Regulatory role of exercise-induced autophagy for sarcopenia

Abstract

Sarcopenia is an aging-related disease, described as the progressive reduction in mass and strength of skeletal muscle. Sarcopenia is typically characterized as the accumulation of damaged products due to an imbalance between protein synthesis and protein degradation. This imbalance between protein synthesis and degradation is attributed to impaired autophagic signal pathways. Sarcopenia can predispose elderly patients to several complications that may significantly impact patient quality of life. Recent evidence indicates that autophagy is required for the control of skeletal muscle mass under catabolic conditions and plays a crucial role in maintaining the homeostasis and integrity of skeletal muscle, specifically at appropriate level of autophagy. Exercise may be considered as a stress stimulus that can substantially modulate cellular signaling to promote metabolic adaptations. Appropriate exercise can induce autophagy or regulate the functional status of autophagy. Additionally, exercise-induced autophagy is the most effective treatment available in slowing down sarcopenia, improving mitochondrial quality, and the number of quiescent satellite cells, as a process that depends on basal autophagy. The molecular mechanisms underpinning the development of sarcopenia, however, remained largely unknown. In this narrative review, the current molecular mechanisms of sarcopenia are discussed from the perspective of exercise-induced autophagy and the effect of different exercise modalities on this response. This narrative review will aim to provide the references for developing scientific and optimal intervention strategies including exercise intervention for the prevention and treatment of sarcopenia through regulating autophagic signal pathways.