Effects of resistance training on alleviating hypoxia-induced muscle atrophy: Focus on acetylation of FoxO1.

J Cell Mol Med

Key Laboratory of Physical Fitness and Exercise, Ministry of Education, Beijing Sport University, Beijing, China.

Published: February 2024

AI Article Synopsis

  • * Forty male rats were assigned to different groups to undergo resistance training or stay in a low-oxygen environment for four weeks, with muscle samples analyzed afterwards.
  • * Results showed that resistance training reversed muscle loss caused by hypoxia by reducing FoxO1 activity and autophagy, leading to improvements in muscle mass and size.

Article Abstract

This study aims to explore the role of FoxO1 and its acetylation in the alleviation of hypoxia-induced muscle atrophy by resistance training. Forty male Sprague-Dawley rats were randomly divided into four groups: normoxic control group (C), normoxic resistance training group (R), hypoxic control group (H) and hypoxic resistance training group (HR). Rats in R and HR groups were trained on an incremental weight-bearing ladder every other day, while those in H and HR groups were kept in an environment containing 12.4% O . After 4 weeks, muscles were collected for analysis. Differentiated L6 myoblasts were analysed in vitro after hypoxia exposure and plasmids transfection (alteration in FoxO1 acetylation). The lean body mass loss, wet weight and fibre cross-sectional area of extensor digitorum longus of rats were decreased after 4 weeks hypoxia, and the adverse reactions above was reversed by resistance training. At the same time, the increase in hypoxia-induced autophagy was suppressed, which was accompanied by a decrease in the expression of nuclear FoxO1 and cytoplasmic Ac-FoxO1 by resistance training. The L6 myotube diameter increased and the expression of autophagic proteins were inhibited under hypoxia via intervening by FoxO1 deacetylation. Overall, resistance training alleviates hypoxia-induced muscle atrophy by inhibiting nuclear FoxO1 and cytoplasmic Ac-FoxO1-mediated autophagy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10844693PMC
http://dx.doi.org/10.1111/jcmm.18096DOI Listing

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