The effect of sleep restriction, with or without high‐intensity interval exercise, on myofibrillar protein synthesis in healthy young men

Abstract

The 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, <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mover><mml:mi>V</mml:mi><mml:mo>̇</mml:mo></mml:mover><mml:msub><mml:mi>O</mml:mi><mml:mrow><mml:mn>2</mml:mn><mml:mspace></mml:mspace><mml:mi>peak</mml:mi></mml:mrow></mml:msub></mml:msub></mml:math> , 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-AKT^ser473 and p-mTOR^ser2448 ) 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.