Six Weeks of Low-Load Blood Flow Restricted and High-Load Resistance Exercise Training Produce Similar Increases in Cumulative Myofibrillar Protein Synthesis and Ribosomal Biogenesis in Healthy Males.

Peter Sieljacks,Thomas Groennebaek,Andreas B Møller,Robert V Musci,Emil Rindom,Jesper Emil Jakobsgaard,Anders Gravholt,Benjamin F Miller,Karyn L Hamilton,Jon Herskind,Kristian Vissing,Jakob Wang,Frank V De Paoli

doi:10.3389/fphys.2019.00649

Abstract

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.

Highlights

When compared to high-load resistance exercise (HLRE), BFRRE training was characterized by a higher number of performed repetitions, but a lower training load and training volume
The present study comprehensively investigated skeletal muscle adaptive responses to 6 weeks of BFRRE or HLRE conducted by recommended exercise principles
The main findings were; (1) that BFRRE and HLRE produced similar increases in longterm myofibrillar muscle protein synthesis (MPS) and RNA synthesis without concomitant increases in muscle fiber CSA; (2) that increases in satellite cell content was observed in responders, and; (3) that muscle strength increased with both training regimens, albeit to greater extent with HLRE

Summary

Introduction

Disease and advanced ageing can negatively affect muscle mass (Lexell et al, 1988; Mancini et al, 1992; Lindle et al, 1997) and muscle protein quality (Haus et al, 2007; Gouveia et al, 2017), which can contribute to impaired muscle contractile function (Harrington et al, 1997; Lindle et al, 1997; Brocca et al, 2017). Stimulating protein turnover during ageing and disease may be important for preserving a functional muscle mass. Recent studies using deuterium oxide (D2O) tracer methodology have demonstrated that prolonged HLRE training can stimulate cumulative increases in MPS to produce muscle hypertrophy (Brook et al, 2015; Damas et al, 2016). This impact of HLRE on MPS may partially rely on the translational capacity and activity of ribosomes (West et al, 2016). Satellite cell-mediated addition of myonuclei to existing muscle fibers has been proposed to contribute to muscle hypertrophy (Petrella et al, 2008), the notion on the importance of satellite cells for muscle hypertrophy has later been challenged (McCarthy et al, 2011)

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