Light weights.... RESTRICTED blood flow.... bigger gains?

[NO HYPE]

1: J Appl Physiol. 2007 Sep;103(3):903-10. Epub 2007 Jun 14. Links

Blood flow restriction during low-intensity resistance exercise increases S6K1 phosphorylation and muscle protein synthesis.

Low-intensity resistance exercise training combined with blood flow restriction (REFR) increases muscle size and strength as much as conventional resistance exercise with high loads. However, the cellular mechanism(s) underlying the hypertrophy and strength gains induced by REFR are unknown. We have recently shown that both the mammalian target of rapamycin (mTOR) signaling pathway and muscle protein synthesis (MPS) were stimulated after an acute bout of high-intensity resistance exercise in humans. Therefore, we hypothesized that an acute bout of REFR would enhance mTOR signaling and stimulate MPS. We measured MPS and phosphorylation status of mTOR-associated signaling proteins in six young male subjects. Subjects were studied once during blood flow restriction (REFR, bilateral leg extension exercise at 20% of 1 repetition maximum while a pressure cuff was placed on the proximal end of both thighs and inflated at 200 mmHg) and a second time using the same exercise protocol but without the pressure cuff [control (Ctrl)]. MPS in the vastus lateralis muscle was measured by using stable isotope techniques, and the phosphorylation status of signaling proteins was determined by immunoblotting. Blood lactate, cortisol, and growth hormone were higher following REFR compared with Ctrl (P < 0.05). Ribo****l S6 kinase 1 (S6K1) phosphorylation, a downstream target of mTOR, increased concurrently with a decreased eukaryotic translation elongation factor 2 (eEF2) phosphorylation and a 46% increase in MPS following REFR (P < 0.05). MPS and S6K1 phosphorylation were unchanged in the Ctrl group postexercise. We conclude that the activation of the mTOR signaling pathway appears to be an important cellular mechanism that may help explain the enhanced muscle protein synthesis during REFR. http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum



Maybe we should put down the NO products.... and hold our breath at the gym?



1: J Physiol. 2007 Jul 15;582(Pt 2):813-23. Epub 2007 May 3. Links

Nutrient signalling in the regulation of human muscle protein synthesis.

The mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) are important nutrient- and energy-sensing and signalling proteins in skeletal muscle. AMPK activation decreases muscle protein synthesis by inhibiting mTOR signalling to regulatory proteins associated with translation initiation and elongation. On the other hand, essential amino acids (leucine in particular) and insulin stimulate mTOR signalling and protein synthesis. We hypothesized that anabolic nutrients would be sensed by both AMPK and mTOR, resulting in an acute and potent stimulation of human skeletal muscle protein synthesis via enhanced translation initiation and elongation. We measured muscle protein synthesis and mTOR-associated upstream and downstream signalling proteins in young male subjects (n=14) using stable isotopic and immunoblotting techniques. Following a first muscle biopsy, subjects in the 'Nutrition' group ingested a leucine-enriched essential amino acid-carbohydrate mixture (EAC). Subjects in the Control group did not consume nutrients. A second biopsy was obtained 1 h later. Ingestion of EAC significantly increased muscle protein synthesis, modestly reduced AMPK phosphorylation, and increased Akt/PKB (protein kinase B) and mTOR phosphorylation (P<0.05). mTOR signalling to its downstream effectors (S6 kinase 1 (S6K1) and 4E-binding protein 1 (4E-BP1) phosphorylation status) was also increased (P<0.05). In addition, eukaryotic elongation factor 2 (eEF2) phosphorylation was significantly reduced (P<0.05). Protein synthesis and cell signalling (phosphorylation status) was unchanged in the control group (P>0.05). We conclude that anabolic nutrients alter the phosphorylation status of both AMPK- and mTOR-associated signalling proteins in human muscle, in association with an increase in protein synthesis not only via enhanced translation initiation but also through signalling promoting translation elongation. http://www.ncbi.nlm.nih.gov/sites/en...RVAbstractPlus



So now I'm curious.... how can we further limit the AMPK-induced inhibition of mTOR phosphorylation?

What are the negatives of over-inhibiting AMPK phosphorylation during skeletal muscle contraction, since it plays a significant role in skeletal muscle homeostasis?

Now if significant AMPK inhibition during exercise is not a wise approach (which I have a feeling it might not be), then how can we further limit the AMPK-induced inhibition of mTOR phosphorylation, thereby resulting in a significant enhancement in protein synthesis?

[leonidas300]

I saw some studies about this coming out of Japan where they would use tourniquets to restrict blood flow to the muscle and the gains in muscular size were quite pronounced. I have heard that in some gyms in Japan they are already implementing this while lifting light weights. I fail to comprehend how you could use this technique for your chest.

[NO HYPE]

I saw some studies about this coming out of Japan where they would use tourniquets to restrict blood flow to the muscle and the gains in muscular size were quite pronounced. I have heard that in some gyms in Japan they are already implementing this while lifting light weights.

Interesting.

In any case.... a 46% increase in MPS vs 0% increase in control, is rather impressive.

I fail to comprehend how you could use this technique for your chest.

