scholarly journals Blood Flow Restriction during Low-Intensity Resistance Exercise Increases Muscle Protein Synthesis through the mTOR Signaling Pathway

2007 ◽  
Vol 39 (Supplement) ◽  
pp. S36
Author(s):  
Satoshi Fujita ◽  
Takashi Abe ◽  
Micah J. Drummond ◽  
Jerson G. Cadenas ◽  
Hans C. Dreyer ◽  
...  
2012 ◽  
Vol 112 (9) ◽  
pp. 1520-1528 ◽  
Author(s):  
David M. Gundermann ◽  
Christopher S. Fry ◽  
Jared M. Dickinson ◽  
Dillon K. Walker ◽  
Kyle L. Timmerman ◽  
...  

Blood flow restriction (BFR) to contracting skeletal muscle during low-intensity resistance exercise training increases muscle strength and size in humans. However, the mechanism(s) underlying these effects are largely unknown. We have previously shown that mammalian target of rapamycin complex 1 (mTORC1) signaling and muscle protein synthesis (MPS) are stimulated following an acute bout of BFR exercise. The purpose of this study was to test the hypothesis that reactive hyperemia is the mechanism responsible for stimulating mTORC1 signaling and MPS following BFR exercise. Six young men (24 ± 2 yr) were used in a randomized crossover study consisting of two exercise trials: low-intensity resistance exercise with BFR (BFR trial) and low-intensity resistance exercise with sodium nitroprusside (SNP), a pharmacological vasodilator infusion into the femoral artery immediately after exercise to simulate the reactive hyperemia response after BFR exercise (SNP trial). Postexercise mixed-muscle fractional synthetic rate from the vastus lateralis increased by 49% in the BFR trial ( P < 0.05) with no change in the SNP trial ( P > 0.05). BFR exercise increased the phosphorylation of mTOR, S6 kinase 1, ribosomal protein S6, ERK1/2, and Mnk1-interacting kinase 1 ( P < 0.05) with no changes in mTORC1 signaling in the SNP trial ( P > 0.05). We conclude that reactive hyperemia is not a primary mechanism for BFR exercise-induced mTORC1 signaling and MPS. Further research is necessary to elucidate the cellular mechanism(s) responsible for the increase in mTOR signaling, MPS, and hypertrophy following acute and chronic BFR exercise.


2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Christopher S Fry ◽  
Erin L Glynn ◽  
Micah J Drummond ◽  
Kyle L Timmerman ◽  
Satoshi Fujita ◽  
...  

2007 ◽  
Vol 103 (3) ◽  
pp. 903-910 ◽  
Author(s):  
Satoshi Fujita ◽  
Takashi Abe ◽  
Micah J. Drummond ◽  
Jerson G. Cadenas ◽  
Hans C. Dreyer ◽  
...  

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). Ribosomal 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.


2007 ◽  
Vol 39 (Supplement) ◽  
pp. S82-S83
Author(s):  
Hans C. Dreyer ◽  
Micah J. Drummond ◽  
Satoshi Fujita ◽  
Erin L. Glynn ◽  
Bart Pennings ◽  
...  

2010 ◽  
Vol 108 (5) ◽  
pp. 1199-1209 ◽  
Author(s):  
Christopher S. Fry ◽  
Erin L. Glynn ◽  
Micah J. Drummond ◽  
Kyle L. Timmerman ◽  
Satoshi Fujita ◽  
...  

