivity, we decided to assess changes in other variables of interest (body composition, blood lipids, glucose and insulin levels, etc.).

In our study, which has just been published in the prestigious journal, Diabetes Care, a total of 63 metabolically-healthy obese men and women and 43 metabolically-unhealthy obese men and women participated in 3-6 months of exercise and/or diet weight-loss intervention.

And what did we find?

First, body weight, waist circumference, and total and abdominal fat mass were significantly reduced in all subjects – regardless of gender, modality of weight loss, and metabolic status.

Second, in contrast to the findings of Karelis et al., insulin sensitivity IMPROVED after weight loss in both the metabolically-healthy (by about 20%) and metabolically-unhealthy obese individuals. However, the improvement was greater in the metabolically-unhealthy subjects. See figure below.

Importantly, this improvement was similar across all weight loss modalities. In other words, dietary caloric restriction did not have a unique negative effect on insulin sensitivity.

Finally, while the metabolically-unhealthy obese individuals also showed improvement in numerous other outcomes (triglycerides, fasting glucose and insulin, HDL-cholesterol, and total cholesterol), a reduction in fasting insulin was the only other metabolic improvement among the metabolically-healthy obese. This latter finding is not surprising given the normal baseline levels of most metabolic risk factors among metabolically-healthy obese individuals. That is, since they were healthy to begin with – they can only get so much healthier after weight loss (ceiling effect).

Thus, we found no evidence of deterioration in metabolic profile among metabolically-obese individuals who lost weight via a lifestyle intervention.

While limited health care resources dictate the need to prioritize high-risk obese individuals for aggressive treatment, to imply that obese individuals who are metabolically healthy should not lose weight may not be the most appropriate public health message. Such a public health message may be particularly misguided at a time when the prevalence of obesity continues to increase, despite a greater public awareness of the benefits of weight loss. In this context, our findings reinforce current recommendations which suggest that all obese individuals should be encouraged to lose 5-10% body weight.

Bottom line?

Although a fair number of obese individuals may have a perfect metabolic profile, it appears they may still experience negative consequences of their excess weight. Furthermore, weight loss achieved via lifestyle intervention appears to still bring about some metabolic benefit among previously healthy obese individuals (it certainly doesn’t seem to harm health). Given the numerous non-metabolic benefits of weight loss (mobility, joint problems, psychological status, sexual function, etc.), all obese individuals have something to gain from a modest 5-10% weight loss. 5,⁵

Peter Janiszewski has a PhD in clinical exercise physiology. He's a medical writer/editor, a published obesity researcher, university lecturer, and an advocate of new media in scientific knowledge translation. You can connect with Peter on Twitter. For more information please visit his website.

Published under a Creative Commons Attribution License (CCAL) from the The Public Library of Science (PLoS). Only minimal changes have been made to the original articles in order to fit this format. The author's original intentions or the meaning of the articles have been in no way affected by these slight changes.

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by EricT

By Eric Troy

I was just reading a review of Mark Young's new "How to Read Fitness Research" product. A few questions occurred to me. One, what in the heck is fitness research? There are so many different types of studies and different types of subjects, all of which could fall under the "fitness" umbrella. Many of these have their own specific pitfalls and unique challenges. A person would need to have a more thorough background in the sub-disciplines before simply "learning how to read a study".

Just what the fitness industry needs is another crowd of Pubmed dreamers constructing the latest and greatest "training program" based on their new understanding of "studies". Let's take some short linear periodization, paste in some magical fruit from a study or two, and make a million! Nah, I disagree that most trainees or gym trainers need to be scouring Pubmed because they think they understand how to read studies based on some online product they purchased. Likely they will just "think" they know what they are doing. Most would do better to build a good library of resources written by professionals who actually do know what they are doing and did not get their expertise from an online product, but from a lifetime of professional endeavor.

The reason I say all this is not to attempt to criticize Mark's product as I am sure it is a fine one. After all, one of the major differences between those who can read studies and those who can't, usually, is that those who can read studies have letters after their names..as does Mark. I am criticizing those who are recommending it willy-nilly to everyone. A product that would be great for coaches and others who already have a large amount of foundational knowledge could actually be damaging to a casual or beginning strength trainee.

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However, having an idea how to read and understand research is a must. Fortunately there are some free resources available. Yep, usually you can get everything for free. You just have to look. For these I simply looked at Jamie Hale's blog "Knowledge Summit" where he has provided permanent links to some pertinent resources: How to Read a Paper by S. Keshav and How to Read a Scientific Paper by John W. Little and Roy Parker, the latter being the most useful for non-scientists.

Critical Thinking Versus Research

There is a lot more to it than a PowerPoint presentation of how to read studies. Critical thinking is, in large part, developing a very good BS meter. Research is not necessarily an indication that one is applying critical thought. How to conduct research and how to think critically are not necessarily one in the same. It is critical thinking, however, that the average person needs to develop in order to see through the BS in the fitness industry more than it is learning how to read research papers. Part of doing that goes way beyond scouring Pubmed for studies and actually reading these things I like to refer to as "books". What ever happened to books, folks? They are still pretty darn useful. The idea is to develop a good sense not of what we do know but what we DO NOT know. Do this long enough and thoroughly enough and after a while you will not even need to search Pubmed for studies. You can make what we call an EWAG (An Educated Wild-Ass Guess).

Somebody Told Me…Wide Gut Equals Big Strength

For instance, not long ago somebody told me that those with the widest abdominal areas were consistently the strongest individuals. Notwithstanding that we need to be clear on what activity we are talking about my BS meter went off. This statement makes it seem as if there is some statistical data that can be readily called on to show a direct correlation between abdominal girth (I had to translate "width" into girth) and physical strength by some consistent measure. There absolutely is not any such data and I did not need to go searching to confidently point out that there was no such data. I was able to make this EWAG not because I had specific data to point to but because I have enough knowledge of the subject matter in general to make my guesses very good ones.

