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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Aged Muscle Demonstrates Fiber-Type Adaptations in Response to Mechanical Overload, in the Absence of Myofiber Hypertrophy, Independent of Satellite Cell Abundance
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Aged Muscle Demonstrates Fiber-Type Adaptations in Response to Mechanical Overload, in the Absence of Myofiber Hypertrophy, Independent of Satellite Cell Abundance

机译：在没有肌纤维肥大的情况下，老年肌肉表现出对机械超负荷的响应，纤维类型的适应与卫星细胞的丰度无关

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Although sarcopenia, age-associated loss of muscle mass and strength, is neither accelerated nor exacerbated by depletion of muscle stem cells, satellite cells, we hypothesized that adaptation in sarcopenic muscle would be compromised. To test this hypothesis, we depleted satellite cells with tamoxifen treatment of Pax7(CreER)-DTA mice at 4 months of age, and 20 months later subjected the plantaris muscle to 2 weeks of mechanical overload. We found myofiber hypertrophy was impaired in aged mice regardless of satellite cell content. Even in the absence of growth, vehicle-treated mice mounted a regenerative response, not apparent in tamoxifen-treated mice. Further, myonuclear accretion occurred in the absence of growth, which was prevented by satellite cell depletion, demonstrating that myonuclear addition is insufficient to drive myofiber hypertrophy. Satellite cell depletion increased extracellular matrix content of aged muscle that was exacerbated by overload, potentially limiting myofiber growth. These results support the idea that satellite cells regulate the muscle environment, and that their loss during aging may contribute to fibrosis, particularly during periods of remodeling. Overload induced a fiber-type composition improvement, independent of satellite cells, suggesting that aged muscle is very responsive to exercise-induced enhancement in oxidative capacity, even with an impaired hypertrophic response.
机译：尽管肌肉衰弱与肌肉衰老有关，但肌肉干细胞，卫星细胞的耗竭既不会加速也不会加剧与年龄相关的肌肉质量和力量的丧失，但我们推测，对肌肉减少症的适应可能会受到损害。为了验证该假设，我们在4个月大时用他莫昔芬处理Pax7（CreER）-DTA小鼠来消除卫星细胞，然后在20个月后对plant肌进行2周的机械超负荷。我们发现无论卫星细胞含量如何，老年小鼠的肌纤维肥大都会受到损害。即使在没有生长的情况下，用媒介物处理的小鼠也会产生再生反应，这在他莫昔芬处理的小鼠中并不明显。此外，在没有生长的情况下发生了肌核的增生，这被卫星细胞的消耗所阻止，这表明肌核的添加不足以驱动肌纤维肥大。卫星细胞的消耗增加了老年肌肉的细胞外基质含量，这种过载会因超负荷而加剧，可能会限制肌纤维的生长。这些结果支持以下观点：卫星细胞调节肌肉环境，并且在衰老过程中丢失可能导致纤维化，特别是在重塑期间。超负荷导致纤维类型组成的改善，独立于卫星细胞，这表明，即使肥大性反应受损，衰老的肌肉也对运动引起的氧化能力增强非常敏感。

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