Fascia stretching and muscle growth: Flimsy evidence in support

[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=Dr Pangloss;650276]

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=Dr Pangloss;650276]

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. 1994 May-Jun;22(3):272-9.
Mechanical and biochemical analyses of tibial compartment fascia in chronic compartment syndrome.

Hurschler C, Vanderby R Jr, Martinez DA, Vailas AC, Turnipseed WD.
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-e...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-e...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.