Waist Circumference and Abdominal Fat

Now, this individual was undoubtedly thinking of very well developed obliques and the massive and blocky look. In fact, the same look that many modern bodybuilders sport. Although many bodybuilders are very strong and a few individuals are notably strong most of them would be out-lifted by a less blocky and relatively skinny powerlifter. Likely, what this individual did not know is that intra-abdominal fat deposition is highly correlated with abdominal girth (not in women). Intra-abdominal fat is fat that is visceral, meaning it is stored between the organs of the abdominal cavity rather than under the skin, i.e. subcutaneous. For men, a waist size greater than 40 inches (about 102cm) means that it is highly likely that this individual has a great amount of intra-abdominal fat. However, it is absolutely not appropriate to rely on abdominal circumference alone as an indication of risk. It is possible that subcutaneous fat could lead to an increased abdominal circumference measurement in an individual who had otherwise normal risk factors and it is important to realize that a waist circumference measurement measures both visceral and subcutaneous fat. When compared with CT (CAT scans) high waist circumferences can show a very large variation in fat distribution between visceral and subcutaneous.

However, waist circumference is still a good estimate and has been suggested to be a better predictor of intra-abdominal adipose tissue than BMI alone. A BMI between 30 and 39 is referred to as obese and above 40 as morbidly obese.¹ But those with large muscle masses may easily have a BMI of 30 or above that has no association with adiposity. Also those who are very tall and/or thin, have a different range of BMI's associated with excessive fat. 1, 2

I'm Bloated!

This intra-abdominal fat is also likely to be the origin of abdominally "gifted" powerlifters claiming they are "bloated" all the time. These same individuals may actually have somewhat visible abs. However, if they were truly "bloated" they would look smooth and puffy. Please trust that I have no problem with fat powerlifters. I only have problems with those who make excuses about it. As a matter of fact, I simply do not care at all whether a lifter is overweight unless I myself am engaged in training them and I must optimize training and performance.

Subcutaneous belly fat will tend to look soft and will hang in folds over the belt. A big puffy belly that sticks out and feels firm is the result of a large amount of visceral fat. Obviously there will tend to be a mixture of both visceral and subcutaneous fat but the largest bellies have the highest amount of visceral fat and this tends to counter-act the folds of subcutaneous fat. To illustrate this to yourself notice how many overweight men have large fat folds in the pectoral region as compared to in the belly region. These individuals may not even have love handles. This clearly shows the different ways adipose tissue is deposited in different areas of the body.

Anthropometric Measures and Body Composition

There is a very good reason why the way fat is stored in different body areas is considered important and it is based on observations about abdominal fat. Individuals who have a predominance of abdominal visceral fat have been seen to exhibit many metabolic differences compared with those who have fat distributed subcutaneously over the lower extremities, such as the hip and thigh area. This led to examining disease risk by looking at these fat mass distributions. The waist-to-hip circumference ratio was the most commonly used measure.

According to the American Heart Association a waist-to-hip ratio of 0.96 in men and greater than 0.88 in women is considered to be an indicator of central obesity (also termed "android obesity"). The waist is measured at the narrowest point while standing in a relaxed position and avoiding sucking in the gut. The hip girth is measured at the widest point over the buttocks. This ratio correlates much better to abdominal fatness in men than in women because of men's increased tendency to store fat in the abdominal region. However, these measurements are very difficult to perform accurately and even a slight change in the area measured can produce significantly different results.5, 3

There are many problems with this approach, not the least of which is a lack of standardization of measurement technique and persons with different levels of training performing the measurements. It is not clear at all whether there is any real biological reason to suspect that the ratio of hip to waist should be a general indicator of risk factors. Abdominal measurement alone may be a better indicator of risk with advancing age due to the BMI's decreasing usefulness in this population.3 Intra-abdominal fat accumulation has been shown to be greater at any given BMI (or %BF) in older individuals.6

According to Willet, it could also be that hip and waist measurements should be considered as two independent factors in a multi-variate model that considered the impact of greater muscularity. In this way hip measurement could be seen as an indicator of muscularity and thus physical activity whereas abdominal measurement would be a more confident predictor of "fatness". For example, while abdominal fat could increase the risk of insulin sensitivity, gluteal mass could indicate a relatively large level of lean mass and this would decrease such risk. These factors and correlations differ across sexes and age brackets and the relationships are highly complex.3 For further discussion of the value of anthropometric measures for assessing body composition as well as a dietary assessment see Nutritional Epidemiology. For the lay person, however, it is prudent to expect a correlation between waist circumference alone, visceral fat, and health risk.

Subcutaneous belly fat is clearly distinguishable in appearance

Yes, It Applies to Strength Trainees

These correlations are not magically and mysteriously erased in a strength training population and there is not a special "squat and milk" program that can erase them. The appearance of a wide belly is much more likely to be an indicator of central obesity and a corresponding excess of caloric intake. The external appearance, over the muscles and under the skin is an indication of where that individual tends to store these calories.

The general rule of thumb is that if you cannot grab a hold of it with your hand or fingers..it's visceral fat rather than subcutaneous fat. In the buttock and thigh areas fat will tend to be subcutaneous but the origin of the beer belly, the "middle aged spread", or muffin top, is caused by this intra-abdominal visceral fat and this is termed "central obesity". This fat pushes the abdominal muscles outward into a tight position. Rather than the subcutaneous fat stored elsewhere on the body, central obesity is what puts one at risk for cardiovascular disease, diabetes, etc. This type of fat deposition should be considered high risk, resulting in complications such as insulin resistance, impaired lipid and glucose metabolism, hypertension, cardiac dysfunction, and sleep apnea disorder. 4 Many people mistakenly expect this type of abdominal fat to appear similar to fat in other parts of the body, such as having a cellulite appearance or showing pockets of fat cell storage. The skin of the abdomen is thicker than on other areas of the body so even subcutaneous fat will not appear as it does in the hips or thighs, and elsewhere.

It is quite common to observe a male with a large "beer belly" but with a clearly visible linea alba² and some will even display the slight appearance of a six pack. It is common to mistake visible abdominals with the absence of belly fat in general. These bellies may feel somewhat firm, but not as hard as well developed and well-visible abs. Remember that an excessive beer belly will not tend to be as "squishy" due to the stretching affect of the intra-abdominal fat.

