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.

中文翻译：

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运动诱导的自噬对少肌症的调节作用。

肌肉减少症是一种与衰老相关的疾病，被描述为骨骼肌质量和强度的逐渐降低。肌肉减少症的典型特征是由于蛋白质合成和蛋白质降解之间的不平衡而导致受损产物的积累。蛋白质合成与降解之间的这种不平衡归因于自噬信号通路的受损。肌肉减少症会使老年患者易患多种并发症，这些并发症可能会严重影响患者的生活质量。最近的证据表明自噬是分解代谢条件下控制骨骼肌质量所必需的，并且在维持骨骼肌的稳态和完整性方面，特别是在适当的自噬水平上，起着至关重要的作用。运动可以被认为是一种压力刺激，可以实质上调节细胞信号传导以促进代谢适应。适当的运动可以诱发自噬或调节自噬的功能状态。此外，运动诱导的自噬是减慢肌肉减少症，改善线粒体质量和静止卫星细胞数量的最有效方法，而这一过程取决于基础自噬。然而，少肌症发展的分子机制仍是未知之数。在这篇叙述性综述中，从运动引起的自噬以及不同运动方式对这种反应的影响的角度讨论了当前的肌肉减少症的分子机制。