Age-related loss of muscle mass and strength is widely attributed to limitation in the capacity of muscle resident satellite cells to perform their myogenic function. This idea contains two notions that have not been comprehensively evaluated by experiment. First, it entails the idea that we damage and lose substantial amounts of muscle in the course of our normal daily activities. Second, it suggests that mechanisms of muscle repair are in some way exhausted, thus limiting muscle regeneration. A third potential option is that the aged environment becomes inimical to the conduct of muscle regeneration. In the present study, we used our established model of human muscle xenografting to test whether muscle samples taken from cadavers, of a range of ages, maintained their myogenic potential after being transplanted into immunodeficient mice. We find no measurable difference in regeneration across the range of ages investigated up to 78 years of age. Moreover, we report that satellite cells maintained their myogenic capacity even when muscles were grafted 11 days postmortem in our model. We conclude that the loss of muscle mass with increasing age is not attributable to any intrinsic loss of myogenicity and is most likely a reflection of progressive and detrimental changes in the muscle microenvironment such as to disfavor the myogenic function of these cells.

中文翻译：

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人体肌肉干细胞不易老化

与年龄相关的肌肉质量和力量损失广泛归因于肌肉常驻卫星细胞执行其生肌功能的能力受限。这个想法包含两个尚未通过实验全面评估的概念。首先，它包含了我们在正常的日常活动过程中会损伤和失去大量肌肉的想法。其次，它表明肌肉修复机制在某种程度上已经耗尽，从而限制了肌肉再生。第三种可能的选择是老化的环境变得不利于肌肉再生的进行。在本研究中，我们使用我们建立的人类肌肉异种移植模型来测试从不同年龄段的尸体中提取的肌肉样本在移植到免疫缺陷小鼠体内后是否保持了它们的生肌潜能。我们发现在调查的 78 岁以下的年龄范围内，再生没有可测量的差异。此外，我们报告说，即使在我们的模型中死后 11 天移植了肌肉，卫星细胞仍能保持其生肌能力。我们得出结论，随着年龄的增长，肌肉量的减少不能归因于肌原性的任何内在损失，很可能是肌肉微环境中进行性和有害变化的反映，例如不利于这些细胞的肌原性功能。