The Infamous GH Gut and Circular Thinking

None of this should be confused with the infamous plague of modern bodybuilding: the so-called "GH Gut" or "roid gut."³ Some modern bodybuilders are displaying grossly distended abdomens but with highly developed and visible six packs over them. This is said to have nothing to do with belly fat but instead be caused by the use of Human Growth Hormone (HGH) and in particular IGF-I which is supposed to cause the lower intestine to grow in size, thus pushing it against the abdominal wall and causing this highly unnatural distended appearance. To my knowledge there has been no clinical investigation into this and it is unclear what is causing these swollen bellies in bodybuilders.

The reason I bring this up is because some (quite idiotically) have tried to blame "powerlifting movements" for these guts on professional bodybuilders. Basically, they are saying big lifts like squatting and deadlifting give you a distended gut. The reason they come to this conclusion is because they look at many of today's upper weight class powerlifters and see that they have…big guts. These powerlifters have big guts because they have a higher body fat proportion. But that hasn't stopped some individuals from making the ridiculous leap to "big lifts equal big gut". As most things in strength training and bodybuilding are circular, others borrow on this spurious logic to justify their belief that a portly appearance is correlated with a "stronger individual". So, not only do the big lifts give you a big belly, having a big belly is a powerlifting "credential". Conclusion: powerlifters should over-eat, eat big and lift big. Now, this, clearly, is not the 'critical thinking' I referred to at the beginning of this post. It is simply bro-science in a big circle-je…umm..goat rope.

I've mentioned this before in my post on breathing, ribcage expansion, and abdominal hollowing when I said:

"The stretched rib cage and hollowed abdomen is not so much a part of modern bodybuilding. Bodybuilding has gone to the extreme opposite and much has been made of the distended abdomens that many professionals display. And many think that these huge protruding abdomens are caused by a lack of abdominal vacuum exercises and thus a weak transverse abdominis. It is true that a weak TA can be a contributor to a "poofy" gut, but in the absence of fat I doubt very much it's the sole cause of these unnatural looking midsections." - Troy8

Weak and Stretched Abdominal Walls? Sheesh…

I should also mention that many like to blame powerlifters' big guts on high intra-abdominal pressure from frequent heavy lifting. They say this results in stretching of the abdominal wall. This stretching is also thought to weaken the abdominal wall, thus, conveniently, resulting in hernias which cause further distension. Although I'm sure Paul Chek would love this idea it is simply an indication of how far some people will go to continue gorging themselves on food. Why should I say I am fat when I can say I am bloated, or my belly is stretched due to all the hardcore lifting I do? If it quacks like a duck…you get the picture. It's belly fat. As for hernias, they stem from a congenital weakness in one area of the abdominal wall where an opening exists or where an opening was supposed to close and failed to do so, such as the umbilical. While heavy lifting may exacerbate certain hernias, it doesn't cause them.

Stubborn Fat and Belly Fat

It just so happens that this visceral abdominal fat is highly receptive to diet and physical activity. Especially exercise. I am not suggesting that one should control body fat through diet alone and some data suggests that this is one reason why. Visceral fat, more prominent in men, seems more correlated to physical activity than subcutaneous fat. But diet should still be considered the key to maintaining healthy weight. While there is some decidedly preliminary "data" suggesting that those who control body fat through diet alone may be prone to having visceral fat, those who are obese will tend to have more.

I have mentioned before, however, when I explained how strength training was not the key to fat loss that exercise may be of particular importance for controlling visceral fat accumulation. This certainly seems to be a key. And strength training, given all it's parameters, fits this bill.

However, the relative ease (for so-called hardgainers) with which fat can be accumulated and then controlled, at first, leads many strength trainees to adopt the "bulk and cut" methods of geared bodybuilders. Some few individuals find some immediate success as they are able to quickly progress in strength and body weight while storing a good proportion of the fat in the belly. They are then able to lose this fat fairly easily with some dietary control and changes in activity level and are left with not too much subcutaneous fat on their hands. This will not work forever though and even these lucky few will find that the body responds to this constant yo-yo in undesirable ways, including a slow but sure deposition of subcutaneous fat that will not be so amendable to a simple decrease in caloric intake. It is this subcutaneous belly fat that is the "stubborn fat".

So Eating Too Much Makes Me Fat and Strong?

Even, so most trainees will utterly fail with this approach and will simply find themselves getting fat in general. The large caloric surplus, depending on macro-nutrient proportions and their own sensitivities will likely make them feel like crap and have the gastrointestinal discomfort (and swelling!) to show for it. This should be somewhat intuitive. If you suddenly start purposely gorging yourself you're going to feel sick and, yes, bloated. But this is just what many strength trainees are being told to do! Recommendations of 5000 to 6000 calories a day, across the board, are not uncommon. Despite the misconception about huge "powerlifters" only a few large framed individuals will ever need these amounts. These amounts are much more appropriate to endurance athletes.

I have shown some of the reasons and silly justifications used for these recommendations but many will see through these ridiculous claims. So, further claims are made as to the validity of "eating big to lift big". Remember, eating big means eating great excess. Clearly rigorous strength training requires rigorous attention to adequate diet and caloric intake. The emphasis here is on the excessive nature of the recommendations. The excess, then, is said to simply make it "easier" to gain strength. Similar to the claims of excess protein, excess food calories in general, together with fat storage, is said to result in greater strength and muscle gains in a shorter period. While adequate nutritional intake, based on ones individual needs will certainly make it easier "excess" calories will simply make you fat. More fat makes it harder to gain muscle, not easier.

Fat Has Mechanical Properties? Check Your BS Meter

Then we have another little strength myth. Now, there is absolutely NO correlation between fat storage and physical strength. How could there be? Fat is not functional in human movement. Yet, that has not stopped some, in the past, from claiming it to be! I touched on this in the GUS "Strength Training Versus Bodybuilding" eBook when I discussed the idea that being "fat and swole" in the off-season allows bodybuilders to lift more weight and thus be bigger after trimming down. The weight gain is postulated to, quite magically, improve leverage around the joints, these ideas were then extended from bodybuilding to powerlifting:

"Improved leverage around the joints by bigger muscles is probably related to an idea called “tissue leverage” which is a bodybuilding idea that attempts to explain why “getting fat and swole” during the off-season will allow a bodybuilder to lift more weight thus being bigger when he trims down again. Apparently it doesn’t matter whether the “bigness” is due to fat deposition, water retention, or actual functional tissue." (Troy 7)

If you were to read about "tissue leverage" alone you should darn well find your BS meter peaking! Now, should you really need to look for justification in "fitness studies" to say this is bullshit? NO! If you cannot already recognize this as bullshit then you are far from the need for Pubmed. You need some foundation in biomechanics, kinesiology, and physiology. So, instead of spending your hard earned money on a "how to read fitness studies" package, spend it on some basic foundational texts.

