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Monico-Neto M.,University of Sao Paulo | Monico-Neto M.,Laboratorio Interdisciplinar em Fisiologia e Exercicio | Antunes H.K.M.,Laboratorio Interdisciplinar em Fisiologia e Exercicio | Antunes H.K.M.,Federal University of Sao Paulo | And 13 more authors.
Applied Physiology, Nutrition and Metabolism | Year: 2015

Sleep deprivation (SD) can induce muscle atrophy. We aimed to investigate the changes underpinning SD-induced muscle atrophy and the impact of this condition on rats that were previously submitted to resistance training (RT). Adult male Wistar EPM-1 rats were randomly allocated into 1 of 5 groups: control, sham, SD (for 96 h), RT, and RT+SD. The major outcomes of this study were muscle fiber cross-sectional area (CSA), anabolic and catabolic hormone profiles, and the abundance of select proteins involved in muscle protein synthesis and degradation pathways. SD resulted in muscle atrophy; however, when SD was combined with RT, the reduction in muscle fiber CSA was attenuated. The levels of IGF-1 and testosterone were reduced in SD animals, and the RT+SD group had higher levels of these hormones than the SD group. Corticosterone was increased in the SD group compared with the control group, and this increase was minimized in the RT+SD group. The increases in corticosterone concentrations paralleled changes in the abundance of ubiquitinated proteins and the autophagic proteins LC3 and p62/SQSTM1, suggesting that corticosterone may trigger these changes. SD induced weight loss, but this loss was minimized in the RT+SD group.Weconclude that SD induced muscle atrophy, probably because of the increased corticosteroneandcatabolic signal. High-intensityRTperformedbeforeSDwasbeneficial in containingmuscleloss induced by SD. It also minimized the catabolic signal and increased synthetic activity, thereby minimizing the body’s weight loss. © 2015, National Research Council of Canada. All rights reserved. Source

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