Exercise, mitochondrial biogenesis and disuse-induced atrophy
1Exercise and Sport Physiology Department, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey
2Department of Pathology, Gulhane Training and Research Hospital, Ankara, Turkey
3Department of Sports Medicine, Faculty of Medicine, Hacettepe University, Ankara, Turkey
Keywords: muscle atrophy, fusion and fission dynamics, Ca2+ homeostasis, mitochondrial disease
In addition to the physiological and cellular effects of exercise, many studies demonstrated that exercise could prevent skeletal muscle atrophy due to disuse. Mitochondria, which are powerhouses in cells, are at the top of the molecular mechanisms that control muscle function. Mitochondria play an essential role in regulating protein synthesis and degradation through various signaling pathways such as ubiquitin-proteolysis, mitochondrial biogenesis, fusion, and fission dynamics autophagy, and apoptosis. Regular exercise protects the skeletal muscle against different stresses by improving cellular oxidative capacity. Eventually, exercise controls the expression of proteins that have been shown to protect muscle from atrophy caused by disuse and activates many cellular signaling pathways. In this review, the role of mitochondria in muscle cells, the effect of disuse atrophy on mitochondria, and the effect of exercise on peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α) that plays a crucial role in mitochondrial biogenesis are discussed.
Cite this article as: Akin S, Kubat GB, Demirel HA. Exercise, mitochondrial biogenesis and disuse-induced atrophy. Turk J Sports Med. 2021;56(2).91-7.; http://dx.doi.org/10.47447/tjsm.0491
The authors declared no conflicts of interest with respect to authorship and/or publication of the article.
The authors received no financial support for the research and/or publication of this article.