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GUS Member Comments

by EricT

Apparently there is a debate about whether training to failure is better than doing one single set of exercise. Well, okay, no there is not really a debate about this but sometimes those who do a lot of "research" about resistance training while simultaneously not having a clue about resistance training think that these kinds of debates exist. The actual debate is about multiple versus single sets to failure. That is a bit different than training to failure versus training with single sets, is it not?

Those who advocate for single set training say that training to failure over one set maximally recruits the muscle motor units and thus should be all that is needed to realize continual gains in muscular strength. Others say that just recruiting enough motor units is not going to do it, we need enough stimulus and a certain amount of exhaustion to get strong. Well, I think that is what they say; the truth is I don't listen very closely. I'm too busy getting busy with strength training to worry about academic debates like that one. And the reason I say it's academic is because there is nothing which is not useful at some point and time, given the proper circumstances!

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I read this interesting article That misses this point completely. It is about training to "task failure" over multiple sets versus using single set training. Or at least I think that is what the article is about. It's hard to be sure. When you see a heading named "Optimum Strength Training Protocol" you CAN be sure, however, that you've entered the Twilight Zone of strength training..

Here is how it goes. When we do multiple reps of an exercise to the point where we can no longer perform another rep immediately we are working to "task failure". If we end up doing 10 reps then we performed a "10RM - 10 rep maximum". We have worked to momentary muscular exhaustion which means that as the set goes on we have recruited more and more motor units in order to maintain the same force output. Thus we have "maximally recruited" the muscle units. This has been considered an important component in progressive training for muscular strength. But let's back up a bit before I get to the point of this post.

Training to Failure is not Just ONE Thing

I explained about rep maximums and training to failure in the article "Training to Fail Part 3: The Failure of Intensity Cycling" under the heading Failure Modes.

Training to task failure as this article in question discusses means that we are training to the point where another rep cannot be completed with good form. We can also train to momentary muscular failure which is when we cannot complete the final rep we attempt. Or, we can training to post failure which means we "force" another rep in some way, either after a brief pause or with assistance or a cheating movement. DC training is an example of post failure training (really post post failure training). All of this is training to failure but it is clearly not all the same thing.

Although all of these modes of failure should not be treated as equal, especially post failure training, they can all be useful some of the time. Especially in the area of muscular endurance.

Explosive Strength Training?

Interestingly the article is entitled "Explosive Strength Training" and yet is about the development of maximum strength. How odd. It ignores the fact that training for "explosiveness" or rate of force development requires sub-maximal loads and that training for maximal strength requires near maximal loads. The language here is a symptom of a bigger problem that I have mentioned in many of my previous posts. Much of the terms and jargon we take for granted has no real consistent meaning. The term "explosive" is thrown about with abandonment in scientific studies and lay articles, many of which are about completely different subjects.

Training for 'explosiveness' to many, is training for high rate of force development. And specifically, exerting the greatest force possible at the very beginning of a movement, say up to the first 200 to 400 ms at the most.

Training for rate of force development and for maximal strength are two different things. They intersect and interact in many training programs but they are not the same goal. What has happened here is one of the false dilemmas I hinted about in the title. The term "explosive" itself is a bit of jargon that is not very useful for actual scientific inquiry because it does not have a specific definition. Yet this term is used often in studies. This should not be surprising, since the word "power" is used inconsistently as well even though it has a very precise biomechanical definition.

The article discusses some research regarding "slow" versus "fast" resistance training. One group performed 4 sets of exercise using a 6RM. The other group performed 4 sets of 4 reps presumably also using a 6RM..so in other words not to failure like the first group. Now get this, its the important part: The first group used a "controlled" cadence and was asked to make sure that the concentric lasted two seconds. The second group was asked to complete the reps as quickly as possible: "explosively". They found similar strength gains. Leading them to get very excited about the idea that the second group did less work but got the same results.

It's all very exciting and everything. Albeit hardly front page news. The "false dilemma" is that there are only two choices "slow" and "fast". Depending on the movement 2 seconds can be a very long time to complete a rep (concentric). Not even considering the "controlled eccentric". And since they were told to purposely slow the movement down we can assume that 2 seconds was slow. Let me clear this up. Nobody does this in STRENGTH TRAINING. At least nobody with a clue. Why slow or fast? Why were the sets to failure done slow? What does going slow, using a RM versus lifting with as much explosiveness as possible have to do with anything? What if both groups lifted explosively but one went to failure and one did not? Would the explosive effort combined with MORE WORK have meant better gains in the first group?

We also lift with the intention of moving the weight as explosively as possible. Now, if this actually results in the weight moving very fast we are not using maximal load. The word "fast" used by the researchers is unfortunate, therefore. How fast were the movements? Only fast compared to the first group? OR actually very fast. Because if they were actually very fast they could have gotten BETTER results with heavier relative loads lifted with the intention of moving the weight as quickly as possible. Ignoring the force velocity relationship of skeletal muscles is like building a bridge out of plastic because it's cheaper than steel. That is, you cannot ignore the intrinsic mechanical properties of the "material" you are working with, regardless of what you would wish to have happen.

Let me put this in perspective. When someone goes to test a new pharmaceutical that is supposed to have X affect in the body, such as relieving pain, ideally, they already have a plausible physiological mechanism to explain why and how this drug exerts this affect. No one likes to randomly test chemicals for pain relief without at least a hint that it has the potential to do what you are testing it for. Biochemical studies performed outside the body BEFORE clinical testing are much more efficient. If you cannot find a biochemical affect, you aren't going to bother doing a clinical trial. Yet, with studies involving human strength development it is often like the researchers are just throwing darts at a board. Let's just see what happens when the subjects do this or that and let's ignore what we already have surmised about muscle physiology in general.

When they are not just throwing darts at a board they are wasting a lot of precious time investigating fads or trends in strength training, such as SuperSlow training.

