Fascia stretching and muscle growth: Flimsy evidence in support

[Dr Pangloss]

After really fucking exhaustive searching of the literature on this subject, I conclude that there is very little support for it in the literature. The best support is posted below.

on FST-7.com (a site based on working out to stretch the fascia), I've seen Hanny Rimbod claim that "the best bodybuilders have really thin fascia so they grow faster and more." something like that. Anyway, the only support for variation in thickness of fascia comes from a few studies on patients with "compartment syndrome," a painful syndrom in which exercise causes great pain, probably because the fascia is restricting blood flow.

It HAS been reported that muscle on patients with compartment syndrome appear to be restricted by thicker, perhaps less elastic fascia.

However, Hanny is talking out his ass when he says fast gainers have thinner fascia. There is absolutely nothing in the literature to support this.

In fact, it's not even clear if people with compartment syndrome exhibit slow or restricted muscle growth.

That said, the following study looks at the results of fasciotomy (ie, cutting the fascia), which clearly lessens fascial restriction on the muscle, on muscle fiber growth in patients with compartment syndrome 1 year after fasciotomy.

the study finds significant growth of muscle fibers 1 year after fasciotomy (in the tibialis i think). What is notable however, is that patients with compartment syndrome already have larger mean fiber diameter than controls.

This, of course, doesnt really say anything about normal people, and doesnt' say anything about whether fascia actually restrict muscle growth in normal people. In fact, it appears to be believed that the fascia should NOT restrict growth.

One other notable finding is that patients with compartment syndrome appear to have blunted angiogenesis and resultant capillary density.


Scand J Med Sci Sports. (javascript:AL_get(this, 'jour', 'Scand J Med Sci Sports.');) 2009 Oct 4. [Epub ahead of print]
Evidence for low muscle capillary supply as a pathogenic factor in chronic compartment syndrome.

Edmundsson D (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Edmundsson%20D%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Toolanen G (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Toolanen%20G%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Thornell LE (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Thornell%20LE%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Stål P (http://www.ncbi.nlm.nih.gov/pubmed?term=%22St%C3%A5l%20P%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract).
Department of Surgery and Perioperative Science, Division of Orthopedics, Umeå University Hospital, Umeå, Sweden.
There is a paucity of data regarding the pathogenesis of chronic exertional compartment syndrome (CECS), its consequences for the muscles and the effects of treatment with fasciotomy. We analyzed biopsies from the tibialis anterior muscle, from nine patients, obtained during a decompressing fasciotomy and during follow-up 1 year later. Control biopsies were obtained from nine normal subjects. Muscle capillarity, fiber-type composition and fiber area were analyzed with enzyme- and immunohistochemistry and morphometry. At baseline, CECS patients had lower capillary density (273 vs 378 capillaries/mm(2), P=0.008), lower number of capillaries around muscle fibers (4.5 vs 5.7, P=0.004) and lower number of capillaries in relation to the muscle fiber area (1.1 vs 1.5, P=0.01) compared with normal controls. The fiber-type composition and fiber area did not differ, but focal signs of neuromuscular damage were observed in the CECS samples. At 1-year follow-up after fasciotomy, the fiber area and the number of fibers containing developmental myosin heavy chains were increased, but no enhancement of the capillary network was detected. Thus, morphologically, patients with CECS seemed to have reduced microcirculation capacity. Fasciotomy appeared to trigger a regenerative response in the muscle, however, without any increase in the capillary bed.

[Dr Pangloss]

There is a substantial literature also demonstrating that longitundinal stretching of myofibers (over the corse of many hours) causes hypertrophy also.

However, the time course of the stretching (I'll post up studies later) is sufficiently long as to cast doubt on it's applicability to training programs like fst-7 or dogcrap. These hypertrophy paradigms use stretching on the order of 12 to 72 hours or more.

What's interesting also is that acute (short term) stretching actually has a negative effect on subsequent strength and as far as i can tell no effect on long-term growth.

The only fascial stretching bodybuilding concept that fits is site-enhancement oil.

It should also be noted that in these stretch paradigms, at least one study had determined that a significant portion of the growth was due to non-contractile tissue.

[Dr Pangloss]

by the way, if someone wants a copy of the above paper, pm me with an email address. Be warned, however, that i may get tired of doing this...

[Dr Pangloss]

It is a strongly held myth that site-enhancement oil used to stretch the fascia produces muscle growth.

If you believe this, then greg valentino should be able to curl 300 lbs. My guess is, his strength actually dropped after he loaded his arms with oil because of poor perfusion and excessive scarring.

and again, as indicated above, muscle fiber stretching can result in significant development of non-contractile tissue.

38629

[bigtimektz]

Great read Dr.

[blondee]

Thank you dr!

[Frosty]

What about reports from Poliquin on fascia stretching massage increasing size...especially places like the forearms? He states that people that have trains for much longer see more benefit.

[natron]

What about reports from Poliquin on fascia stretching massage increasing size...especially places like the forearms? He states that people that have trains for much longer see more benefit.

Yeah, unfortunately Poliquin also suggest taking 45 grams of fish oil per day as well???

[Frosty]

Yeah, unfortunately Poliquin also suggest taking 45 grams of fish oil per day as well???


And according to him and his experience it works for fast results....I don't see the issue.

[natron]

And according to him and his experience it works for fast results....I don't see the issue.

yep, 29lbs of lean muscle mass in 30 days, in a trained athlete!

That screams bullshit

[Frosty]

yep, 29lbs of lean muscle mass in 30 days, in a trained athlete!

That screams bullshit

This is where I start to get slightly irritated.

Let me put it this way--I will listen to a coach that has encyclopedic knowledge and an incredible track record with producing results over people that look at research ANY day. I get sick of hearing people that read research say all this shit when the literature is usually limited for what we want to do, and you have people out there with not only the education, but broad knowledge of many fields as well as extraordinary amounts of experience AND producing results, and we just say they're full of shit because of "research" or whatever the hell you want to say.

I'm not buying it. That's horse shit.

[Frosty]

Back to the subject here...

[natron]

Back to the subject here...

owned! haha

the man has some great views, this was just not one of them, just sayin.

back to the topic

[-BLP-]

poliquin did affect my training positively,, i love tempo time control , plyometric to some level , and truly a big circuit training advocate

[Frosty]

owned! haha

the man has some great views, this was just not one of them, just sayin.

back to the topic

Sorry for the outburst.

He's made some crazy claims with gains and fat loss with athletes. However keep in mind there may be circumstances that aren't exactly "normal". It's not like he took Jay Cutler and had him put on 29 lbs of mass in a month during a bulk. It was probably some athlete that let his diet go to shit during season, lost mass as well, and then Poliquin got his hands on him and got his diet, training, and supplementation back in order and BAM. Add to that that the athlete probably is well conditioned (which IMO helps with faster results) and also may have good genetics.

I've had some things happen to me that were similar and I've produced insane before and after pics in a matter of 6 weeks. In fact for shits and giggles, this fat loss occurred in just 6 weeks:

[natron]

Sorry for the outburst.

