Wang Jiayin, Jia Dandan, Zhang Zhiwang, Wang Dan
School of Exercise and Health, Shanghai University of Sport, Shanghai 200438, China.
School of Athletic Performance, Shanghai University of Sport, Shanghai 200438, China.
Metabolites. 2025 Jan 16;15(1):59. doi: 10.3390/metabo15010059.
: Sarcopenia, characterized by the progressive loss of muscle mass and strength, is linked to physical disability, metabolic dysfunction, and an increased risk of mortality. Exercise therapy is currently acknowledged as a viable approach for addressing sarcopenia. Nevertheless, the molecular mechanisms behind exercise training or physical activity remain poorly understood. The disruption of mitochondrial homeostasis is implicated in the pathogenesis of sarcopenia. Exercise training effectively delays the onset of sarcopenia by significantly maintaining mitochondrial homeostasis, including promoting mitophagy, improving mitochondrial biogenesis, balancing mitochondrial dynamics, and maintaining mitochondrial redox. Exerkines (e.g., adipokines, myokines, hepatokines, and osteokines), signaling molecules released in response to exercise training, may potentially contribute to skeletal muscle metabolism through ameliorating mitochondrial homeostasis, reducing inflammation, and regulating protein synthesis as a defense against sarcopenia. : In this review, we provide a detailed summary of exercise-induced exerkines and confer their benefit, with particular focus on their impact on mitochondrial homeostasis in the context of sarcopenia. : Exercise induces substantial adaptations in skeletal muscle, including increased muscle mass, improved muscle regeneration and hypertrophy, elevated hormone release, and enhanced mitochondrial function. An expanding body of research highlights that exerkines have the potential to regulate processes such as mitophagy, mitochondrial biogenesis, dynamics, autophagy, and redox balance. These mechanisms contribute to the maintenance of mitochondrial homeostasis, thereby supporting skeletal muscle metabolism and mitochondrial health. : Through a comprehensive investigation of the molecular mechanisms within mitochondria, the context reveals new insights into the potential of exerkines as key exercise-protective sensors for combating sarcopenia.
肌肉减少症的特征是肌肉质量和力量逐渐丧失，与身体残疾、代谢功能障碍及死亡风险增加有关。运动疗法目前被认为是解决肌肉减少症的一种可行方法。然而，运动训练或体育活动背后的分子机制仍知之甚少。线粒体稳态的破坏与肌肉减少症的发病机制有关。运动训练通过显著维持线粒体稳态，包括促进线粒体自噬、改善线粒体生物发生、平衡线粒体动力学和维持线粒体氧化还原状态，有效延缓肌肉减少症的发生。运动因子（如脂肪因子、肌动蛋白、肝动蛋白和骨动蛋白）是运动训练后释放的信号分子，可能通过改善线粒体稳态、减轻炎症和调节蛋白质合成来促进骨骼肌代谢，从而抵御肌肉减少症。在本综述中，我们详细总结了运动诱导的运动因子，并阐述了它们的益处，特别关注它们在肌肉减少症背景下对线粒体稳态的影响。运动可引起骨骼肌的显著适应性变化，包括增加肌肉质量、改善肌肉再生和肥大、提高激素释放以及增强线粒体功能。越来越多的研究表明，运动因子有潜力调节线粒体自噬、线粒体生物发生、动力学、自噬和氧化还原平衡等过程。这些机制有助于维持线粒体稳态，从而支持骨骼肌代谢和线粒体健康。通过对线粒体内分子机制的全面研究，本文揭示了运动因子作为对抗肌肉减少症的关键运动保护传感器的潜力的新见解。
