Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production of the endogenous peptide apelin, induced by muscle contraction, is reduced in an age-dependent manner in humans and rodents and is positively associated with the beneficial effects of exercise in older persons. Mice deficient in either apelin or its receptor (APLNR) presented dramatic alterations in muscle function with increasing age. Various strategies that restored apelin signaling during aging further demonstrated that this peptide considerably enhanced muscle function by triggering mitochondriogenesis, autophagy and anti-inflammatory pathways in myofibers as well as enhancing the regenerative capacity by targeting muscle stem cells. Taken together, these findings revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy.

中文翻译：

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exerkine apelin可逆转与年龄相关的肌肉减少症。

骨骼肌减少，骨骼肌质量，质量和力量的退化性丧失，缺乏早期诊断工具和新的治疗策略来防止通常导致老年人医疗机构化的脆弱至残疾过渡。本文中我们报道了由肌肉收缩引起的内源性肽apelin的产生在人类和啮齿动物中以年龄依赖性的方式减少，并且与老年人运动的有益作用正相关。缺少apelin或其受体（APLNR）的小鼠会随着年龄的增长而出现肌肉功能的显着变化。在衰老过程中恢复apelin信号转导的各种策略进一步表明，该肽通过触发线粒体发生显着增强了肌肉功能，并通过靶向肌肉干细胞增强肌纤维的自噬和抗炎途径。综上所述，这些发现揭示了体育活动，apelin和肌肉功能之间的积极调节反馈，并确定了apelin既可以作为早期肌肉减少症的诊断工具，又可以作为预防年龄相关性肌肉无力并恢复身体自主性的创新药理策略的目标。