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Please note: The purpose of this entry is to provide simple explanations and should by no means be considered comprehensive or above reproach. These topics are much more complicated than many trainers maintain, so while this may seem highly technical to some, it is in fact, highly basic.
The Myotatic Reflex
The stretch reflex, or myotatic reflex is a neural mechanism that responds to changes in muscle length (stretching) by attempting to resist that the change in length. The changes in length are detected by proprioceptors called muscle spindles. Changes in muscle tension are detected by another important proprioceptor, the Golgi tendon organ (note: there may be other processes at work).
Myotatic reflex is part of a feeback system of proprioception that is highly important for a sense of body position and for posture maintenance and motor control.
For instance, if one stands for long periods of time and the extensor muscles maintaining position relax and thus lengthen, causing the body to lean to one side or other, the muscle spindles cause the muscles to contract and thus return the body back to correct positioning without conscious involvement.
The joints of the body have two opposing sets of muscles, extensors and flexors. The myotatic reflex, together with reciprocal inhibition, allows these muscles to work in synchrony, as opposed to against each other.
The myotatic reflex is initiated by receptors in muscles called muscle spindles which convey information to the spine used to trigger the response.
Muscle spindles are fusiform structures scattered widely throughout though the muscle body (but not everywhere). They are attached to the tendon, the endomysium, or the perimysium in parallel with the extrafusal fibers (regular fibers outside the spindle).
These spindles contain two types of intrafusal (within the fusiform spindle) fibers: nuclear bag fibers and nuclear chain fibers. Nuclear bag fibers are also divided into dynamic and static fibers.
Dynamic nuclear bag fibers are highly sensitive to the rate or change or velocity of the change in muscle length. Static nuclear bag fibers and nuclear chain fibers are more sensitive to static or steady state muscle length change.
When you stretch a muscle there is an initial stretch reflex which is quick and strong. The strength of this reflex depends upon the rate of change. This is the dynamic component. There is a second, weaker but longer acting, static component which responds to the new length. The static component persists as the new length is held. The static fibers respond to the new length in a sustained, tonic fashion and the discharge of both static fiber types is continued for as long as the new length is held.
One misconception of the stretch reflex is that the muscle spindles are only active when stretching or otherwise stimulating a muscles. In fact the job of the spindles is to signal muscle length continuously as part of the proprieceptive system. Both primary and secondary fiber types discharge tonically when the muscle is at it’s resting length and increase their rate of discharge when there is a change in length. The muscle spindles themselves, due to their short lengths, size, and other factors, do not generate any appreciable muscle tension.
Autogenic Inhibition
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The Golgi tendon organs are proprioceptors which, instead of monitoring change in muscle length, monitor change in muscle tension. There is an active and passive component here as well, with the threshold for tension developed through stretch relatively lower than that of active contraction. Previously it was thought that the golgi tendon organs only reacted to extreme changes in tension and were simply a protective device. But it is now known that the receptors are simply more insensitive to passive tension but extremely sensitive to active tension. The gogi tendon organs initiate autogenic inhibition in the stretched muscle.
The misunderstandings about the stretch reflex are based on this. Different muscles can have different tonus. Some muscles may be hypertonic and show a marked increase in reaction to stretch. Whereas some muscles may be flaccid and have a muted response. It is important to note that “normal” tone in a muscle is a very ill-defined concept. All muscles in any given individual do not react the same to stretch.
The relaxation response is part of a cyclical reaction. Once the muscle is “relaxed” via autogenic inhibition is is free to stretch and thus lengthen again and thus the muscle spindles are free to react to stretch again initating another stretch reflex, upon which time, at a certain point, the golgi tendon organs may react again, so on and so forth.
It is not well excepted that the golgi tendon is sensitive enough to passive or static stretch conditions to contribute greatly to muscle relaxation via autogenic inhibition. It is certainly not an optimal condition for GTO involvement. But earlier theories suggested that one response to prolonged passive stretch was the subsequent relaxation after contraction of the stretched muscle, by one means or another, which should theoretically lessen resistance to further stretch.
Although there is indeed less restistance during slow, static stretching these simplistic theories about muscle relaxation should be considered incomplete. The idea that complete relaxation is needed to increase flexibility certainly doesn’t hold up in real training.
Many people think that once a stretch is “held” for a long enough period of time then the stretch response simply vanishes. Instead the response is part of a feedback circuit that continuously monitors muscle length and tension. Simply pausing a stretch does not eliminate the stretch reflex entirely, only ameliorates it. Furthermore, any great change in muscle activity has not been shown after a hold of 30 seconds or more. Longer durations will not result in greater exceptance of stretch reducing the stretch reflex.
