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

Texas A&M University - Galveston, Galveston, Texas, United States
Journal of Applied Physiology (Impact Factor: 3.06). 10/2007; 103(3):903-10. DOI: 10.1152/japplphysiol.00195.2007
Source: PubMed


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.

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    • "Resistance exercise performed to failure elevates muscle protein synthesis independent of volume (sets × reps) or % one repetition maximum (1RM) load (Burd et al., 2010b; Mitchell et al., 2012). For example, low-load blood flow-restricted exercise has been shown to elicit significant increases in muscle hypertrophy and strength (Fujita et al., 2007; Takada et al., 2012). Furthermore , investigations that controlled relative %1RM training load and volume reported that repetition failure led to significantly greater gains in muscular strength (Rooney et al., 1994; Drinkwater et al., 2005). "
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    ABSTRACT: This investigation sought to determine the effect of resistance training to failure on functional, structural and neural elbow flexor muscle adaptation. Twenty-eight males completed a 4-week familiarization period and were then counterbalanced on the basis of responsiveness across; non-failure rapid shortening (RS; rapid concentric, 2 s eccentric), non-failure stretch-shortening (SSC; rapid concentric, rapid eccentric), and failure control (C, 2 s concentric, 2 s eccentric), for a 12-week unilateral elbow flexor resistance training regimen, 3 × week using 85% of one repetition maximum (1RM). 1RM, maximal voluntary contraction (MVC), muscle cross-sectional area (CSA), and muscle activation (EMGRMS ) of the agonist, antagonist, and stabilizer muscles were assessed before and after the 12-week training period. The average number of repetitions per set was significantly lower in RS 4.2 [confidence interval (CI): 4.2, 4.3] and SSC 4.2 (CI: 4.2, 4.3) compared with C 6.1 (CI: 5.8, 6.4). A significant increase in 1RM (30.5%), MVC (13.3%), CSA (11.4%), and agonist EMGRMS (22.1%) was observed; however, no between-group differences were detected. In contrast, antagonist EMGRMS increased significantly in SSC (40.5%) and C (23.3%), but decreased in RS (13.5%). Similar adaptations across the three resistance training regimen suggest repetition failure is not critical to elicit significant neural and structural changes to skeletal muscle. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
    Scandinavian Journal of Medicine and Science in Sports 04/2015; DOI:10.1111/sms.12445 · 2.90 Impact Factor
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    • "On the other hand, the mTOR signalling pathway is a potent positive regulator of skeletal muscle size and plays a significant role in stimulating translation initiation and muscle protein synthesis. A previous BFR study (Fujita et al., 2007) reported that increased muscle protein synthesis through the mTOR signalling pathway was observed in LI-BFR exercise as well as HI exercise. Therefore, it appears that both myostatin and mTOR signalling pathways may have a potent influence on decreases in muscle size during a detraining period. "
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    ABSTRACT: We investigated the effects of 3 weeks of detraining on muscle cross-sectional area (CSA) and one-repetition maximum strength (1-RM) in young men who had previously participated in 6 weeks (3 days week−1) of bench press training [blood flow restricted low-intensity (LI-BFR; n = 10, 20% 1-RM) or high-intensity (HI; n = 7, 75% 1-RM)]. Bench press 1-RM and muscle CSA of triceps brachii (TB) and pectoralis major (PM) were evaluated before (pre) and after training period (post) as well as after detraining period (detraining). Bench press 1-RM was higher at both post and detraining than at pre for LI-BFR (P<0·01) and the HI (P<0·01). TB and PM muscle CSA were higher at both post and detraining than at pre for the HI group (P<0·01), while the LI-BFR group only increased (P<0·01) at post. Relative dynamic strength (1-RM divided by TB muscle CSA) was higher at both post and detraining than at pre for the HI group (P<0·01), while the LI-BFR group only increased (P<0·01) at detraining. In conclusion, increased muscle strength following 6 weeks of training with LI-BFR as well as HI was well preserved at 3 weeks of detraining. HI-induced muscle strength appears to be dependent upon both neural adaptations and muscle hypertrophy with training and detraining. On the other hand, LI-BFR-induced muscle strength appears to be related primarily to muscle hypertrophy with training and to neural adaptations with detraining.
    Clinical Physiology and Functional Imaging 05/2014; 35(1). DOI:10.1111/cpf.12165 · 1.44 Impact Factor
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    • "pported in part by Fry et al . ( 2010 ) who observed greater increases in muscle size ( measured by circumference ) with LI - BFR compared with low - intensity resistance exercise without BFR . The authors suggested that this acute swelling might mechanistically explain part of the increase in muscle protein synthesis observed following LI - BFR ( Fujita et al . , 2007 ; Fry et al . , 2010 ; Gundermann et al . , 2012 ) . We pre - viously showed that LI - pBFR resulted in an acute increase in muscle swelling and size following a resistance exercise bout ( Wilson et al . , 2013 ) . However , to our knowledge , this is the first study to look chronically at changes in muscle size compared with high - int"
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    ABSTRACT: Resistance training in combination with practical blood flow restriction (pBFR) is thought to stimulate muscle hypertrophy by increasing muscle activation and muscle swelling. Most previous studies used the KAATSU device; however, little long-term research has been completed using pBFR. To investigate the effects of pBFR on muscle hypertrophy. Twenty college-aged male participants with a minimum of 1 year of resistance training experience were recruited for this study. Our study consisted of a randomized, crossover protocol consisting of individuals either using pBFR for the elbow flexors during the first 4 weeks (BFR-HI) or the second 4 weeks (HI-BFR) of an 8-week resistance training programme. Direct ultrasound-determined bicep muscle thickness was assessed collectively at baseline and at the end of weeks 4 and 8. There were no differences in muscle thickness between groups at baseline (P = 0·52). There were time (P<0·01, ES = 0·99) but no condition by time effects (P = 0·58, ES = 0·80) for muscle thickness in which the combined values of both groups increased on average from week 0 (3·66 ± 0·06) to week 4 (3·95 ± 0·05) to week 8 (4·11 ± 0·07). However, both the BFR-HI and HI-BFR increased significantly from baseline to week 4 (6·9% and 8·6%, P<0·01) and from weeks 4 to 8 (4·1%, 4·0%, P<0·01), respectively. The results of this study suggest that pBFR can stimulate muscle hypertrophy to the same degree to that of high-intensity resistance training.
    Clinical Physiology and Functional Imaging 11/2013; 34(4). DOI:10.1111/cpf.12099 · 1.44 Impact Factor
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