Exercise, mitochondrial biogenesis and disuse-induced atrophy

• Main Authors: Şenay Akın, Gökhan Burçin Kubat1, 2, Haydar A. Demirel1, 3
• Format: Article
• Language: English
• Published: Turkish Sports Medicine Association 2021-06-01
• Series: Spor Hekimligi Dergisi
• Subjects: muscle atrophy; fusion and fission dynamics; ca2+ homeostasis; mitochondrial disease
• Online Access: https://journalofsportsmedicine.org/eng/full-text-pdf/568/eng

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.