LyleMcD on loaded stretching

Dood

New Member
I came across this over at Avant. Thoughts?

"It takes somwhere between 30 minutes and 8 hours of chronic stretch for any effect to be seen (in terms of stretch induced gene expression for hypertrophy or hyperplasia). All of this idiotic 'do weighted stretch for 30 seconds betwee sets' won't do anything in this regards."

http://forum.avantlabs.com/index.p....ic=6851
 
If mechanical strain is the fundamental cause of hypertrophy (it is), and if loaded stretching induces mechanical strain capable of inducing hypertrophy (I don't see why it couldn't), then I'd have to disagree.
 
On top of what Mikey said, stretch models show the most trauma, causing macrophage increases. Macrophage increases in satellite cell activity is well documented as one of the earliest signs of proliferation. Granted most of the models used are in vitro, but IMHO in vivo stretch models will show the same. I guess Lyle's contention is the dose reponse, which is understandable.
 
[b said:
Quote[/b] (dkm1987 @ May 22 2005,10:48)]I guess Lyle's contention is the dose reponse, which is understandable.
Are you saying you agree with him that a 30 second loaded stretch is useless?
From the book of V: "I think loaded stretches make most sense during negatives. You could use your stretch-point movements and just hold it at the bottom of the negative. This may amount to no more than 10-15 seconds tops."

Or is the length of time less important because you've already been strectching under load with the negative?
 
I guess I find the ongoing controversy with loaded stretches so bewildering given the popularity of flexibility training and plyometrics.

Lyle is correct, in the sense, that if you were to hold muscle fibers in a passive stretch, the response won't be all that significant without a super-lengthy amount of time. However, that is not the actual intent of loaded stretches and other forms of stretch.

LS and PS are methods to trigger the stretch reflex. The stretch reflex causes a neural signal that increases the effective tension. That signal can get very, very high. I read one piece a long time ago where it said that the reflex (albeit in a very extreme reflex reaction) can create a burst double the tension that the muscle was originally producing. Of course, you did that, you also run the risk of producing pulling the muscle and/or surrounding connective tissue. And that is why your PE teacher told you not to bounce while touching your toes.

You basically have two schools with that reflex. Flexibility training teaches you how to relax against the reflex, so your ROM increases. Plyometrics teaches you how to amplify that reflex, so that you produce massive amounts of force.

LS and PS are hypertrophy-specific versions of these two schools. They enable you to effectively use peak tensions that theoretically go beyond 120% of your training 1rm. With a normal weight. Way, way beyond. Moreover, they would be applied at where the muscle is most sensitive to damage, which is through a more stretched range of motion.

The problem with the stretch reflex is exactly the same problems that are in flexibility training and plyo. The reflex resets itself according to the new range of motion and training weight.

So, if you were to do LS, you have to either go longer and longer, or use heavier weight, or go even deeper. The problem with going longer is that, eventually, a relaxation response kicks in, meaning however long you go, the tension will either peak or start to decrease. This is why flexibility training works at all. The conditioning response is similar in behaviour to the RBE.

But, I feel that as long as you progressively load and wait until the 5s or post-5s to implement these stretches, you'll always get a pretty strong reflex response before it doesn't become a useful technique. The key thing here is that the stretch reflex effectively increases the training load. If this reflex is high enough that it exceeds the peak tension generated through an eccentric contraction, then you can say that the LS is the "primary disruptor" for that muscle.

If it doesn't, then well, you've done a static hold with a heavy weight at a stretch. That's pretty good at generating strain too.

In theory, pulses stretches with >100% of 1RM is as high as you can possibly go with producing mechanical strain. It would be like suddenly applying a 300-500lbs bench press onto your muscle for 100millieseconds. Pain! :D