What does SuperSlow Training have to do with Training to Failure versus One Set

So, I was discussing the article. It starts out with the idea that there is conflicting evidence concerning the use of multiple (2 or 3) sets to failure versus using only single sets of exercise. Remember I hinted above that the difference between the two is the idea that we do or do not need a certain amount of exhaustion. Even if you performed your single set to failure you would be more "exhausted" if you did multiple sets to failure.

Yet the article in question, after bringing this up, completely abandons it and goes on to talk about research involving multiple sets of exercise and comparing relative levels of exhaustion. This is the "non sequitor" I referred to in the title and it is the kind of thing that is prevalent in the strength training world. It seems like a "train of thought" is hard to maintain when it comes to resistance training. This is where the author gets into seriously muddy waters:

"Repetitions can be performed quickly or slowly and both methods have been used across research in the area."

Repetitions can of course be performed with the "intention" of moving slowly or quickly but they cannot use the same relative loads if they actually move quickly versus moving slowly. The more people talk about such "research" the harder it is for me to explain the basic tenants of force production. Beginning trainees are asking whether they should bench press slow or fast yet have never been told that you CANNOT move a maximal weight QUICKLY. Let me repeat this. If the weight moves very quickly it ain't maximal. Moving the weight intentionally very slowly means much the same thing. It takes more muscular tension and the relative load must be reduced.

Are you getting what I am saying here? If the wrong questions are being asked which are questions which ignore the basic properties of the musculoskeletal system, then any research done to answer the questions is meaningless. The question is moot! Therefore the research is moot!

As mentioned above, if we were to investigate a medication, normally, we would already have an idea about how this medicine would physiologically exert it's effect. We wouldn't just shoot in the dark. Well, we have knowledge of the physiological adaptations the body makes and we have knowledge of the mechanical properties of muscle - both intrinsic and neuro-mechanical. We have knowledge of the biomechanics of movement. Etc. and so on. Much of the research regarding strength training routinely ignores this foundational knowledge. It has been said many times before that the those who engage in strength training research may do well to speak to those who spend their lives applying the strength training.

This is why you hear "iron veterans" say things like "just lift the damn weights". Sure they are being unhelpful and over-simplistic but they are expressing a sort of intuitive insight which tells them that many of the questions that are being asked are the wrong questions and have very little to do, in the big picture, with getting strong. "Should I lift fast or slow?" is certainly one of those.

Why are these questions asked and articles like the one I am talking about here written? You know why. The word is "optimal". The idea that there is a better or best way to train for everybody is what drives the engine of "strength training" today. This is not like searching for a needle in a haystack. It is like searching a haystack for no good reason at all! There is not, and never will be a best or most optimal way to train at all times for all people. I would sincerely like to be able to say that there was. And that I'd found it and that you can get it here, come one come all. But to do that I'd have to be a sleazy and dishonest strength training marketer¹ rather than a simple and honest strength training writer. And I'd rather sleep at night than do that.

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Comments

by EricT

By Roger B. McDonald and Rodney C. Ruhe

Department of Nutrition, University of California, One Shields Ave, Davis, CA 95616, USA
Nutrients 2010

Life expectancies after the age of 70 and the number of individuals living with age-related chronic conditions that affect daily activities continue to increase. Age-specific nutritional recommendations may help to decrease the incidence or severity of age-related debilitating chronic disorders. However, research in this area has seen limited success in identifying nutrition-related mechanisms that underlie the functional loss and chronic conditions that occur as a function of time. We believe that the limited success in establishing age-specific nutrition recommendations for the older population reflects, at least in part, research designs that fail to consider the evolutionary and biological bases of aging and longevity. Longevity has evolved as a by-product of genes selected for their contribution in helping the organism survive to the age of reproduction. As such, the principle of genetic determinism provides an appropriate underlying theory for research designs evaluating nutritional factors involved with life span. Aging is not a product of evolution and reflects stochastic and/or random events that most likely begin during the early, reproductively-active years. The genetic determinism model by which young (normal, control) are compared to old (abnormal, experimental) groups will not be effective in identifying underlying mechanisms and nutritional factors that impact aging. The purpose of this commentary is to briefly discuss the difference between aging and longevity and why knowing the difference is important to nutrition research and to establishing the most precise nutritional recommendations possible for the older population.

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More Aging and Longevity Articles

Introduction

Life expectancies after the age of 70 and especially after the age of 85 have yet to reach a plateau. While life expectancy after the age of 70 continues to increase, so too do the number of individuals living with age-related chronic conditions that affect daily activities. Many believe that age-specific nutritional recommendations for the older population may help to decrease the incidence or severity of debilitating, non-disease disorders that occur with increasing age. However, research in this area has seen limited success in identifying nutrition-related mechanisms that underlie the functional loss and chronic conditions that occur as a function of time.

We suggest that lack of success in establishing age-specific nutritional recommendations for the older population reflects, at least in part, research designs that do not consider the biological differences between aging and longevity. Failure to consider these differences may also lead to difficulty in precisely defining aging or longevity, a prerequisite to efficient experimental designs. Distinguishing human biological aging from longevity can be difficult due to the fact that the rate of aging may affect the length of the life span. Moreover, the lack of predation, control of childhood diseases, and effective therapies for life-threatening disease have extended the human post-reproductive life span, making the distinction between aging and longevity even more difficult. Nonetheless, such a distinction will be necessary to develop the most effective research designs evaluating the mechanisms that underlie the impact of nutrition on aging or longevity. Although we acknowledge that there are many valid definitions for aging, we suggest that biological aging be defined as the progressive, event-dependent decline in the ability to maintain biochemical/physiological function. Longevity is the length of the life span independent of the biological aging process. This brief commentary will provide justification for these two definitions.

The ability to define aging and longevity separately has become possible only in recent years. Biogerontological research conducted during the last two decades has, to a large degree, solved the
evolutionary problem of longevity and aging. Evolutionary theorists have mathematically and empirically demonstrated that longevity is genetically determined from genes that are selected for a reproductive advantage [1,2]. As such, the principle of genetic determinism provides an appropriate underlying theory for research designs evaluating nutritional factors involved with life span. Investigations evaluating possible gene-nutrient interaction should prove valuable in the search for nutrients that affect longevity. On the other hand, aging is not a product of selective evolution. The aging process more closely reflects chance events that affect biological systems during development or during the early reproductively-active years [3]. The genetic determinism model by which young (normal, control) are compared to old (abnormal, experimental) groups will not be effective in identifying mechanisms by which nutritional factors affect aging. Aging will be best understood by evaluating biological systems during development that are most susceptible to time- or event-dependent alteration leading to functional loss and chronic conditions in old age.