He's made some crazy claims with gains and fat loss with athletes. However keep in mind there may be circumstances that aren't exactly "normal". It's not like he took Jay Cutler and had him put on 29 lbs of mass in a month during a bulk. It was probably some athlete that let his diet go to shit during season, lost mass as well, and then Poliquin got his hands on him and got his diet, training, and supplementation back in order and BAM. Add to that that the athlete probably is well conditioned (which IMO helps with faster results) and also may have good genetics.

I've had some things happen to me that were similar and I've produced insane before and after pics in a matter of 6 weeks. In fact for shits and giggles, this fat loss occurred in just 6 weeks:

No worries, and nice cut by the way! Impressive.

ASll these guys have there ups and downs, Lyle Mcdonald is another fine example, lots of his shit is brilliant, other shit is just that.

My stance is to gain knowledge and experience, and be able to employ the best techniques from each where applicable.

[Dr Pangloss]

What about reports from Poliquin on fascia stretching massage increasing size...especially places like the forearms? He states that people that have trains for much longer see more benefit.


I dont read baseless assertion. i read science. i dont give a damn about someone's anecdotal knowledge either.

there is so much delusion and bias in anecdotal knowledge that it's almost worthless.

[Dr Pangloss]

This is where I start to get slightly irritated.

Let me put it this way--I will listen to a coach that has encyclopedic knowledge and an incredible track record with producing results over people that look at research ANY day. I get sick of hearing people that read research say all this shit when the literature is usually limited for what we want to do, and you have people out there with not only the education, but broad knowledge of many fields as well as extraordinary amounts of experience AND producing results, and we just say they're full of shit because of "research" or whatever the hell you want to say.

I'm not buying it. That's horse shit.

The bold is exactly why you are a moron frosty.

Remember this: i dont post for you, because your mind is soft and lacks the discipline to remain evidence-based.

[Frosty]

You're welcome to remain years behind while waiting for the research to come out on the things coaches are already finding to work :D Good luck with that.

[natron]

You're welcome to remain years behind while waiting for the research to come out on the things coaches are already finding to work :D Good luck with that.

Flawed logic IMO. Science is what helps us continue to progress. Scientific thinking as well, is what developes the most effective training/cardio/drug/supplement/diet programs.

Not gain 1" in a day muscletech ads

[Dr Pangloss]

You're welcome to remain years behind while waiting for the research to come out on the things coaches are already finding to work :D Good luck with that.


you're welcome to wallow in your ignorance and make-believe.

This forum is called "bodybuilding science," and if you dont like the rigor of science, stay in your little gnc world. In fact, i'm quite happy to have used car-salesmen with no formal scientific training not participate in my threads at all.

Your input isnt worth shit. Never has been. Never will be.

[Dr Pangloss]

Some of you brighter people who dont find my analysis satisfying might try and find more evidence in support of the role of the fascia in restricting muscle growth, or more evidence that engorging muscles with blood effectively stretches myofibers into growth.


I dont think you will find anything more compelling than what i have posted, but give it a try.

[Tatyana]

This is where I start to get slightly irritated.

Let me put it this way--I will listen to a coach that has encyclopedic knowledge and an incredible track record with producing results over people that look at research ANY day. I get sick of hearing people that read research say all this shit when the literature is usually limited for what we want to do, and you have people out there with not only the education, but broad knowledge of many fields as well as extraordinary amounts of experience AND producing results, and we just say they're full of shit because of "research" or whatever the hell you want to say.

I'm not buying it. That's horse shit.

The majority of modern training techniques and diet are based off scientific research.

I think most people think the fascia is just the covering of the muscle, but it also wraps all the individual muscle fibres and runs through all the muscle.

To stretch out the fascia would be to lose the structural integrity of muscle.


I think it is things like the fascia that make a steak that hasn't been aged properly tough and chewy.

Good steak is aged at least 30 days, or you have to cook roasts for ages to tenderise this.

http://www.alterchiropractic.com/images/skeletalmuscle.gif

[TPT]

After really fucking exhaustive searching of the literature on this subject, I conclude that there is very little support for it in the literature. The best support is posted below.

on FST-7.com (a site based on working out to stretch the fascia), I've seen Hanny Rimbod claim that "the best bodybuilders have really thin fascia so they grow faster and more." something like that. Anyway, the only support for variation in thickness of fascia comes from a few studies on patients with "compartment syndrome," a painful syndrom in which exercise causes great pain, probably because the fascia is restricting blood flow.

It HAS been reported that muscle on patients with compartment syndrome appear to be restricted by thicker, perhaps less elastic fascia.

However, Hanny is talking out his ass when he says fast gainers have thinner fascia. There is absolutely nothing in the literature to support this.

In fact, it's not even clear if people with compartment syndrome exhibit slow or restricted muscle growth.

That said, the following study looks at the results of fasciotomy (ie, cutting the fascia), which clearly lessens fascial restriction on the muscle, on muscle fiber growth in patients with compartment syndrome 1 year after fasciotomy.

the study finds significant growth of muscle fibers 1 year after fasciotomy (in the tibialis i think). What is notable however, is that patients with compartment syndrome already have larger mean fiber diameter than controls.

This, of course, doesnt really say anything about normal people, and doesnt' say anything about whether fascia actually restrict muscle growth in normal people. In fact, it appears to be believed that the fascia should NOT restrict growth.

One other notable finding is that patients with compartment syndrome appear to have blunted angiogenesis and resultant capillary density.


Scand J Med Sci Sports. (http://javascript<b></b>:AL_get(this, 'jour', 'Scand J Med Sci Sports.');) 2009 Oct 4. [Epub ahead of print]
Evidence for low muscle capillary supply as a pathogenic factor in chronic compartment syndrome.

Edmundsson D (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Edmundsson%20D%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Toolanen G (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Toolanen%20G%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Thornell LE (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Thornell%20LE%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Stål P (http://www.ncbi.nlm.nih.gov/pubmed?term=%22St%C3%A5l%20P%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract).
Department of Surgery and Perioperative Science, Division of Orthopedics, Umeå University Hospital, Umeå, Sweden.
There is a paucity of data regarding the pathogenesis of chronic exertional compartment syndrome (CECS), its consequences for the muscles and the effects of treatment with fasciotomy. We analyzed biopsies from the tibialis anterior muscle, from nine patients, obtained during a decompressing fasciotomy and during follow-up 1 year later. Control biopsies were obtained from nine normal subjects. Muscle capillarity, fiber-type composition and fiber area were analyzed with enzyme- and immunohistochemistry and morphometry. At baseline, CECS patients had lower capillary density (273 vs 378 capillaries/mm(2), P=0.008), lower number of capillaries around muscle fibers (4.5 vs 5.7, P=0.004) and lower number of capillaries in relation to the muscle fiber area (1.1 vs 1.5, P=0.01) compared with normal controls. The fiber-type composition and fiber area did not differ, but focal signs of neuromuscular damage were observed in the CECS samples. At 1-year follow-up after fasciotomy, the fiber area and the number of fibers containing developmental myosin heavy chains were increased, but no enhancement of the capillary network was detected. Thus, morphologically, patients with CECS seemed to have reduced microcirculation capacity. Fasciotomy appeared to trigger a regenerative response in the muscle, however, without any increase in the capillary bed.


compartment syndrome cannot be used to validate the differences in the properties of fascia across people since it occurs secondary to a traumatic event. the fascia is already different because of injury. the limitations of fascia itself and how the body adapts to injury causes compartment syndrome. no evidence exists of correlations between thicker or less elastic fascia and compartment syndrome.

fascia does not limit growth or muscle hypertrophy beyonds its inherent function to provide tension forces and structure. theories of muscle restrictions due to fascia are flawed on every level including physiological processes.

more of these limitations in a bit.

