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Blood Flow Restriction Only Increases Myofibrillar Protein Synthesis with Exercise.

ABSTRACT: PURPOSE:Combining blood flow restriction (BFR) with exercise can stimulate skeletal muscle hypertrophy. Recent observations in an animal model suggest that BFR performed without exercise can also induce anabolic effects. We assessed the effect of BFR performed both with and without low-load resistance-type exercise (LLRE) on in vivo myofibrillar protein synthesis rates in young men. METHODS:Twenty healthy young men (age = 24 ± 1 yr, body mass index = 22.9 ± 0.6 kg·m) were randomly assigned to remain in resting condition (REST ± BFR; n = 10) or to perform LLRE (LLRE ± BFR at 20% one-repetition maximum; n = 10), combined with two 5-min cycles of single leg BFR. Myofibrillar protein synthesis rates were assessed during a 5-h post-BFR period by combining a primed continuous L-[ring-C6]phenylalanine infusion with the collection of blood samples, and muscle biopsies from the BFR leg and the contralateral control leg. The phosphorylation status of anabolic signaling (mammalian target of rapamycin pathway) and metabolic stress (acetyl-CoA carboxylase)-related proteins, as well as the mRNA expression of genes associated with skeletal muscle mass regulation, was assessed in the collected muscle samples. RESULTS:Under resting conditions, no differences in anabolic signaling or myofibrillar protein synthesis rates were observed between REST + BFR and REST (0.044% ± 0.004% vs 0.043% ± 0.004% per hour, respectively; P = 0.683). By contrast, LLRE + BFR increased myofibrillar protein synthesis rates by 10% ± 5% compared with LLRE (0.048% ± 0.005% vs 0.043% ± 0.004% per hour, respectively; P = 0.042). Furthermore, compared with LLRE, LLRE + BFR showed higher phosphorylation status of acetyl-CoA carboxylase and 4E-BP1 as well as the elevated mRNA expression of MuRF1 (all P < 0.05). CONCLUSION:BFR does not increase myofibrillar protein synthesis rates in healthy young men under resting conditions. When combined with LLRE, BFR increases postexercise myofibrillar protein synthesis rates in vivo in humans.

SUBMITTER: Nyakayiru J

PROVIDER: S-EPMC6553970 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Purpose: High-load resistance exercise contributes to maintenance of muscle mass, muscle protein quality, and contractile function by stimulation of muscle protein synthesis (MPS), hypertrophy, and strength gains. However, high loading may not be feasible in several clinical populations. Low-load blood flow restricted resistance exercise (BFRRE) may provide an alternative approach. However, the long-term protein synthetic response to BFRRE is unknown and the myocellular adaptations to prolonged BFRRE are not well described. Methods: To investigate this, 34 healthy young subjects were randomized to 6 weeks of low-load BFRRE, HLRE, or non-exercise control (CON). Deuterium oxide (D2O) was orally administered throughout the intervention period. Muscle biopsies from m. vastus lateralis were collected before and after the 6-week intervention period to assess long-term myofibrillar MPS and RNA synthesis as well as muscle fiber-type-specific cross-sectional area (CSA), satellite cell content, and myonuclei content. Muscle biopsies were also collected in the immediate hours following single-bout exercise to assess signaling for muscle protein degradation. Isometric and dynamic quadriceps muscle strength was evaluated before and after the intervention. Results: Myofibrillar MPS was higher in BFRRE (1.34%/day, p < 0.01) and HLRE (1.12%/day, p < 0.05) compared to CON (0.96%/day) with no significant differences between exercise groups. Muscle RNA synthesis was higher in BFRRE (0.65%/day, p < 0.001) and HLRE (0.55%/day, p < 0.01) compared to CON (0.38%/day) and both training groups increased RNA content, indicating ribosomal biogenesis in response to exercise. BFRRE and HLRE both activated muscle degradation signaling. Muscle strength increased 6-10% in BFRRE (p < 0.05) and 13-23% in HLRE (p < 0.01). Dynamic muscle strength increased to a greater extent in HLRE (p < 0.05). No changes in type I and type II muscle fiber-type-specific CSA, satellite cell content, or myonuclei content were observed. Conclusions: These results demonstrate that BFRRE increases long-term muscle protein turnover, ribosomal biogenesis, and muscle strength to a similar degree as HLRE. These findings emphasize the potential application of low-load BFRRE to stimulate muscle protein turnover and increase muscle function in clinical populations where high loading is untenable.

