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The Performance Lab A place to discuss the role of physical exercise on health in diseased and non-diseased states.

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Old 17-03-2009, 02:14 AM   #1
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Default Long Duration Static Stretching

Hi all,

Recently I've been seeing more and more recommendations for long duration, low load static stretching to reduce pain and improve function. For example, in the case of plantar fascitis, it is often recommended that a person wear a Strausberg Sock, which provides this stretch. I've also seen it applied in patello-femoral pain with long duration rectus femoris and supine hip internal rotation stretching.

I am having difficulty locating any literature on the topic, but would love to know of any, and would also love to hear Soma Simple's opinions regarding the strategy.

Thanks, and have a great week!

Carson Boddicker
Flagstaff, AZ
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Old 17-03-2009, 05:57 AM   #2
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Dig around and you'll find plenty of studies that contradict one another and leave the whole question open for further debate. Many studies on the efficacy of stretching are badly flawed and of dubious merit.

As a massage therapist and personal trainer, I have very low regard for static stretching in general. However, I do not argue when a medical pro prescribes such methods for treatment of a medical condition.

For most individuals, static stretching is of very limited value when compared to alternatives like dynamic joint mobility drills, active isolated stretching, PNF stretching, or yoga (which is dynamic even in static poses). All of these methods actively incorporate the nervous system to achieve superior results over the long run. I prefer to spend some extra time teaching these more effective stretching methods rather than waste time on static stretches that will have little or no long-term positive impact.
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Old 17-03-2009, 06:23 AM   #3
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I did some reading and nothing really jumps out at me that can specifically address your issue. I did find this full article here. It doesn't speak directly of how pain maybe addressed through static stretching, but what i found interesting was that it showed the myriad events associated with static stretching at the myotendinous junction. This part was very interesting to me, quoted from the above article;

"Growth factors and their cognate receptors.
Another possibility of how muscle may adapt to passive stretch is based on the autocrine (ie, the muscle fiber itself) or paracrine (ie, the fibroblasts or other cells contiguous with the muscle fiber) regulation of muscle growth. Growth factors are molecules, secreted by cells, and have a potent biological activity.69–72 In addition to specific effects, growth factors, in general, stimulate cell proliferation.69–72 Several growth factors are involved in muscle development and have been identified. Insulin-like growth factor 1 (IGF-1),69,70 platelet-derived growth factor (PDGF),71 and fibroblastic growth factor (FGF)72 have been documented to stimulate either myoblast proliferation or, to a certain extent, muscle maturation.

The release of an IGF-1-like molecule from muscle fibers during passive stretch was described by Goldspink and colleagues,70 and these findings provide support for the theory that a similar mechanism might occur during the passive stretching of a muscle. Whether IGF-1 is directly involved in stretch-induced hypertrophy needs to be verified, and the molecular mechanisms of a stretch-sensitive increase in IGF-1 or other molecules during stretch-based rehabilitation protocols is not known. Insulin-like growth factor 1 (secreted with passive stretch)69 and PDGF (there are relatively more PDGF receptors at the myotendinous junction than at the nonjunctional membrane)71 are the likeliest candidates to regulate satellite cell proliferation during stretch-based rehabilitation. These growth factors could stimulate cell division of the myosatellite cells. The addition of more sarcomeres (ie, myofibrillogenesis) could be the result of the proliferating myosatellite cells, which have fused with preexisting muscle fiber cells. The proliferation of myosatellite cells is proposed to explain overload-induced muscle enlargement,73–75 and perhaps they could also be stimulated by passive stretch as it is applied therapeutically to function in a manner similar to how they behave during limb lengthening (growth).33 Such adaptation seems to occur preferentially at the distal portion of the muscle.34 Based on the literature, it seems that the distal portion of a muscle, and the myotendinous junction in particular, is important in the adaptive response of muscle to altered loading. However, the role of satellite cells and the formation of de novo muscle fibers in response to a changed nontraumatic mechanical event is not fully known and needs more study.

Ion channels.
Transmission of a mechanical stimulus could lead to changes in ion flux (eg, mechanical transduction similar to the hair cells in the inner ear). Stretch-activated ion channels have been found in muscle cells and in many other systems.76–78 The electrophysiological characteristics (determined by patch clamping) of these channels have been well documented, but their function in muscle remains unclear. Mechanosensitive ion channels may be organized by a submembranous actin cytoskeleton. Whether these ion channels play a role in passively stretched muscle fibers is not yet fully determined, in part because few reagents are available that could analyze the mechanosensitive ion channels. Undoubtedly, as more of the gene sequences are discovered, specific reagents (eg, cDNA and antibodies) can be made, providing researchers with the necessary tools."

Now it is very interesting to see how much we DON'T know about the effects of the various stimuli that may be applied to patients. If nothing else, this article shows that much research is needed before we can really just blindly go and discount or talk up certain treatment modalities. I think the author does a great job of not making assumptions and claims that are ungrounded in research, but he brings forth many interesting 'takes' on what may happen. It is not such a great leap of faith, IMO, to say that there might be some sort of neurochemical or other such mechanism at work to explain the anecdotal reports of increased ROM, decreased pain etc.
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Old 05-04-2009, 07:00 AM   #4
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The jury is definately still out on the whole static stretching debate. I personally use long-duration/low-load static stretches at night a couple of times per week on muscles that have a tendency to lose suppleness and/or extensibility. Notice I didn't say "flexibility" since that is more about joint range of motion which includes both muscle and passive (i.e. capsular, ligamentous) restraints.

Subjectively and anecdotally, I do seem to sleep better when I stretch at night in this fashion and even feel a little less "stiff" in the morning. I often hold these stretches for 1-3 minutes depending on the specific stretch. During theses stretches I try to add slow movements of other distant bodyparts (including the head/neck) to add stress/strain to all the associated connective tissues of both muscle and nerve. I fool around with some longer duration neurodynamic type of stretches as well.

It's fun to use your own body as a scientific lab experiement and see what works for you; regardless of what the research literature says!
Keats Snideman CSCS, LMT
"Keep an open mind, but not so open that your brains fall out."
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