[TPT]

It is a strongly held myth that site-enhancement oil used to stretch the fascia produces muscle growth.

If you believe this, then greg valentino should be able to curl 300 lbs. My guess is, his strength actually dropped after he loaded his arms with oil because of poor perfusion and excessive scarring.

and again, as indicated above, muscle fiber stretching can result in significant development of non-contractile tissue.

38629


foriegn substances such as oil would cause mechanical changes of tissue and fascia. but, these changes do not suggest muscle hypertrophy nor strength changes.

[Dr Pangloss]

compartment syndrome cannot be used to validate the differences in the properties of fascia across people since it occurs secondary to a traumatic event. the fascia is already different because of injury. the limitations of fascia itself and how the body adapts to injury causes compartment syndrome. no evidence exists of correlations between thicker or less elastic fascia and compartment syndrome.

fascia does not limit growth or muscle hypertrophy beyonds its inherent function to provide tension forces and structure. theories of muscle restrictions due to fascia are flawed on every level including physiological processes.

more of these limitations in a bit.

There is an old paper cited in the publication i posted that suggested there were differences in thickness and elasticity with compartment syndrome.

would you like me to give the citation?

I was somewhat surprised myself.

Finally, i agree that this idea seems unfounded, and the above paper represents the most supportive data i could find.

There are no fasciotomies performed on control patients to judge what effect (if any) loosening the fascia would have on normal muscle growth.


The only other place to go is myofibril stretching, which would reasonably also result from muscle engorgement or site-enhancement oil.

In any case, Greg valentino and other's hideous growth demands an explanation as to what is "growing." Like i said, there is some suggestion that it can be non-contractile tissue, which seems more likely to me than muscle.


And now folks, we have a real scientific discussion going on this subject....

thanks pt.

[TPT]

This is where I start to get slightly irritated.

Let me put it this way--I will listen to a coach that has encyclopedic knowledge and an incredible track record with producing results over people that look at research ANY day. I get sick of hearing people that read research say all this shit when the literature is usually limited for what we want to do, and you have people out there with not only the education, but broad knowledge of many fields as well as extraordinary amounts of experience AND producing results, and we just say they're full of shit because of "research" or whatever the hell you want to say.

I'm not buying it. That's horse shit.

The bold is exactly why you are a moron frosty.

Remember this: i dont post for you, because your mind is soft and lacks the discipline to remain evidence-based.


pangloss, these moral lablels are functionally analogous to anectodes. they are all subjective. they are not scientific and do not function scientifically.

im just sayin, be cool.

[Dr Pangloss]

[quote=Dr Pangloss;648675]


pangloss, these moral lablels are functionally analogous to anectodes. they are all subjective. they are not scientific and do not function scientifically.

im just sayin, be cool.


I should be cool and he can call my analysis bullshit? I think you'd better take a second and read the thread.

Secondly, the bold makes no sense.

[TPT]

The majority of modern training techniques and diet are based off scientific research.

I think most people think the fascia is just the covering of the muscle, but it also wraps all the individual muscle fibres and runs through all the muscle.

To stretch out the fascia would be to lose the structural integrity of muscle.


I think it is things like the fascia that make a steak that hasn't been aged properly tough and chewy.

Good steak is aged at least 30 days, or you have to cook roasts for ages to tenderise this.

http://www.alterchiropractic.com/images/skeletalmuscle.gif


fascia is usually descibed in three categories: superficial, deep or visceral. i assume when people reference fascial stretching by dc or rambod, they are speaking of superficial or deep. someone can correct me on this. so fasica wraps around not just muscle but bones, organs, tendons, ligaments, etc. this further argues that increasing the extensibility of fascia is not necessarily what we waht.

for a moment, im going to skip over whether we can actually perform this. but, if we could stretch the deep fasica we might cause further orthopaedic involvement because of the tight relationship between fascia, muscle, tendons, ligaments, joint capsule, etc. "loose" fasica would set the occasion for "loose" joints.

[Tatyana]

fascia is usually descibed in three categories: superficial, deep or visceral. i assume when people reference fascial stretching by dc or rambod, they are speaking of superficial or deep. someone can correct me on this. so fasica wraps around not just muscle but bones, organs, tendons, ligaments, etc. this further argues that increasing the extensibility of fascia is not necessarily what we waht.

for a moment, im going to skip over whether we can actually perform this. but, if we could stretch the deep fasica we might cause further orthopaedic involvement because of the tight relationship between fascia, muscle, tendons, ligaments, joint capsule, etc. "loose" fasica would set the occasion for "loose" joints.

Muscle anatomy, any anatomy really, is not my area of expertise by any means.

My limited study have revealed to me that the structure of muscle is incredibly complicated, right down to the actin and myosin fibres.

However, it is fairly obvious that there is a LOT of fascia, as you have stated, and I would think that stretching it out would be analogous to a muscle hernia.

[TPT]

There is an old paper cited in the publication i posted that suggested there were differences in thickness and elasticity with compartment syndrome.

would you like me to give the citation?

I was somewhat surprised myself.

Finally, i agree that this idea seems unfounded, and the above paper represents the most supportive data i could find.

There are no fasciotomies performed on control patients to judge what effect (if any) loosening the fascia would have on normal muscle growth.


The only other place to go is myofibril stretching, which would reasonably also result from muscle engorgement or site-enhancement oil.

In any case, Greg valentino and other's hideous growth demands an explanation as to what is "growing." Like i said, there is some suggestion that it can be non-contractile tissue, which seems more likely to me than muscle.


And now folks, we have a real scientific discussion going on this subject....

thanks pt.

yes. please cite it. ill look into it further.

noncontraticle tissues would not "grow." articular cartilage, bone or collagenous tissues such as tendons and ligaments do derform but not in the cases of site injections.

we'll have to investigate other structures.

[Dr Pangloss]

In the discussion of old paper cited in the work above, the idea that fascia may restrict hypertrophy is actually brought up, and dealt with quite skeptically. No evidence to support it at all.

that is the ONLY mention in the literature i could find. It's just not a question people in this area have taken seriously.

[Dr Pangloss]

yes. please cite it. ill look into it further.

noncontraticle tissues would not "grow." articular cartilage, bone or collagenous tissues such as tendons and ligaments do derform but not in the cases of site injections.

we'll have to investigate other structures.


you want to pm me an email addy bro. I'm going to send you the paper and perhaps another.