cheers,
Jules
 
[b said:
Quote[/b] (Dood @ May 22 2005,10:02)]
[b said:
Quote[/b] (dkm1987 @ May 22 2005,10:48)]I guess Lyle's contention is the dose reponse, which is understandable.
Are you saying you agree with him that a 30 second loaded stretch is useless?  
From the book of V: "I think loaded stretches make most sense during negatives. You could use your stretch-point movements and just hold it at the bottom of the negative. This may amount to no more than 10-15 seconds tops."
Or is the length of time less important because you've already been strectching under load with the negative?
No, I'm saying that until a definative looks at the dose reponse it hard to say HOW LONG is best. I firmly believe loaded stretches increase the signalling for satellite cell proliferation. From myofibrillar alignment, T-Tubule disruption causing CA2+ reduction, to integrin signalling it all fits loaded stretches very well. The question that remains is how long (in time, they've already looked at length in mm of stretch) of a static stretch is neccesary. Speaking of a dynamic movement, the eccentric portion of the lift has been proven to cause enough disruption to the cell membrane to cause the satellite cell activity, but Vicious' point on myotatic reflex with the pulsed stretches surely would also enact the strain on the cellular level, at least IMHO, so adding a 10 to 30 sec (if you can stand 30 secs) static strech at the end of the movement surely isnt going to hurt and again IMHO would probably help considerably.
 
Just to open old wounds and give Mikeynov some flashbacks,  ;) He brought up this subject a while back and I will post Bryan's comments from that thread
[b said:
Quote[/b] ]    
I think its clear from the whole body of research that the mechanical stimulus of passive stretch does indeed play a role in hypertrophy. Here are a couple of studies unraveling the genetic link between stretch and growth.
1: Kemp TJ, Sadusky TJ, Simon M, Brown R, Eastwood M, Sassoon DA, Coulton GR. Identification of a novel stretch-responsive skeletal muscle gene (Smpx). Genomics. 2001 Mar 15;72(3):260-71.Erratum in: Genomics 2001 Jun 1;74(2):251.
2: Kemp TJ, Sadusky TJ, Saltisi F, Carey N, Moss J, Yang SY, Sassoon DA, Goldspink G, Coulton GR. Identification of Ankrd2, a novel skeletal muscle gene coding for a stretch-responsive ankyrin-repeat protein. Genomics. 2000 Jun 15;66(3):229-41.
I also agree with what Mikey said.
I think I disagree with Lyle in my apraisal of the value of stretch overload research to understand the mechanisms of muscle hypertrophy. Then again, my passion is hypertrophy and I tend to squeeze as much as I can out of all the clues that I find, obvious or obscure.
I do have a few questions about the study he references. For example, although they didn't explore what happened inside the cells, I would be curious to know if there was any effect on gene expression. Is it possible that there was a trend towards hypertrophic gene expression that did not translate immediately into elevated levels of protein synthesis? Was there any impact on satellite cells? Would their results be different after multiple bouts of passive stretch instead of just one?
 
I dug up the thread you referenced and at this point I'm thinking like Mikey:
"In answering the question, what causes a muscle to grow, it seems to be the consensus in this part that 'sufficient' strain borne by the contractile components of muscle tissue kicks off the various processes regulating growth (e.g. MGF leaking out of distorted muscle fiber and so forth, activates nearby satellite cells which then differentiate and donate their nuclei, upregulating the nuclei:volume ratio of the fiber).
Now, as far as I know, this strain is quite simply a product of tension. To me, whether this tension comes from passive stretch, active stretch, or an isotonic contraction, I don't really see the difference, nor do I particularly see how the muscle tissue itself 'knows' anything other than it's being strained sufficiently or not.
As such, why the heck WOULDN'T stretch result in growth in the same way that an isotonic contraction against some weight would? This is really what I don't get."

Thread:
http://www.hypertrophy-specific.com/cgi-bin....+growth
 
[b said:
Quote[/b] (Dood @ May 23 2005,5:55)]I dug up the thread you referenced and at this point I'm thinking like Mikey:
"In answering the question, what causes a muscle to grow, it seems to be the consensus in this part that 'sufficient' strain borne by the contractile components of muscle tissue kicks off the various processes regulating growth (e.g. MGF leaking out of distorted muscle fiber and so forth, activates nearby satellite cells which then differentiate and donate their nuclei, upregulating the nuclei:volume ratio of the fiber).
Now, as far as I know, this strain is quite simply a product of tension. To me, whether this tension comes from passive stretch, active stretch, or an isotonic contraction, I don't really see the difference, nor do I particularly see how the muscle tissue itself 'knows' anything other than it's being strained sufficiently or not.
As such, why the heck WOULDN'T stretch result in growth in the same way that an isotonic contraction against some weight would? This is really what I don't get."
Thread:
http://www.hypertrophy-specific.com/cgi-bin....+growth
I agree with this mikey character too!
 
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