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1 Internal Medicine, University of Texas Medical Branch, Galveston, Texas, United States; Human and Engineered Environment, Graduate School of Frontier Sciences, University of Tokyo, Tokyo, Texas, Japan
2 Human and Engineered Environment, Graduate School of Frontier Sciences, University of Tokyo, Tokyo, Japan
3 Physical Therapy, University of Texas Medical Branch, Galveston, Texas, United States
4 Internal Medicine, University of Texas Medical Branch, Galveston, Texas, United States
5 Internal Medicine - Geriatrics, University of Texas Medical Branch, Galveston, Texas, United States
* To whom correspondence should be addressed. E-mail: safujita{at}gmail.com.
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 the mTOR signaling pathway is involved in the increase in muscle protein synthesis 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 muscle protein synthesis (MPS). We measured MPS and phosphorylation status of mTOR-associated signaling proteins in 6 young male subjects. Subjects were studied once during blood flow restriction (REFR, bilateral leg extension exercise at 20% of 1-RM while a pressure cuff was placed on the proximal end of both thighs and inflated at 200mmHg) and a second time using the same exercise protocol but without the pressure cuff (CTRL). MPS in the vastus lateralis muscle was measured by using stable isotope techniques and the phosphorylation status of signaling proteins were determined by immunoblotting. Blood lactate, cortisol, and growth hormone were higher following REFR as compared to CTRL (P<0.05). S6K1 phosphorylation, a downstream target of mTOR, increased concurrently with a decreased eEF2 phosphorylation and a 46% increase in MPS following REFR (P<0.05). MPS and S6K1 phosphorylation were unchanged in the CTRL group post-exercise. We conclude that the activation of the mTOR signaling pathway appears to be an important cellular mechanism which may help explain the enhanced muscle protein synthesis during REFR.
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