[TPT]

[quote=ThePhysicalTherapist;650262]


I should be cool and he can call my analysis bullshit? I think you'd better take a second and read the thread.

Secondly, the bold makes no sense.


im just saying- if we promote science/objectivity, we dont need to label people "morons." those are implications of value, morality, and subjectivity.

come on! im a experimental researcher myself! : )

ok. back to fascia.

[TPT]

you want to pm me an email addy bro. I'm going to send you the paper and perhaps another.


definately. thank you. and thanks for the discussion.

[Dr Pangloss]

papers sent.

[TPT]

Muscle anatomy, any anatomy really, is not my area of expertise by any means.

My limited study have revealed to me that the structure of muscle is incredibly complicated, right down to the actin and myosin fibres.

However, it is fairly obvious that there is a LOT of fascia, as you have stated, and I would think that stretching it out would be analogous to a muscle hernia.


very complex. that is what i suspect proponents of fascia stretching are not discriminating. the rate at which fascia adapts to muscle hypertrophy would not limit muscle hypertrophy (in normal humans). the fascia will progressivly deform whether in states of hypertrophy or atrophy.

[natron]

Dr.P or PT,

do either of you have any studies linked to the FST-7 that Hany has wrote?

I'd like to look over some of them and I don't have a reference point

[Dr Pangloss]

Dr.P or PT,

do either of you have any studies linked to the FST-7 that Hany has wrote?

I'd like to look over some of them and I don't have a reference point


far as i know, there are no controlled studies using fst-7. He has a website; go join and read up. Its all the rage with pros and ams.

to me, he's just using both a volume and a high intensity system together. It might work well, but why it does appears--in spite of claims--to be elusive.

[Frosty]

[quote=ThePhysicalTherapist;650262]


I should be cool and he can call my analysis bullshit? I think you'd better take a second and read the thread.

Secondly, the bold makes no sense.


I was speaking to natron. That's why he was quoted above my text.

[natron]

far as i know, there are no controlled studies using fst-7. He has a website; go join and read up. Its all the rage with pros and ams.

to me, he's just using both a volume and a high intensity system together. It might work well, but why it does appears--in spite of claims--to be elusive.

I searched his site, and older MD articles. I'm specifically looking for referenced studies in any of the articles he has written on said topic, and I'm batting 0%.

I'm getting the feeling he's is using other studies based on high volume etc and painting his own picture?

[TPT]

papers sent.


the study you sent me by turnipseed et al. (1989) found increased thickness in 40% of the cases. also, the following study found those with compartment syndrome to have stiffer and thicker fascia than normal controls.

thus, its quite plausible that those with pathology of some compartments have thicker fascia. the correlation does not suggest whether thicker fascia limits muscle hypertrophy. we might have to cite other research to validate the efficacy of stretching fascia and muscle hypertrophy. maybe work in hyperplasia.


Ann Biomed Eng. (javascript:AL_get(this, 'jour', 'Ann Biomed Eng.');) 1994 May-Jun;22(3):272-9.
Mechanical and biochemical analyses of tibial compartment fascia in chronic compartment syndrome.

Hurschler C (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Hurschler%20C%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Vanderby R Jr (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Vanderby%20R%20Jr%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Martinez DA (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Martinez%20DA%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Vailas AC (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Vailas%20AC%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Turnipseed WD (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Turnipseed%20WD%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract).
Department of Surgery, University of Wisconsin, Madison.
Increases in compartment pressure associated with chronic compartment syndrome (CCS) may be due to changes in the mechanical properties and/or thickness of fascia (4,22). To explore this possibility, we compared the mechanical and biochemical characteristics (stiffness, thickness, time-dependent response, collagen content, and collagen crosslinking) of fascia from patients with symptomatic anterior compartment syndrome to fascia from adjacent collateral compartments. We tested 43 specimens harvested from 20 individuals during surgical fasciectomy. Properties of normal (lateral)-compartment (NC) and pathological (anterior)-compartment (PC) fascia were mechanically tested in the axial and transverse directions forming four groups. An external control group (EX) of six specimens of anterior and lateral-compartment fascia harvested from amputated legs was also included in the study. PC fascia was found to be thicker and structurally stiffer (elastic modulus times thickness) in the axial direction than was NC fascia (p < or = 0.05). No significant differences were found between NC and PC time-dependent response, although significant differences between percent relaxation in the pooled axial and transverse direction specimens were observed. No differences were found in the collagen content, as measured by hydroxyproline (Hyp) concentration, between NC and PC fascia. PC fascia was found to have less collagen crosslinking by hydroxylyslpyridinoline (HP) concentration. In conclusion, although this study does not elucidate etiological factors in CCS, the changes found in PC fascia suggest that fascial mechanical properties contribute to the pathology.

PMID: 7978548 [PubMed - indexed for MEDLINE]

[Scott Stevenson]

Dr. P et al.

Here's a post of mine from a thread on another board focusing on the data supporting DC training-style "extreme stretching." I think you might find it interesting.

------------
The thread:

http://www.intensemuscle.com/33935-extreme-stretching-how-effective-really-5.html?

-------------------------

My post (modified slightly to remove out of context comments - it was written to a poster in that thread, not this one or you of course, Dr. P):

-----------------------

The stretch-induced chronic overload literature has poor (if that) external validity in supporting a DC-style extreme stretching. I've read through this thread (albeit cursorily over the past few days), but it seems you're mostly just asking if there are more applicable data to support extreme stretching.

As you've been saying, to do this, the duration (1-2 min) and tensile overload would have to be equivalent, as well as using a human model. Naturally (and I don't recall this being mentioned), it is possible that while an extreme stretching protocol in and of itself might not be a hypertrophic stimulus (in lieu of other exercise), this does not preclude the possibility that there could be an *interaction* between the resistance exercise stimulus and that of an extreme stretch such that adding the stretching enhances the growth adaptation.

For example here is a study which supports the above notion (of an experimental interaction of a treatment without a main effect of that treatment in isolation). You might also say that this study could lend support to the notion that small "doses" of tension and vascular occlusion (as in extreme stretching) may produce hypertrophy.
-------------------
1. Takarada Y, Tsuruta T, Ishii N. Cooperative effects of exercise and occlusive stimuli on muscular function in low-intensity resistance exercise with moderate vascular occlusion. Jpn J Physiol 2004;54:585-592.

To obtain insight into the relative contributions of exercise and occlusive stimuli to these muscular adaptations, the present study investigated the short- and long-term effects of varied combinations of low-intensity exercise and vascular occlusion. The subjects were separated into 3 groups (n = 6 for each group): low-intensity with vascular occlusion (LIO), low-intensity without vascular occlusion (LI), and vascular occlusion without exercise (VO). LIO and LI groups performed bilateral knee extension exercises in seated positions with an isotonic extension machine. In the LIO group, both sides of the thigh were pressure-occluded at the proximal end by means of a tourniquet during the entire session of exercise (approximately 10 min), whereas only the occlusion with the same pressure and duration was given in the VO group. The mean occlusion pressure was 218 +/- 8.1 mmHg (mean +/- SE). The exercise session consisted of five sets of exercise at an intensity of 10-20% 1RM and was performed twice a week for 8 wk. After the period of exercise training, isometric and isokinetic strengths at all velocities examined increased significantly in the LIO group (p < 0.05), whereas no significant change in strength was seen in the LI and VO groups. The increase in muscular strength in LIO was associated with a significant increase in the cross-sectional area of knee extensor muscles by 10.3 +/- 1.6%. The plasma growth hormone concentration measured 15 min after the session of exercise showed a marked increase only in LIO. The results showed that the low-intensity exercise and occlusive stimuli have cooperative effects in the long-term adaptation of muscle and an acute response to growth hormone.