Hypothetically speaking, I would think that restriction of blood flow to the pecs could be accomplished with a rubber-like tourniquet placed on the top portion of the shoulder, then around the bottom portion of the armpit and tied at the top (I am NOT recommending this technique... just entertaining the thought).

[NO HYPE]

So now I'm curious.... how can we further limit the AMPK-induced inhibition of mTOR phosphorylation?

What are the negatives of over-inhibiting AMPK phosphorylation during skeletal muscle contraction, since it plays a significant role in skeletal muscle homeostasis?

Now if significant AMPK inhibition during exercise is not a wise approach (which I have a feeling it might not be), then how can we further limit the AMPK-induced inhibition of mTOR phosphorylation, thereby resulting in a significant enhancement in protein synthesis?

.... Any thoughts?

[bigmanwalking]

.... Any thoughts?

How long until they start peeing dark brown?

[Skigazzi]

I read something along these lines with leg training, and the results were good.

Everyone is gonna be looking like the ultimate warrior at the gym with their arms all tied up with bandanna's and stuff...

[DRP7]

... I fail to comprehend how you could use this technique for your chest.

Hypothetically speaking, I would think that restriction of blood flow to the pecs could be accomplished with a rubber-like tourniquet placed on the top portion of the shoulder, then around the bottom portion of the armpit and tied at the top (I am NOT recommending this technique... just entertaining the thought).

just rub a good vasoconstrictor onto your chest (e.g. some *******) and there you go with restricted blood flow. j/k


P.S.: good thread, NO HYPE!

[Dr.Dave1]

Maybe we should put down the NO products.... and hold our breath at the gym?

interesting stuff . . . check out a thread I started on this very topic a while back, it contains some related studieshttp://forum.bodybuilding.com/showthread.php?t=750704

[vegasdsm]

Everyone is gonna be looking like the ultimate warrior at the gym with their arms all tied up with bandanna's and stuff...

nice....

[5Six]

This is interesting, I must say.

Edit: NO HYPE (I really need to know your name. I hate calling people by their screen name) if you want me to grab you the studies, let me know.

[NO HYPE]

Edit: NO HYPE (I really need to know your name. I hate calling people by their screen name) if you want me to grab you the studies, let me know.

It's Tim.... and the full versions are ALWAYS welcomed.

[5Six]

Aights, Tim. If I can get access to 'em, I will have them up in maybe 15 min.

[5Six]

1. blood flow restriction during low-inensity resistance exercise.pdf

2. 2. nutrient signalling in the regulation of human muscle protein synthesis.pdf

[Jules Verne]

I don't remember the authors name, but in a t-nation article he suggested inseat of using a torinquet, to simply do a low weight but high rep set as the last set. This would have a similar effect but (I think) keeping the muscle under tension.

The idea was interesting enouugh (and my lack of any real epxlanation) that it shouuld probably be linked to in this thread. It seemed like a better proposition than tying stuff aroound ones body.

It was fairly reecent.

[in10city]

I don't remember the authors name, but in a t-nation article he suggested inseat of using a torinquet, to simply do a low weight but high rep set as the last set. This would have a similar effect but (I think) keeping the muscle under tension.

The idea was interesting enouugh (and my lack of any real epxlanation) that it shouuld probably be linked to in this thread. It seemed like a better proposition than tying stuff aroound ones body.

It was fairly reecent.

Probably this one: http://www.t-nation.com/readTopic.do?id=1633676

Regardless, you'll get better constant occlusion by holding a contracted / semi-contracted (static) position or by pulsing at the contracted position.

[ksamurai]

Pseudoephedrine a couple hours pre-WO? Wouldn't use it more than once or twice a week though...

[Autobody]

Researchers Solve a Molecular Mystery in Muscle

ScienceDaily (Mar. 15, 2010) — The muscle-building abilities of hormones known as insulin-like growth factors (IGFs) are legendary. Just do an online search and you'll find not only scientific papers discussing the effects of IGFs on the cells that give rise to muscle tissue, but also scores of ads touting the purported benefits of IGF supplements for bodybuilding.

But in spite of widespread interest in these potent molecules, key details about how IGFs work on muscle cells have been lacking.

A research by a team led by University of Michigan molecular biologist Cunming Duan has cleared up a longstanding mystery about the workings of IGFs. The team's findings, scheduled to be published online in the Proceedings of the National Academy of Sciences, could lead to new treatments for muscle-wasting diseases and new ways of preventing the muscle loss that accompanies aging.

And because IGFs also are implicated in the growth and spread of malignant tumors, the new insights may have implications in cancer biology.

Like other peptide and protein hormones, IGFs work by binding to receptors on the cells they target. The binding then sets off a cascade of reactions that ultimately direct the cell to do something. You might think that a given hormone, binding to a particular receptor, would always elicit the same response from the cell, but that's not what happens in the case of IGF and myoblasts (immature cells that develop into muscle tissue).

During muscle formation, the binding of IGF to its receptor can prompt either of two very different responses in myoblasts, said Duan, a professor in the Department of Molecular, Cellular and Developmental Biology. Some of the cells are stimulated to divide, while others interpret the very same signal as an order to differentiate (become specialized).