Project description:Key pointsSleep restriction has previously been associated with the loss of muscle mass in both human and animal models. The rate of myofibrillar protein synthesis (MyoPS) is a key variable in regulating skeletal muscle mass and can be increased by performing high-intensity interval exercise (HIIE), although the effect of sleep restriction on MyoPS is unknown. In the present study, we demonstrate that participants undergoing a sleep restriction protocol (five nights, with 4 h in bed each night) had lower rates of skeletal muscle MyoPS; however, rates of MyoPS were maintained at control levels by performing HIIE during this period. Our data suggest that the lower rates of MyoPS in the sleep restriction group may contribute to the detrimental effects of sleep loss on muscle mass and that HIIE may be used as an intervention to counteract these effects.AbstractThe present study aimed to investigate the effect of sleep restriction, with or without high-intensity interval exercise (HIIE), on the potential mechanisms underpinning previously-reported sleep-loss-induced reductions to muscle mass. Twenty-four healthy, young men underwent a protocol consisting of two nights of controlled baseline sleep and a five-night intervention period. Participants were allocated into one of three parallel groups, matched for age, V̇O2peak , body mass index and habitual sleep duration; a normal sleep (NS) group [8 h time in bed (TIB) each night], a sleep restriction (SR) group (4 h TIB each night), and a sleep restriction and exercise group (SR+EX, 4 h TIB each night, with three sessions of HIIE). Deuterium oxide was ingested prior to commencing the study and muscle biopsies obtained pre- and post-intervention were used to assess myofibrillar protein synthesis (MyoPS) and molecular markers of protein synthesis and degradation signalling pathways. MyoPS was lower in the SR group [fractional synthetic rate (% day-1 ), mean ± SD, 1.24 ± 0.21] compared to both the NS (1.53 ± 0.09) and SR+EX groups (1.61 ± 0.14) (P < 0.05). However, there were no changes in the purported regulators of protein synthesis (i.e. p-AKTser473 and p-mTORser2448 ) and degradation (i.e. Foxo1/3 mRNA and LC3 protein) in any group. These data suggest that MyoPS is acutely reduced by sleep restriction, although MyoPS can be maintained by performing HIIE. These findings may explain the sleep-loss-induced reductions in muscle mass previously reported and also highlight the potential therapeutic benefit of HIIE to maintain myofibrillar remodelling in this context.

Project description:Background: Blood flow restriction or KAATSU exercise training is associated with greater muscle mass and strength increases than non-blood flow restriction equivalent exercise. Blood flow restriction exercise has been proposed as a possible alternative to more physically demanding exercise prescriptions (such as high-load/high-intensity resistance training) in a range of clinical and chronic disease populations. While the maintenance of muscle mass and size with reduced musculoskeletal tissue loading appeals in many of these physically impaired populations, there remains a disconnect between some of the desired clinical measures for chronic disease populations and those commonly measured in the literature examining blood flow restriction exercise. While strength does play a vital role in physical function, task-specific objective measures of physical function indicative of activities of daily living are often more clinically relevant and applicable for evaluating the success of medical and surgical interventions or monitoring age- and disease-related physical decline. Objective: To determine whether exercise interventions utilizing blood flow restriction are able to improve objective measures of physical function indicative of activities of daily living. Methods: A systematic search of Medline, Embase, CINAHL, SPORTDiscus, and Springer identified 13 randomized control trials utilizing an exercise intervention combined with blood flow restriction, while measuring at least one objective measure of physical function. Participants were ≥18 years of age. Systematic review of the literature and quality assessment of the included studies used the Cochrane Collaboration's tool for assessing risk bias. Results: Data from 13 studies with a total of 332 participants showed blood flow restriction exercise, regardless of modality, most notably increased performance on the 30 s sit-to-stand and timed up and go tests, and generally improved physical function on other tests including walking tests, variations of sit-to-stand tests, and balance, jumping, and stepping tests. Conclusions: From the evidence available, blood flow restriction exercise of multiple modalities improved objective measures of physical function indicative of activities of daily living.

Project description:BACKGROUND:Leucine-enriched essential amino acids (LEAAs) acutely enhance post-exercise myofibrillar protein synthesis (MyoPS), which has been suggested to be important for muscle repair and recovery. However, the ability of LEAAs to concurrently enhance MyoPS and muscle damage recovery in free-living humans has not been studied. METHODS:In a randomized, double-blind, placebo-controlled, parallel-group design, twenty recreationally active males consuming a controlled diet (1.2 g/kg/d of protein) were supplemented thrice daily with 4 g of LEAAs (containing 1.6 g leucine) or isocaloric placebo for four days following an acute bout of lower-body resistance exercise (RE). MyoPS at rest and integrated over 96 h of recovery was measured by D2O. Isometric and isokinetic torque, muscle soreness, Z-band streaming, muscle heat shock protein (HSP) 25 and 72, plasma creatine kinase (CK), and plasma interleukin-6 (IL-6) were measured over 96 h post-RE to assess various direct and indirect markers of muscle damage. RESULTS:Integrated MyoPS increased ~72% over 96 h after RE (p < 0.05), with no differences between groups (p = 0.98). Isometric, isokinetic, and total peak torque decreased ~21% by 48 h after RE (p < 0.05), whereas total peak torque was ~10% greater overall during recovery in LEAAs compared to placebo (p < 0.05). There were moderate to large effects for peak torque in favour of LEAAs. Muscle soreness increased during recovery with no statistical differences between groups but small to moderate effects in favour of LEAAs that correlated with changes in peak torque. Plasma CK, plasma IL-6, and muscle HSP25 increased after RE (p < 0.05) but were not significantly different between groups (p ? 0.13). Consistent with a trend toward attenuated Z-band streaming in LEAAs (p = 0.07), muscle HSP72 expression was lower (p < 0.05) during recovery in LEAAs compared with placebo. There were no correlations between MyoPS and any measures of muscle damage (p ? 0.37). CONCLUSION:Collectively, our data suggest that LEAAs moderately attenuated muscle damage without concomitant increases in integrated MyoPS in the days following an acute bout of resistance exercise in free-living recreationally active men.

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Blood Flow Restriction Only Increases Myofibrillar Protein Synthesis with Exercise.

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