-------------

In the above case, neither the resistance training stimulus nor vascular occlusion alone were sufficient to produce muscle growth, but combined, they did. JUST A LITTLE TENSION in combination with occlusion produced muscle growth - and a 10% increase in CSA in just 8 weeks is A LOT.

Although I've never seen a direct test of DC training sans stretching in the literature, I also haven't seen a direct study demonstrating that it will not stimulate skeletal muscle growth. Perhaps the stretching isn't about fascial manipulation per se, but rather about the vascular occlusion that occurs under tension during the stretch (per the above study)?... Food for thought... (And yes, I do recognize that the above study used isotonic contractions not isometrics as in DC training, but as the above study shows, and you and I are aware, neither isometric contractions nor isotonic training with <20%1RM will produce substantial muscle growth in non-pathological situations.)

Another study that I find interesting:

The same group of researchers has studied vascular occlusion per se and found it had an anti-atrophic effect (granted their protocol was a total of 15min / day - FAR from a single DC stretch). Prevention of atrophy is of course also found with fixation in a stretched position (again long term studies). OTOH, its fairly certain that weighted stretch models produce ischemia at least at the initiation of the protocol and gene expression is turned on pretty rapidly on those models. (Again, maybe there's something to this ischemia thing...)

1. Takarada Y, Takazawa H, Ishii N. Applications of vascular occlusion diminish disuse atrophy of knee extensor muscles. Med Sci Sports Exerc 2000;32:2035-2039.

PURPOSE: We have previously shown that the combination of low-intensity resistive exercise and moderate vascular occlusion induces in humans a marked increase in growth hormone secretion and muscular hypertrophy. The present study investigated the effects of vascular occlusion on the size of thigh muscles in patients who underwent an operation for the reconstruction of the anterior cruciate ligament to see whether it attenuates the disuse muscular atrophy without any exercise combined. METHODS: Two sessions of occlusive stimulus, each consisting of five repetitions of vascular occlusion (mean maximal pressure, 238 mm Hg) for 5 min and the release of occlusion for 3 min, were applied daily to the proximal end of the thigh from 3rd to 14th days after the operation. Changes in the cross-sectional area (CSA) of thigh muscles were analyzed with magnetic resonance images taken on the 3rd and 14th day after the operation. RESULTS: Without occlusive stimulus (control), the CSAs of knee extensors and flexors decreased by 20.7 +/- 2.2% and 11.3 +/- 2.6% (mean +/- SEM, N = 8), whereas with the occlusive stimulus, they decreased by 9.4 +/- 1.6% and 9.2 +/- 2.6% (N = 8), respectively. The relative decrease in CSA of knee extensors was significantly (P < 0.05) larger in the control group than in the experimental group. CONCLUSION: The results indicate that the occlusive stimulus effectively diminishes the postoperation disuse atrophy of knee extensors.

---------------------

And here's a really nifty one I thought you'd like. The model was not an extreme stretch per se, but a hell of a lot closer that the animal models we've been talking about: Human model, stretch (less than a 30 min bout / day) and the stretch was an intermittent ACTIVE one - under intermittent voluntary tension that persisted until volitional fatigue. Compared to an extreme stretch, the difference was the voluntary force produced, that it was intermittant and the the time under tension was longer.

They found:
-Passive stretch: No increase in protein turnover with the same joint angle (roughly) and duration of stretch.
-ACTIVE stretch: Nearly a 50% increase in muscle protein synthetic rate when an active voluntary contraction was added to the stretch. (Note that the 40% MVC force likely produced significant ischemia / vascular occlusion, as well!)

1. Fowles JR, MacDougall JD, Tarnopolsky MA, Sale DG, Roy BD, Yarasheski KE. The effects of acute passive stretch on muscle protein synthesis in humans. Can J Appl Physiol 2000;25:165-180.

We examined the effect of an isolated bout of maximal tolerated passive stretch on fractional muscle protein synthetic rate in human soleus muscle. Eight healthy males performed two separate trials with the same leg: one session of passive stretch and one of intermittent active isometric contraction at a force equivalent to that which occurred during the passive stretch trial. This force was approximately 40% of maximum voluntary contraction force and produced volitional fatigue in approximately 27 min. Intermittent passive stretch, for the same duration, elicited a 6.1 degrees increase in joint angle (P<.0005) with silent electromyography. Fractional protein synthetic rate from experimental and control soleus in each trial was assessed from biopsy samples over the period 10-22 hr postexercise by the incorporation rate of L-[1-13C] leucine into muscle. Protein synthesis was elevated in the soleus of the exercised leg following the active contraction trial by 49% (P<.05) but not following the passive stretch trial. Results indicate that a single bout of maximal passive stretch does not significantly elevate fractional muscle protein synthetic rate in humans and thus suggests that muscle stretch per se is not the stimulus for the muscle hypertrophy that occurs with resistance training.

--------------------

....Again, I'm in agreement about the lack of direct scientific (peer-reviewed, etc.) evidence. The above is not an attempt to convince you of anything - actually more of an enjoyable exercise on my part to dig in the literature for a little bit and find some new tidbits.

-Scott

[TPT]

Dr. P et al.

Here's a post of mine from a thread on another board focusing on the data supporting DC training-style "extreme stretching." I think you might find it interesting.

------------
The thread:

http://www.intensemuscle.com/33935-extreme-stretching-how-effective-really-5.html?

-------------------------

My post (modified slightly to remove out of context comments - it was written to a poster in that thread, not this one or you of course, Dr. P):

-----------------------

The stretch-induced chronic overload literature has poor (if that) external validity in supporting a DC-style extreme stretching. I've read through this thread (albeit cursorily over the past few days), but it seems you're mostly just asking if there are more applicable data to support extreme stretching.

As you've been saying, to do this, the duration (1-2 min) and tensile overload would have to be equivalent, as well as using a human model. Naturally (and I don't recall this being mentioned), it is possible that while an extreme stretching protocol in and of itself might not be a hypertrophic stimulus (in lieu of other exercise), this does not preclude the possibility that there could be an *interaction* between the resistance exercise stimulus and that of an extreme stretch such that adding the stretching enhances the growth adaptation.

For example here is a study which supports the above notion (of an experimental interaction of a treatment without a main effect of that treatment in isolation). You might also say that this study could lend support to the notion that small "doses" of tension and vascular occlusion (as in extreme stretching) may produce hypertrophy.
-------------------
1. Takarada Y, Tsuruta T, Ishii N. Cooperative effects of exercise and occlusive stimuli on muscular function in low-intensity resistance exercise with moderate vascular occlusion. Jpn J Physiol 2004;54:585-592.