Why should a nutrition researcher know the difference between aging and longevity? In the next decade and a half in economically-developed countries, the population of individuals who will be over the age of 70 years will rise from the current 13% to almost 20%. In the United States that percent increase represents an additional 35 million people. Given the disproportionate amount of health care dollars spent on this population, much of which is covered by entitlement programs, we must do all we can to insure a healthy aging population—anything less could be economically catastrophic. Dietary recommendations are a significant part of the overall strategy for improving the health of the aged population.

In an effort to improve the health of older Americans through dietary recommendations, the Committee on the Dietary Reference Intakes (CDRI) has added two age classifications, 51–70 and 70+. However, after 12 years of having these new age classifications, recommendations in the 51–70 and 70+ age groups do not, in general, differ significantly from younger adult age groups [4]. The CDRI attributes the lack of age-specific recommendations to insufficient research. While more research will be necessary, the inability to establish age-specific recommendations also reflects results from research designs that have based their hypotheses on outdated theory. We believe that precise and sustainable recommendations for the older population will come from research designs that consider the most up-to-date findings from biogerontology, including the related but distinct biological processes of aging and longevity [5–7]. Knowing the difference between aging and longevity will be fundamental to developing the strongest designs for nutrition research aimed at establishing recommendations and improving the health of the older population.

In this commentary, we discuss the difference between aging and longevity and why knowing this difference is important to nutrition research. To this end, a brief review will be presented of evolutionary and genetic findings showing that aging lacks genetic determinism whereas longevity evolved. Through this scientific evidence we will show why knowing the difference between aging and longevity is critically important to designing appropriate nutrition research that can be used for nutritional recommendations in the elderly population. A brief discussion will follow as to why establishing nutritional recommendations for the older population will be best achieved by first evaluating genetic/metabolic pathways in young populations that are most susceptible to the chance events leading to age-related functional loss. The interaction between aging and disease will not be covered here. Previous reviews have described thoroughly the differences between aging and disease and the reasons why using disease as a research model for aging may not be tenable [5,6].

Imprecise Terminology: Aging vs. Longevity

In 1952, Sir Peter Medawar delivered a lecture at the University of London focusing on the evolutionary problem of aging entitled .The Unsolved Problem of Biology. [8]. He argued that natural selection could not have worked to fix genes causing the loss in physiological function that begins as reproductive success declines. Medawar reasoned that the extrinsic hazards of the environment present throughout evolutionary history would result in an age distribution that favored a young, reproductively-active population. The younger population would have had greater fitness simply because there were more of them than the population of reproductively-active older individuals. The high rate of reproduction (fitness) in young vs. old age groups would result in traits important for survival to reproduction age being selected over alleles expressing proteins that insure the maintenance of physiological function well past reproduction age. Aging could not have evolved through natural selection.

Medawar’s suggestion that aging did not arise from natural selection came at a time when genetic determinism through natural section was universally accepted as the only explanation for evolution. Therefore, a hypothesis that could explain, in term of genetic determinism, how alleles giving rise to aging could be selected in the absence of natural selection was needed. To this end, Medawar turned to genetic drift, a population genetics theory predicting that alleles in small populations can be fixed in the general population’s genome as a matter of chance. Medawar was building on the ideas of Haldane [9] that a small population of late-life reproducers carried genes conveying the aging phenotype. This small population could contribute to the establishment of an aging phenotype because nonlethal but physiologically detrimental genes expressed only in late life could arise in a population because they would not have had any effect on reproduction. Natural selection would have selected neither for nor against these genes. Medawar named his evolutionary aging theory mutation accumulation.

Medawar’s verbal postulations on aging provided the foundation for scores of researchers investigating the evolutionary, genetic, and biological basis of aging and longevity. However, his theory on aging contained a significant flaw that has been perpetuated in research designs for over 50 years. That is, he used the terms aging and longevity interchangeably even though his theoretical models focused exclusively on longevity. Medawar’s model for aging/longevity did not consider the possibility that life span and the functional loss characterizing aging could have arisen through different evolutionary/biological processes. Subsequent work found that longevity and aging are distinct biological events.

The differences between aging and longevity became clearer with the mathematical descriptions by W.D. Hamilton [1] and later by B. Charlesworth [10]. Hamilton’s mathematics agreed with Medawar’s verbal speculation that genes did indeed affect events leading to either aging and/or longevity. However, these genes were not the type that Medawar had suggested, i.e., fixed by genetic drift and specific to the aging phenotype. Rather, Hamilton’s mathematical model predicted that longevity was determined by genes selected for reproductive success and not by genes that were expressed only late in life. His model showed that the force of natural selection on mortality was highest before the start of the reproduction phase and declined thereafter (Figure 1). Because the force of mortality was highest prior to reproduction, evolution would have worked to select genes that were necessary for combating mortality in early life, i.e., surviving to reproduction age. Mortality (life span), therefore, must be related to genes selected for survival to reproduction age. Hamilton provided the first mathematically implicit evidence that life span (longevity) had evolved and was directly related to genes that optimized survival to the age of reproduction. Importantly, his model was specific to longevity and did not include variables of age-related functional loss.

Hamilton’s mathematical theory on longevity was a monumental breakthrough in the understanding of how life span, not aging, evolved. Based on his mathematical models, several laboratories using artificial selection methods to approximate evolution have supported Hamilton’s theories on the evolution of longevity [11–13]. Populations of Drosophila selected in the laboratory for their timing of reproduction showed that late-life reproducers do indeed live significantly longer than flies having their highest rate of reproduction early in the life span (Figure 2). Genetic studies in yeast, C. elegans, and Drosophila have also shown that genes affecting life span have been selected first and foremost for their role in enhancing survival to reproduction age (see review [14]).