Another misconception is that injury due to stretching is entirely due to velocity of stretching and thus only dynamic and ballistic stretching activities will lead to injury. However, the extensiblility of muscles is not without limit and all tissues will eventually reach a point of rupture, regardless of the velocity of the lengthening. The stretch reflex together with the relaxtation response due to inhibition is not an excuse for "extreme" stretching activities. Injuries can and will occur if muscles are stretched too vigorously.
On the other hand a spasticity condition known as the “clasped-knife” can occur in the extensor muscles of a joint, during certain physiological conditions such as “upper motoneuron” disease. See [http://www.uth.tmc.edu/nba/neuroscience/s3/iii6-1.html#clasp_knife_reflex]
The flexion is resisted due to the reflex response to stretch in the extensor but the reflex suddenly “melts away” and the muscle is relaxed due to an exaggeration in the response. Thus when a spastic limb is being passively moved though a range of motion there is a constant restistance and then it seems as if this resistance suddenly lets go, and the limb suddenly easily collapses into full flexion, much like a pocket knife snapping shut.
This response was originally thought to be caused by autogenic inhibition but it is now known to be exaggerated reaction and the activity of the Golgi tendon and autogenic inhibition cannot alone account for it. Even if this inhibition explains the relaxation of the spastic muscle it does not explain the failure of the return to spasticity, since once it relaxes it is free then to react to stretch.
Actually, this gives rise to another frequent misunderstanding. The difference between the stretch reflex and mechanical recoil in the muscles. When you stretch a muscle, mechanical energy is stored in the cross-bridges which basically results in a spring effect. Thus, during the eccentric portion of a bench press, energy is stored in the muscles that contributes greatly to the concentric.
However if one pauses for long enough at the bottom of the press, this energy dissipates. This has caused some to theorize that the stretch reflex is dampened or eliminated and the inhibitory action of the Golgi tendon organ makes the concentric action harder after a pause. This is likely to have very little influence.
How the GTO works and doesn’t work, it should be noted, is not entirely understood.
When flexibility in a muscle increases, it is because the response to repeated bouts of stretching dampens and modulates the reaction to stretch. Thus allowing greater changes in length over time. But it is the repeated exposure over time that is important and it is possible to injure the muscle due to too vigorous a stretch. This could result in a muscle that not only does not achieve the desired flexibility in a timely manner but that becomes less flexible and ameliable to stretch due to many small injures over time.
As stated previously any tissue can reach it’s point of rupture regardless of the velocity of stretching. The stretch reflex may be able to be “downtrained” over time but this leads to other problems. Seeking to continuously downtrain the stretch reflex is probably not going to contribute to athletic success and indeed, more flexilbility is not always good. Useful range of motion should be should be distinguished from excessive range of motion.
The stretch reflex is sometimes confused with the "stretch response" which which has to do with tension generated in parallel muscle fibers at lengths slightly greater than resting length. Both the stretch reflex and the stretch response may be part of the //stretch shortening cycle (SSC). It is unclear to what extent each component is important but the SSC is key in developing explosive power.
This entry is by no means to be taken as a comprehensive theory or overview of reflexes, proprioception, the muscle spindles, the GTO or any other motor process.
For further reading see sources below:
Alter, Michael J. Science of Flexibility. New York: Human Kinetics, 2004.
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References
Hole, John W. Human anatomy and physiology. Dubuque, Iowa: W.C. Brown, 1987.
"Spinal Cord Medicine." NCBI HomePage. Ed. Vernon W. Lin. 2003. Demos Medical Publishing. 15 Mar. 2009 <http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=spinalcord>.
"Chapter 11 - Muscle Receptors." University of Nebraska Medical Center (UNMC). 15 Mar. 2009 <http://www.unmc.edu/physiology/Mann/mann11.html>."Neuroscience Online (iii,2,1)."
Neuroscience Online: A Neuroscience Electronic Textbook | The University of Texas Medical School at Houston." Neuroscience Online. Ed. John H. Byrne. 19 Mar. 2009 <http://www.uth.tmc.edu/nba/neuroscience/index.htm>.
Joan C. Edwards School of Medicine - Marshall University. 19 Mar. 2009 <http://musom.marshall.edu/anatomy/grosshom/spinalreflexes.html>.