To obtain insight into the relative contributions of exercise and occlusive stimuli to these muscular adaptations, the present study investigated the short- and long-term effects of varied combinations of low-intensity exercise and vascular occlusion. The subjects were separated into 3 groups (n = 6 for each group): low-intensity with vascular occlusion (LIO), low-intensity without vascular occlusion (LI), and vascular occlusion without exercise (VO). LIO and LI groups performed bilateral knee extension exercises in seated positions with an isotonic extension machine. In the LIO group, both sides of the thigh were pressure-occluded at the proximal end by means of a tourniquet during the entire session of exercise (approximately 10 min), whereas only the occlusion with the same pressure and duration was given in the VO group. The mean occlusion pressure was 218 +/- 8.1 mmHg (mean +/- SE). The exercise session consisted of five sets of exercise at an intensity of 10-20% 1RM and was performed twice a week for 8 wk. After the period of exercise training, isometric and isokinetic strengths at all velocities examined increased significantly in the LIO group (p < 0.05), whereas no significant change in strength was seen in the LI and VO groups. The increase in muscular strength in LIO was associated with a significant increase in the cross-sectional area of knee extensor muscles by 10.3 +/- 1.6%. The plasma growth hormone concentration measured 15 min after the session of exercise showed a marked increase only in LIO. The results showed that the low-intensity exercise and occlusive stimuli have cooperative effects in the long-term adaptation of muscle and an acute response to growth hormone.

-------------

In the above case, neither the resistance training stimulus nor vascular occlusion alone were sufficient to produce muscle growth, but combined, they did. JUST A LITTLE TENSION in combination with occlusion produced muscle growth - and a 10% increase in CSA in just 8 weeks is A LOT.

Although I've never seen a direct test of DC training sans stretching in the literature, I also haven't seen a direct study demonstrating that it will not stimulate skeletal muscle growth. Perhaps the stretching isn't about fascial manipulation per se, but rather about the vascular occlusion that occurs under tension during the stretch (per the above study)?... Food for thought... (And yes, I do recognize that the above study used isotonic contractions not isometrics as in DC training, but as the above study shows, and you and I are aware, neither isometric contractions nor isotonic training with <20%1RM will produce substantial muscle growth in non-pathological situations.)

Another study that I find interesting:

The same group of researchers has studied vascular occlusion per se and found it had an anti-atrophic effect (granted their protocol was a total of 15min / day - FAR from a single DC stretch). Prevention of atrophy is of course also found with fixation in a stretched position (again long term studies). OTOH, its fairly certain that weighted stretch models produce ischemia at least at the initiation of the protocol and gene expression is turned on pretty rapidly on those models. (Again, maybe there's something to this ischemia thing...)

1. Takarada Y, Takazawa H, Ishii N. Applications of vascular occlusion diminish disuse atrophy of knee extensor muscles. Med Sci Sports Exerc 2000;32:2035-2039.

PURPOSE: We have previously shown that the combination of low-intensity resistive exercise and moderate vascular occlusion induces in humans a marked increase in growth hormone secretion and muscular hypertrophy. The present study investigated the effects of vascular occlusion on the size of thigh muscles in patients who underwent an operation for the reconstruction of the anterior cruciate ligament to see whether it attenuates the disuse muscular atrophy without any exercise combined. METHODS: Two sessions of occlusive stimulus, each consisting of five repetitions of vascular occlusion (mean maximal pressure, 238 mm Hg) for 5 min and the release of occlusion for 3 min, were applied daily to the proximal end of the thigh from 3rd to 14th days after the operation. Changes in the cross-sectional area (CSA) of thigh muscles were analyzed with magnetic resonance images taken on the 3rd and 14th day after the operation. RESULTS: Without occlusive stimulus (control), the CSAs of knee extensors and flexors decreased by 20.7 +/- 2.2% and 11.3 +/- 2.6% (mean +/- SEM, N = 8), whereas with the occlusive stimulus, they decreased by 9.4 +/- 1.6% and 9.2 +/- 2.6% (N = 8), respectively. The relative decrease in CSA of knee extensors was significantly (P < 0.05) larger in the control group than in the experimental group. CONCLUSION: The results indicate that the occlusive stimulus effectively diminishes the postoperation disuse atrophy of knee extensors.

---------------------

And here's a really nifty one I thought you'd like. The model was not an extreme stretch per se, but a hell of a lot closer that the animal models we've been talking about: Human model, stretch (less than a 30 min bout / day) and the stretch was an intermittent ACTIVE one - under intermittent voluntary tension that persisted until volitional fatigue. Compared to an extreme stretch, the difference was the voluntary force produced, that it was intermittant and the the time under tension was longer.

They found:
-Passive stretch: No increase in protein turnover with the same joint angle (roughly) and duration of stretch.
-ACTIVE stretch: Nearly a 50% increase in muscle protein synthetic rate when an active voluntary contraction was added to the stretch. (Note that the 40% MVC force likely produced significant ischemia / vascular occlusion, as well!)

1. Fowles JR, MacDougall JD, Tarnopolsky MA, Sale DG, Roy BD, Yarasheski KE. The effects of acute passive stretch on muscle protein synthesis in humans. Can J Appl Physiol 2000;25:165-180.

We examined the effect of an isolated bout of maximal tolerated passive stretch on fractional muscle protein synthetic rate in human soleus muscle. Eight healthy males performed two separate trials with the same leg: one session of passive stretch and one of intermittent active isometric contraction at a force equivalent to that which occurred during the passive stretch trial. This force was approximately 40% of maximum voluntary contraction force and produced volitional fatigue in approximately 27 min. Intermittent passive stretch, for the same duration, elicited a 6.1 degrees increase in joint angle (P<.0005) with silent electromyography. Fractional protein synthetic rate from experimental and control soleus in each trial was assessed from biopsy samples over the period 10-22 hr postexercise by the incorporation rate of L-[1-13C] leucine into muscle. Protein synthesis was elevated in the soleus of the exercised leg following the active contraction trial by 49% (P<.05) but not following the passive stretch trial. Results indicate that a single bout of maximal passive stretch does not significantly elevate fractional muscle protein synthetic rate in humans and thus suggests that muscle stretch per se is not the stimulus for the muscle hypertrophy that occurs with resistance training.

--------------------

....Again, I'm in agreement about the lack of direct scientific (peer-reviewed, etc.) evidence. The above is not an attempt to convince you of anything - actually more of an enjoyable exercise on my part to dig in the literature for a little bit and find some new tidbits.

-Scott



ill be back to appraise the papers but for now i will say- greater loads and high forces muscle contractions themselves restrict blood flow similar to occlusion of external manipulation. thus, they would negate any effects. applications and effects of vasular occulsion are likely biased towards untrained subjects with lower loads or intensity.

these applications are still quite interesting in understanding the physiological processes in muscle hypertrophy. be back.