"These are opposite and mutually exclusive cellular events -- once a muscle cell divides, it can't differentiate, and once it differentiates, it can never divide again," Duan said. How activation of the same receptor by the same hormone can elicit two such distinctly different responses has been one of the most puzzling questions about IGF, but Duan and colleagues have found the answer.

"The myoblasts' response is controlled by oxygen availability," said Duan. When oxygen levels are normal, IGF promotes muscle cell differentiation; when oxygen levels are below normal, IGF promotes muscle cell division. Teasing out the molecular details, the researchers discovered that low oxygen activates an intermediary called the HIF-1 complex, which reprograms the cascade of steps that ultimately controls the cell's response.

The findings not only reveal how muscle cells respond to varying oxygen levels during normal development, but also have implications for human disease, Duan said. "For example, a major reason that muscle atrophy occurs as people get older is that the IGF signal gets weaker. If we can find a way to affect IGF signaling, we may be able to stop or reverse the loss." Although manipulating the oxygen levels in living cells could be difficult, it may be possible to manipulate HIF-1 in ways that would mimic changing oxygen levels.

The work also could help scientists better understand the processes involved in cancer progression and spread. It's known that IGF can promote tumor cell division and survival and also that oxygen levels are often lower in tumor tissue than in normal tissue. Finding the link between IGF activity and oxygen levels may lead to new strategies for cancer treatment.

Duan's coauthors on the paper are former graduate student Hongxia Ren, now a postdoctoral fellow at Columbia University, and Domenico Accili, professor of medicine at Columbia .

The research was funded by the National Institutes of Health, the National Science Foundation and the University of Michigan.

Which leads to the thinking that the "gains" seen in occlusion training (if they occur) come from this mechanism.

^^puts bro cap on~
~~Begin brophesizing.....

So if occlusion training works by lack of oxygen (here is another study
http://www.ncbi.nlm.nih.gov/pubmed/20019623
done by Japanese people looking at katsuu and the MOA for its gains, they found you only need to limit oxygen, they used a machine to limit oxygen levels.)

Do normal workouts follow this theory as well? Does the above apply when thinking of a normal workout looking at things like "Time under tension" so long as a muscle is contracting there is:

a reduction in oxygen -> motor/fiber failure -> recruit more motors -> motor/fiber failure -> IGF-1 swims in and binds, depending on available oxygen, it either Differentiates the muscle tissue (change in fiber type and motor units) or Cell devision (Hypertrophy).

I am probably wrong, but would like to see if the picture can be completed and the studies above accounted for, and perhaps a better way to optimize training.

you may proceed....

[AphtaLyfe]

Wasn't there a study done on isometric vs isotonic lifting? According to the theory presented in the study that the OP posted... isometric exercises would occlude blood flow and encourage hypertrophy/hyperplasia... yet according to the study on isometric vs isotonic I think isotonic exercises were considerably more hypertrophic?

[Autobody]

Wasn't there a study done on isometric vs isotonic lifting? According to the theory presented in the study that the OP posted... isometric exercises would occlude blood flow and encourage hypertrophy/hyperplasia... yet according to the study on isometric vs isotonic I think isometric exercises were considerably more hypertrophic?

I think you just said isometric is more hypertrophic, but isometric is more hypertrophic... i assume you mean the latter to be isotonic is more hypertrophic according to a study, could you post the study?

[AphtaLyfe]

I think you just said isometric is more hypertrophic, but isometric is more hypertrophic... i assume you mean the latter to be isotonic is more hypertrophic according to a study, could you post the study?

Yes sorry, fixed it.

Took me a while to find one, and this one is pretty outdated (and only have access to the abstract)... I'll post another if I find a more current study. (although human physiology probably doesn't change much in 50 years)

http://jap.physiology.org/cgi/content/abstract/11/1/29

"The 24 subjects who performed isotonic exercises showed greater gains in strength and hypertrophy than did the 25 subjects who exercised isometrically."

[dustinlima]

homeostasis is some interesting ****

[scotties123]

i dont get how decreasing nutrient delivery and removal of wastes can help muscle growth

[Autobody]

i dont get how decreasing nutrient delivery and removal of wastes can help muscle growth

Good thing its only very short term. There are a bunch of studies on Katsuu, and occlusion training.

[pitbull14218]

pretty interesting stuff!

[TrueAmateur]

I saw some studies about this coming out of Japan where they would use tourniquets to restrict blood flow to the muscle and the gains in muscular size were quite pronounced. I have heard that in some gyms in Japan they are already implementing this while lifting light weights. I fail to comprehend how you could use this technique for your chest.

I think everything involving gains is moreso about form, like if you naturally flex your chest hard while pushing up or pulling down. I tend to use light weights and go for more reps, more fluid movements, etc. I'm not a pro or anything, but it works 'for me'. I rather be the nicely built guy whom can maneuver well than a huge muscular one that has to turn sideways to get through a doorway, ya know?

[brogaine]

I've gotten good results using this with my bicep training, but you've got to be on the lookout for thrombosis/embolism.