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The Role of Exercise and TFAM in Preventing Skeletal Muscle Atrophy

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Journal of Cellular Physiology

Published online on

Abstract

Skeletal muscle atrophy is the consequence of protein degradation exceeding protein synthesis. This arises for a multitude of reasons including the unloading of muscle during microgravity, post‐surgery bedrest, immobilization of a limb after injury, and overall disuse of the musculature. The development of therapies prior to skeletal muscle atrophy settings to diminish protein degradation is scarce. Mitochondrial dysfunction is associated with skeletal muscle atrophy and contributes to the induction of protein degradation and cell apoptosis through increased levels of ROS observed with the loss of organelle function. ROS binds mtDNA, leading to its degradation and decreasing functionality. Mitochondrial transcription factor A (TFAM) will bind and coat mtDNA, protecting it from ROS and degradation while increasing mitochondrial function. Exercise stimulates cell signaling pathways that converge on and increase PGC‐1α, a well‐known activator of the transcription of TFAM and mitochondrial biogenesis. Therefore, in the present review we are proposing, separately, exercise and TFAM treatments prior to atrophic settings (muscle unloading or disuse) alleviate skeletal muscle atrophy through enhanced mitochondrial adaptations and function. Additionally, we hypothesize the combination of exercise and TFAM leads to a synergistic effect in targeting mitochondrial function to prevent skeletal muscle atrophy. J. Cell. Physiol. 232: 2348–2358, 2017. © 2016 The Authors. Journal of Cellular Physiology Published by © 2016 Wiley Periodicals, Inc. Skeletal muscle atrophy via unloading and disuse of the musculature is the consequence of protein degradation exceeding protein synthesis. This state is correlated with increased markers of mitochondrial dysfunction. We hypothesize targeting increased mitochondrial function through exercise and mitochondrial transcription factor A treatments will diminish skeletal muscle atrophy after a period of muscle unloading and disuse.