[TPT]

also, im not sure how the previous papers support whether direct or indirect- the effects of fascia stretching. the procedures and mechanisms of occlusion training that increase tension to fasica do not approximate that of fascia stretching of doggycrap and fst7. well, i havent discriminated them.

how are vascular occlusion and extreme stretching similar in effects that they might set the occasion for muscle hypertrophy? in other words, how would the effects of vascular occulsion occur during a stretch? these questions are important as the answeres would validate your arguments further.

[Dr Pangloss]

Dr. P et al.

Here's a post of mine from a thread on another board focusing on the data supporting DC training-style "extreme stretching." I think you might find it interesting.

------------
The thread:

http://www.intensemuscle.com/33935-extreme-stretching-how-effective-really-5.html?

-------------------------

My post (modified slightly to remove out of context comments - it was written to a poster in that thread, not this one or you of course, Dr. P):

-----------------------

The stretch-induced chronic overload literature has poor (if that) external validity in supporting a DC-style extreme stretching. I've read through this thread (albeit cursorily over the past few days), but it seems you're mostly just asking if there are more applicable data to support extreme stretching.

As you've been saying, to do this, the duration (1-2 min) and tensile overload would have to be equivalent, as well as using a human model. Naturally (and I don't recall this being mentioned), it is possible that while an extreme stretching protocol in and of itself might not be a hypertrophic stimulus (in lieu of other exercise), this does not preclude the possibility that there could be an *interaction* between the resistance exercise stimulus and that of an extreme stretch such that adding the stretching enhances the growth adaptation.

For example here is a study which supports the above notion (of an experimental interaction of a treatment without a main effect of that treatment in isolation). You might also say that this study could lend support to the notion that small "doses" of tension and vascular occlusion (as in extreme stretching) may produce hypertrophy.
-------------------
1. Takarada Y, Tsuruta T, Ishii N. Cooperative effects of exercise and occlusive stimuli on muscular function in low-intensity resistance exercise with moderate vascular occlusion. Jpn J Physiol 2004;54:585-592.

To obtain insight into the relative contributions of exercise and occlusive stimuli to these muscular adaptations, the present study investigated the short- and long-term effects of varied combinations of low-intensity exercise and vascular occlusion. The subjects were separated into 3 groups (n = 6 for each group): low-intensity with vascular occlusion (LIO), low-intensity without vascular occlusion (LI), and vascular occlusion without exercise (VO). LIO and LI groups performed bilateral knee extension exercises in seated positions with an isotonic extension machine. In the LIO group, both sides of the thigh were pressure-occluded at the proximal end by means of a tourniquet during the entire session of exercise (approximately 10 min), whereas only the occlusion with the same pressure and duration was given in the VO group. The mean occlusion pressure was 218 +/- 8.1 mmHg (mean +/- SE). The exercise session consisted of five sets of exercise at an intensity of 10-20% 1RM and was performed twice a week for 8 wk. After the period of exercise training, isometric and isokinetic strengths at all velocities examined increased significantly in the LIO group (p < 0.05), whereas no significant change in strength was seen in the LI and VO groups. The increase in muscular strength in LIO was associated with a significant increase in the cross-sectional area of knee extensor muscles by 10.3 +/- 1.6%. The plasma growth hormone concentration measured 15 min after the session of exercise showed a marked increase only in LIO. The results showed that the low-intensity exercise and occlusive stimuli have cooperative effects in the long-term adaptation of muscle and an acute response to growth hormone.

-------------

In the above case, neither the resistance training stimulus nor vascular occlusion alone were sufficient to produce muscle growth, but combined, they did. JUST A LITTLE TENSION in combination with occlusion produced muscle growth - and a 10% increase in CSA in just 8 weeks is A LOT.

Although I've never seen a direct test of DC training sans stretching in the literature, I also haven't seen a direct study demonstrating that it will not stimulate skeletal muscle growth. Perhaps the stretching isn't about fascial manipulation per se, but rather about the vascular occlusion that occurs under tension during the stretch (per the above study)?... Food for thought... (And yes, I do recognize that the above study used isotonic contractions not isometrics as in DC training, but as the above study shows, and you and I are aware, neither isometric contractions nor isotonic training with <20%1RM will produce substantial muscle growth in non-pathological situations.)

Another study that I find interesting:

The same group of researchers has studied vascular occlusion per se and found it had an anti-atrophic effect (granted their protocol was a total of 15min / day - FAR from a single DC stretch). Prevention of atrophy is of course also found with fixation in a stretched position (again long term studies). OTOH, its fairly certain that weighted stretch models produce ischemia at least at the initiation of the protocol and gene expression is turned on pretty rapidly on those models. (Again, maybe there's something to this ischemia thing...)

1. Takarada Y, Takazawa H, Ishii N. Applications of vascular occlusion diminish disuse atrophy of knee extensor muscles. Med Sci Sports Exerc 2000;32:2035-2039.

PURPOSE: We have previously shown that the combination of low-intensity resistive exercise and moderate vascular occlusion induces in humans a marked increase in growth hormone secretion and muscular hypertrophy. The present study investigated the effects of vascular occlusion on the size of thigh muscles in patients who underwent an operation for the reconstruction of the anterior cruciate ligament to see whether it attenuates the disuse muscular atrophy without any exercise combined. METHODS: Two sessions of occlusive stimulus, each consisting of five repetitions of vascular occlusion (mean maximal pressure, 238 mm Hg) for 5 min and the release of occlusion for 3 min, were applied daily to the proximal end of the thigh from 3rd to 14th days after the operation. Changes in the cross-sectional area (CSA) of thigh muscles were analyzed with magnetic resonance images taken on the 3rd and 14th day after the operation. RESULTS: Without occlusive stimulus (control), the CSAs of knee extensors and flexors decreased by 20.7 +/- 2.2% and 11.3 +/- 2.6% (mean +/- SEM, N = 8), whereas with the occlusive stimulus, they decreased by 9.4 +/- 1.6% and 9.2 +/- 2.6% (N = 8), respectively. The relative decrease in CSA of knee extensors was significantly (P < 0.05) larger in the control group than in the experimental group. CONCLUSION: The results indicate that the occlusive stimulus effectively diminishes the postoperation disuse atrophy of knee extensors.

---------------------

And here's a really nifty one I thought you'd like. The model was not an extreme stretch per se, but a hell of a lot closer that the animal models we've been talking about: Human model, stretch (less than a 30 min bout / day) and the stretch was an intermittent ACTIVE one - under intermittent voluntary tension that persisted until volitional fatigue. Compared to an extreme stretch, the difference was the voluntary force produced, that it was intermittant and the the time under tension was longer.

They found:
-Passive stretch: No increase in protein turnover with the same joint angle (roughly) and duration of stretch.
-ACTIVE stretch: Nearly a 50% increase in muscle protein synthetic rate when an active voluntary contraction was added to the stretch. (Note that the 40% MVC force likely produced significant ischemia / vascular occlusion, as well!)

1. Fowles JR, MacDougall JD, Tarnopolsky MA, Sale DG, Roy BD, Yarasheski KE. The effects of acute passive stretch on muscle protein synthesis in humans. Can J Appl Physiol 2000;25:165-180.