Figure 1. Hamilton’s calculation on the force of natural selection on mortality (s(x)) and fecundity (s’(x)). Data used are from life-tables of the United States between 2000 and 2004 (Adapted from [2]).

Figure 2. Life span of female Drosophila artificially selected for early and late life reproduction (Adapted with permission from John Wiley & Sons [12]).

Mathematical models and empirical experimentation have unequivocally established that longevity evolved from genes selected for their impact on survival to the age of reproduction. Because these investigations did not include measures of age-related degeneration, conclusions as to the genetic basis of aging cannot be made. Nonetheless, hundreds if not thousands of publications exist describing research that either directly or indirectly implicate specific genes as being involved in age-related degeneration. Not one gene has been identified that causes osteoarthritis, presbyopia, sarcopenia, or any other of the hundreds of age-related degenerative and chronic disorders observed in the aged population. The reason for this is simple-these genes do not exist.

The Disposable Nature of the Soma and the Cause of Aging

Aging arose serendipitously in evolutionary history as a result of a trade-off between the germ line and somatic cells in the distribution of resources. This trade-off has been developed into a formal
theory by Thomas Kirkwood and is known as the Disposable Soma Theory of Aging [15]. The foundation of this theory lies directly in a basic principle of natural selection, i.e., all environments have finite resources and individuals compete for these resources. Organisms that use the finite resources most efficiently will be the ones to successfully survive to reproduction age. The Disposable Soma Theory posits that the most efficient use of resources in multicellular organisms is to give highest priority to the cells that are responsible for the continuation of the species, i.e., the cells of reproduction, or the germ line. Supporting cells, those of the soma, would only need enough resources to accomplish their primary task of supporting the germ line. That is, the soma could be disposed of once reproduction had occurred.

But, where and how were those resources being spent? The Disposable Soma Theory predicts that that the distribution of resources by the early metazoans was preferentially diverted to repair mechanisms of the DNA in the germ line. This suggestion is consistent with the observation that the energetic cost for maintaining DNA fidelity is rather high. If, because of finite resources, an organism had to make an evolutionary choice between accuracy in the DNA of the germ cell or repair of a somatic cell, the germ cell would be chosen so as to provide the best chance of survival for the next generation. The immortality of the germ line has come at the cost of somatic mortality.

Chance, Aging, and Nutritional Recommendation

The evidence presented thus far leads to the conclusion that aging is a random and/or stochastic phenomenon. A substantial literature exists describing that the primary mechanism associated with the random nature of aging is entropy, a property of the Second Law of Thermodynamics (see reviews [5–7]). Briefly, biological systems defend themselves against the unceasing disorder of entropy by continuously restoring the free energy lost to chemical reactions that maintain molecular fidelity (structure, function). At its very basic level, survival to reproduction age simply reflects the selection of genes that maintain free energy states conducive to life. However, there is no reproductive advantage for an individual to sustain molecular fidelity after the age of reproduction. Genes would not have been selected for the purpose of maintaining the high cost of combating entropy throughout the life span. The age-related decline in physiological function reflects a gradual loss in the ability to defend against the Second Law of Thermodynamics, i.e., entropy. Importantly, the age-related loss in the ability to defend against entropy manifests purely as random events with respect to the physiological systems affected.

The random nature of aging suggests that chance plays a significant part in determining the physiological system or systems that experience declining function in the older population. The role of chance as a factor in the aging process has been reviewed in detail [3]. Chance precludes genetic determinism and introduces an element of uncertainty that cannot be controlled easily in population-based research, the type of research commonly used as the basis for establishing nutritional recommendations. The CDRI recognizes the problem of random variation in the aging population when stating that research investigating dietary recommendations for the older population is confounded by increased error (random variation) in the data [4]. Moreover, the error becomes greater with advancing age, suggesting that nutritional recommendations based on the current scientific rationale, i.e., genetic determinism, are even less accurate for the oldest age groups.

Chance also raises the possibility that every sample population will be unique and that no sample population can be relied upon to provide meaningful predictive results for the entire aged population. Take for example the results from studies investigating the value of nutritional antioxidants as modulators of aging. Nutritional antioxidants prevent damage to the cell in vitro and the accumulation of cellular damage has found wide acceptance as a proximal cause of organism aging. The epidemiological data suggest that the rate of aging and age-related disease may decrease in populations consuming foods high in antioxidants [16,17]. Consistent with the epidemiological data, small sample size cross-sectional supplementation investigations tend to find positive outcomes between experimental (supplemented) and control (non-supplemented). However, several large randomized clinical trials have failed to demonstrate the benefit of antioxidant supplements in the aging population (see review [18]). That is, the small cross-sectional studies have not been reliable indicators of the usefulness of antioxidant nutrition in the general older population.

The dominant role of chance in the aging process (but not longevity) leads to the inevitable conclusion that the fundamental process of biological aging cannot be modulated through interventions during old age. The nutrition researcher may find this statement difficult to accept given the overwhelming successes that nutrition interventions had on infant and childhood health. The reason that nutrition interventions improved the health of infants and children was that nutrients had targets to interact with, i.e., genes selected for survival to reproduction age. Since aging did not arise through selective evolution, nutrients may or may not alter expression of genes in the older population. Recommendations for the older population arrived at by using genetic determinism will be unreliable—without genetic determinism, it is a matter of chance.

If modulating aging by nutritional intervention during old age will not produce the desired results, how then will nutrition intervention be effective in improving the health of the older population? We suggest that the research approach should focus on possible variation in function among individuals in younger age groups that may predispose them to differential rates of functional decline during advancing age. We must focus our attention on the time in the life span in which genetic determinism has the greatest influence on random aging outcomes, i.e., the development, juvenile, and reproductively-active periods. Only after gaining a clear understanding of how chance and randomness shape the genetic pathways in younger populations that, in turn, affect the outcomes in the older population, should nutrition recommendations be considered.

