Skeletal muscle quality and quantity are negatively impacted with age. Part of this decline in function can be attributed to alterations in mitochondrial turnover, and in the mechanisms that regulate mitochondrial homeostasis. Protein quality control within the mitochondria relies on a number of interconnected processes, namely the mitochondrial unfolded protein response (UPRmt), protein import and mitophagy. In particular, the post-transcriptional regulation of protein import into the organelle has generated considerable recent interest in view of its dynamic versatility. The capacity for import can be increased by chronic exercise, and diminished by muscle disuse, and defects in the import pathway can be rescued by exercise. Within mitochondria, the unfolded protein response (UPR) is activated if protein import is altered, or if protein misfolding takes place. This UPR generates retrograde signaling to the nucleus to activate compensatory gene expression and protein synthesis. Mitophagy is also elevated with age, contributing to the lower mitochondrial content in aging muscle. However, mitophagy is amenable to exercise adaptations, as it is activated with each exercise bout, presumably to mediate mitochondrial quality control. However, this response is attenuated in older subjects. Although not yet completely elucidated, numerous molecular processes involved in mitochondrial biogenesis and turnover are affected with age. The contrasting and often opposite consequences of exercise and age suggest that exercise can serve as non-pharmacological "mitochondrial medicine" for aging muscle to ameliorate mitochondrial content and function, via pathways that implicate organelle protein quality control mechanisms.

中文翻译：

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运动和衰老对线粒体蛋白质质量控​​制的影响。

骨骼肌的质量和数量会随着年龄的增长而受到负面影响。这种功能下降的部分原因可归因于线粒体更新和调节线粒体内稳态的机制。线粒体内的蛋白质质量控​​制依赖于许多相互关联的过程，即线粒体未折叠的蛋白质反应（UPRmt），蛋白质输入和线粒体。特别地，鉴于其动态多功能性，蛋白质输入到细胞器中的转录后调节已引起相当大的兴趣。长期锻炼可以增加输入的能力，而肌肉废用可以减少输入的能力，运动可以挽救输入途径中的缺陷。在线粒体内，如果蛋白质进口发生变化，未折叠的蛋白质反应（UPR）就会被激活，或者发生蛋白质错误折叠。该UPR产生向核的逆行信号，以激活补偿性基因表达和蛋白质合成。线粒体也随着年龄增长而增加，导致衰老肌肉中线粒体含量降低。但是，线粒体适合运动适应性，因为每次运动都可以激活线粒体，大概是介导线粒体质量控制。但是，这种反应在老年受试者中减弱。尽管尚未完全阐明，但涉及线粒体生物发生和更新的许多分子过程会随着年龄的增长而受到影响。运动与年龄的对比结果往往是相反的，这表明运动可以用作衰老肌肉以改善线粒体含量和功能的“非线粒体药物”，