We examined the effect of an isolated bout of maximal tolerated passive stretch on fractional muscle protein synthetic rate in human soleus muscle. Eight healthy males performed two separate trials with the same leg: one session of passive stretch and one of intermittent active isometric contraction at a force equivalent to that which occurred during the passive stretch trial. This force was approximately 40% of maximum voluntary contraction force and produced volitional fatigue in approximately 27 min. Intermittent passive stretch, for the same duration, elicited a 6.1 degrees increase in joint angle (P<.0005) with silent electromyography. Fractional protein synthetic rate from experimental and control soleus in each trial was assessed from biopsy samples over the period 10-22 hr postexercise by the incorporation rate of L-[1-13C] leucine into muscle. Protein synthesis was elevated in the soleus of the exercised leg following the active contraction trial by 49% (P<.05) but not following the passive stretch trial. Results indicate that a single bout of maximal passive stretch does not significantly elevate fractional muscle protein synthetic rate in humans and thus suggests that muscle stretch per se is not the stimulus for the muscle hypertrophy that occurs with resistance training.

--------------------

....Again, I'm in agreement about the lack of direct scientific (peer-reviewed, etc.) evidence. The above is not an attempt to convince you of anything - actually more of an enjoyable exercise on my part to dig in the literature for a little bit and find some new tidbits.

-Scott


Yeah i checked out a lot of studies on stretching. You found one i didnt see however--the active flexing with stretch (which i dont believe anyone does)

Stretching definitely works in some laboratory paradigms, but they seem to be unnaturally long, which in my book made them only amenable to the effects of site-enhancement oil.

I think the vascular occlusion stuff is frankly unwise for one simple reason. About 10% of whites exhibit accelerated clotting due to genetic variations in several genes. This kind of thing would put people at risk of deep vein thrombosis.

I'm fascinated that there are any effects on muscle though.

[Scott Stevenson]

also, im not sure how the previous papers support whether direct or indirect- the effects of fascia stretching. the procedures and mechanisms of occlusion training that increase tension to fasica do not approximate that of fascia stretching of doggycrap and fst7. well, i havent discriminated them.

Check the start of my post - the papers are in the context of DC training-style extreme stretching. The point I'm making is that in an attempt to produce a facial stretch ala DC training, there is also vascular occlusion, which may have an effect on muscle growth in and of itself.



how are vascular occlusion and extreme stretching similar in effects that they might set the occasion for muscle hypertrophy? in other words, how would the effects of vascular occulsion occur during a stretch?


Extreme stretching causes vascular occlusion.

-S

[Scott Stevenson]

Yeah i checked out a lot of studies on stretching. You found one i didnt see however--the active flexing with stretch (which i dont believe anyone does)

Stretching definitely works in some laboratory paradigms, but they seem to be unnaturally long, which in my book made them only amenable to the effects of site-enhancement oil.

Agreed, as I note as well.


I think the vascular occlusion stuff is frankly unwise for one simple reason. About 10% of whites exhibit accelerated clotting due to genetic variations in several genes. This kind of thing would put people at risk of deep vein thrombosis.

I'm fascinated that there are any effects on muscle though.

In those with the clotting features you refer too, does this show up with a PT, PTT, etc.?...

Would these folks be at risk in doing, let's say, yoga or a DC style extreme stretch lasting for 1-2 min?...

-S

[Dr Pangloss]

Agreed, as I note as well.



In those with the clotting features you refer too, does this show up with a PT, PTT, etc.?...

Would these folks be at risk in doing, let's say, yoga or a DC style extreme stretch lasting for 1-2 min?...

-S


doesnt necessarily show up with prothrombin time. Jeez bro. starting to think you're a doc or a med student.

most common variant is factor V leiden. Factor V has a variation that takes out a thrombin site that would normally stop it from promoting clot growth.

factor v leiden is present in 5-10% of the population. In minneapolis probably 10%. In new orleans, maybe 1%.

there are other variants that promote clotting as well, but not as common as fVL.

as for the last questions, the overriding factor is immobilization. I think most of those things are ok if they're short-lived.

[natron]

Very interesting,

wish I could chime in, but this is over my head!

learning though

[TPT]

Check the start of my post - the papers are in the context of DC training-style extreme stretching. The point I'm making is that in an attempt to produce a facial stretch ala DC training, there is also vascular occlusion, which may have an effect on muscle growth in and of itself.




Extreme stretching causes vascular occlusion.

-S



i see that as well. however, the processes of reduced blood flow and proposed muscle hypertrophy are different for the two.

[Tatyana]

Agreed, as I note as well.



In those with the clotting features you refer too, does this show up with a PT, PTT, etc.?...

Would these folks be at risk in doing, let's say, yoga or a DC style extreme stretch lasting for 1-2 min?...

-S


Not necessarily.

I am homozygous for the MTHFR mutation which indicates thrombophilia, and my coagulation profile is normal.

It is estimated that 30% of the population has this mutation, and it is only recently discovered.

Coagulation is phenomenally complicated, there are several biochemical cascades of enzymes and clotting factors with quite a few odd polymorphisms.

[TPT]

Yeah i checked out a lot of studies on stretching. You found one i didnt see however--the active flexing with stretch (which i dont believe anyone does)

Stretching definitely works in some laboratory paradigms, but they seem to be unnaturally long, which in my book made them only amenable to the effects of site-enhancement oil.

I think the vascular occlusion stuff is frankly unwise for one simple reason. About 10% of whites exhibit accelerated clotting due to genetic variations in several genes. This kind of thing would put people at risk of deep vein thrombosis.

I'm fascinated that there are any effects on muscle though.



it might have great applications to rehab and people with history of injuries. as you eluded to, any occlusion might be contraindicated for those with history of vascular diseases including diabetics.

[Dr Pangloss]

Not necessarily.

I am homozygous for the MTHFR mutation which indicates thrombophilia, and my coagulation profile is normal.

It is estimated that 30% of the population has this mutation, and it is only recently discovered.

Coagulation is phenomenally complicated, there are several biochemical cascades of enzymes and clotting factors with quite a few odd polymorphisms.


I'm heterozygous for Factor V Leiden. i have had deep vein thrombosis. Some of these thrombophillic mutations like FVL have been positively selected for in the past for a number of reasons.

Now it just seems to be a problem.

[Scott Stevenson]

i see that as well. however, the processes of reduced blood flow and proposed muscle hypertrophy are different for the two.

TPT,

Not quite following you here....


doesnt necessarily show up with prothrombin time. Jeez bro. starting to think you're a doc or a med student.

LOL - Not too far off...



as for the last questions, the overriding factor is immobilization. I think most of those things are ok if they're short-lived.

I can see that. The reactive hyperemia after stopping a high tension stretch is probably advantageous for minimizing clot formation (limiting pooling of blood) as well.

-S

[TPT]

TPT,

Not quite following you here....

-S


ahhh...you do post here. : )

i am suggesting that relative to the processes of vascular occlusion- the consequences of occlusion training cannot be generalized to dc fascia stretching.