Refocusing nutrition and aging research to be consistent with the current understanding of the cause
of aging may not be as difficult as it first may appear. While a personal genomic approach will ultimately be required in humans, several investigative models exist that may prove useful. The Fetal Origins Hypothesis (a.k.a Fetal Basis of Adult Disease) suggests that some diseases have their bases in utero [19]. Most research in this area has focused on the relationship between fetal/maternal nutrition and adult-onset obesity. These investigations suggest that undernutrition in utero leads to higher incidences of adult-onset obesity, hypertension, cardiovascular disease, and type II diabetes [20]. Recently, a link between Parkinson’s and Alzheimer’s Disease and a toxic gestational environment during neurodevelopment has begun to emerge [21]. For example, the amyloidogenic proteins A. and A. precursor as well as BACE1 (the A. cleavage enzyme) are elevated in non-human primates exposed to lead during infancy [22]. Although the current focus of research linking the developmental environment with aging remains on age-related disease, it would not be surprising to find that the rate of aging and the trajectory in the age-related loss of soma maintenance, independent of overt disease, may also have fetal origins.

The age-related alterations to the vascular system and the development of certain types of cancer have been used extensively as models of the aging phenotype. A substantial literature exists describing how dietary habits during childhood may induce dysfunction of various systems during aging. Some recent publications provide additional examples of specific research areas that should be given consideration [3,5,6] in this regard.

Conclusions

Evolutionary and genetic research has clearly established that longevity has evolved whereas aging is a random/stochastic process driven primarily by chance events occurring during development and the reproductive years. Knowing the difference between aging and longevity will determine, in part, the scientific approach to research questions aimed at evaluating the impact that nutrition may have on the aging population. If the primary purpose of the research is to determine the factors involved with longevity, then focusing on altering the expression of specific genes by specific nutrients will be appropriate. If, however, the aim of the research is to evaluate how nutritional interventions can modulate the aging process and improve the health of the older population, then the genetic determinism model will be inappropriate. Research designs that focus on chance events in young populations that lead to altered states of aging will be the more powerful. Effective nutritional recommendations for the aged population will most likely be ones that focus on dietary changes in the younger populations.

Acknowledgements

The author wishes to acknowledge Jon Ramsey for his critical review of the manuscript, and Jennifer Ruhe for her technical assistance.

References

1. Hamilton, W.D. The moulding of senescence by natural selection. J. Theor. Biol. 1966, 12, 12–45.

2. Rose, M.R.; Burke, M.K.; Shahrestani, P.; Mueller, L.D. Evolution of ageing since Darwin. J. Genet. 2008, 87, 363–371.

3. Finch, C.E.; Kirkwood, T.B. Chance, Development, and Aging; Oxford University Press: New York, NY, USA, 2000.

4. Otten, J.J.; Hellwig, J.P.; Meyer, L.D. DRI, Dietary Reference Intakes: Essential Guide to Nutrient Requirments; Academies Press: Washington DC, USA, 2006.

5. Hayflick, L. Entropy explains aging, genetic determinism explains longevity, and undefined terminology explains misunderstanding both. PLoS Genet. 2007, 3, e220.

6. Hayflick, L. Biological aging is no longer an unsolved problem. Ann. N. Y. Acad. Sci. 2007, 1100, 1–13.

7. Lithgow, G.J. Why aging isn’t regulated: A lamentation on the use of language in aging literature. Exp. Gerontol. 2006, 41, 890–893.

8. Medawar, P.B. An Unsolved Problem of Biology; H.K. Lewis and Company: London, UK, 1952.

9. Haldane, J.B.S. New Paths in Genetics; Harper and Brothers: London, UK, 1942.

10. Charlesworth, B. Selection in populations with overlapping generations. I. The use of Malthusian parameters in population genetics. Theor. Popul. Biol. 1970, 1, 352–370.

11. Luckinbill, L.S.; Arking, R.; Clare, M.J.; Cirocco, W.C.; Buck, S.A. Selection for delayed senescence in Drosophlia melanogaster. Evolution 1984, 38, 996–1003.

12. Rose, M.R. Laboratory evolution of postponed senescence in Drosophila melanogaster. Evolution 1984, 38, 1004–1010.

13. Stearns, S.C.; Ackermann, M.; Doebeli, M.; Kaiser, M. Experimental evolution of aging, growth, and reproduction in fruitflies. Proc. Natl. Acad. Sci. USA 2000, 97, 3309–3313.

14. Kenyon, C. The plasticity of aging: Insights from long-lived mutants. Cell 2005, 120, 449–460.

15. Kirkwood, T.B.; Holliday, R. The evolution of ageing and longevity. Proc. R. Soc. Lond. B Biol. Sci. 1979, 205, 531–546.

16. Hirvonen, T.; Virtamo, J.; Korhonen, P.; Albanes, D.; Pietinen, P. Intake of flavonoids, carotenoids, vitamins C and E, and risk of stroke in male smokers. Stroke 2000, 31, 2301–2306.

17. Hung, H.C.; Joshipura, K.J.; Jiang, R.; Hu, F.B.; Hunter, D.; Smith-Warner, S.A.; Colditz, G.A.; Rosner, B.; Spiegelman, D.; Willett, W.C. Fruit and vegetable intake and risk of major chronic
disease. J. Natl. Cancer Inst. 2004, 96, 1577–1584.

18. Thomas, D.R. Vitamins in aging, health, and longevity. Clin. Interv. Aging 2006, 1, 81–91.

19. Barker, D.J.P.; Eriksson, J.G.; Forsen, T.; Osmond, C. Fetal origins of adult disease: Strength of
effects and biological basis. Int. J. Epidemiol. 2002, 31, 1235–1239.

20. McMillen, I.C.; Robinson, J.S. Developmental origins of the metabolic syndrome: Prediction, plasticity, and programming. Physiol. Rev. 2005, 85, 571–633.

21. Barlow, B.K.; Cory-Slechta, D.A.; Richfield, E.K.; Thiruchelvam, M. The gestational environment and Parkinson’s disease: Evidence for neurodevelopmental origins of a neurodegenerative disorder. Reprod. Toxicol. 2007, 23, 457–470.

22. Wu, J.; Basha, M.R.; Brock, B.; Cox, D.P.; Cardozo-Pelaez, F.; McPherson, C.A.; Harry, J.; Rice, D.C.; Maloney, B.; Chen, D.; Lahiri, D.K.; Zawia, N.H. Alzheimer’s disease (AD)-like pathology in aged monkeys after infantile exposure to environmental metal lead (Pb): Evidence for a developmental origin and environmental link for AD. J. Neurosci. 2008, 28, 3–9.

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