The loss of skeletal muscle mass during aging, sarcopenia, increases the risk for falls and dependence. Resistance exercise (RE) is an effective rehabilitation technique that can improve muscle mass and strength; however, older individuals are resistant to the stimulation of muscle protein synthesis (MPS) with traditional high-intensity RE. Recently, a novel rehabilitation exercise method, low-intensity RE, combined with blood flow restriction (BFR), has been shown to stimulate mammalian target of rapamycin complex 1 (mTORC1) signaling and MPS in young men. We hypothesized that low-intensity RE with BFR would be able to activate mTORC1 signaling and stimulate MPS in older men. We measured MPS and mTORC1-associated signaling proteins in seven older men (age 70 ± 2 yr) before and after exercise. Subjects were studied identically on two occasions: during BFR exercise [bilateral leg extension exercise at 20% of 1-repetition maximum (1-RM) with pressure cuff placed proximally on both thighs and inflated at 200 mmHg] and during exercise without the pressure cuff (Ctrl). MPS and phosphorylation of signaling proteins were determined on successive muscle biopsies by stable isotopic techniques and immunoblotting, respectively. MPS increased 56% from baseline after BFR exercise ( P < 0.05), while no change was observed in the Ctrl group ( P > 0.05). Downstream of mTORC1, ribosomal S6 kinase 1 (S6K1) phosphorylation and ribosomal protein S6 (rpS6) phosphorylation increased only in the BFR group after exercise ( P < 0.05). We conclude that low-intensity RE in combination with BFR enhances mTORC1 signaling and MPS in older men. BFR exercise is a novel intervention that may enhance muscle rehabilitation to counteract sarcopenia.


2011 ◽  
Vol 301 (5) ◽  
pp. E873-E881 ◽  
Author(s):  
Yu Chen ◽  
Sumita Sood ◽  
Kevin McIntire ◽  
Richard Roth ◽  
Ralph Rabkin

The branched-chain amino acid leucine stimulates muscle protein synthesis in part by directly activating the mTOR signaling pathway. Furthermore, leucine, if given in conjunction with resistance exercise, enhances the exercise-induced mTOR signaling and protein synthesis. Here we tested whether leucine can activate the mTOR anabolic signaling pathway in uremia and whether it can enhance work overload (WO)-induced signaling through this pathway. Chronic kidney disease (CKD) and control rats were studied after 7 days of surgically induced unilateral plantaris muscle WO and a single leucine or saline load. In the basal state, 4E-BP1 phosphorylation was modestly depressed in non-WO muscle of CKD rats, whereas rpS6 phosphorylation was nearly completely suppressed. After oral leucine mTOR, S6K1 and rpS6 phosphorylation increased similarly in both groups, whereas the phospho-4E-BP1 response was modestly attenuated in CKD. WO alone activated the mTOR signaling pathway in control and CKD rats. In WO CKD, muscle leucine augmented mTOR and 4E-BP1 phosphorylation, but its effect on S6K1 phosphorylation was attenuated. Taken together, this study has established that the chronic uremic state impairs basal signaling through the mTOR anabolic pathway, an abnormality that may contribute to muscle wasting. However, despite this abnormality, leucine can stimulate this signaling pathway in CKD, although its effectiveness is partially attenuated, including in skeletal muscle undergoing sustained WO. Thus, although there is some resistance to leucine in CKD, the data suggest a potential role for leucine-rich supplements in the management of uremic muscle wasting.


2010 ◽  
Vol 42 ◽  
pp. 740
Author(s):  
Haruhiko Madarame ◽  
Miwa Kurano ◽  
Haruhito Takano ◽  
Haruko Iida ◽  
Yoshiaki Sato ◽  
...  

2019 ◽  
Vol 12 (23) ◽  
pp. 11-15
Author(s):  
Tiberiu Puta ◽  
Alexandra Mihaela Stănilă ◽  
Remus Datcu

AbstractIntroduction: The blood flow restriction method is a training method that is based on the partial occlusion of circulation during a workout. This technique combines low-intensity exercise with the occlusion of the bloodstream which produces results similar to high-intensity training.Aim: We aimed to identify the areas in which this method is applicable, its potential benefits and effects, recommendations regarding the rules of use for maximal effects (dosage, intensity, etc.), and also possible contraindications or warnings regarding the use of this method.Methods: We have analyzed a number of 20 articles on this topic from the field literature of the last 10 years, using ”google academic” as a search engine.Results: After this study we concluded that blood flow restriction is a method with wide applicability in the field of sports training, but also in the recovery process; however, it requires attention in choosing the necessary equipment. For healthy individuals, best training adaptations occur when combining low-load blood flow restriction resistance exercise with traditional high-load resistance exercise.Conclusion: Low-intensity resistance exercise with blood flow restriction is as effective as high-intensity training (for strength and muscle mass gains), but only the high-intensity protocol promotes significant hypotensive responses after exercise.


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