One aspect of skeletal muscle memory is the ability of a previously trained muscle to hypertrophy more rapidly following a period of detraining. Although the molecular basis of muscle memory remains to be fully elucidated, one potential mechanism thought to mediate muscle memory is the permanent retention of myonuclei acquired during the initial phase of hypertrophic growth. However, myonuclear permanence is debated and would benefit from a meta-analysis to clarify the current state of the field for this important aspect of skeletal muscle plasticity. The objective of this study was to perform a meta-analysis to assess the permanence of myonuclei associated with changes in physical activity and ageing. When available, the abundance of satellite cells (SCs) was also considered given their potential influence on changes in myonuclear abundance. One hundred forty-seven peer-reviewed articles were identified for inclusion across five separate meta-analyses; (1–2) human and rodent studies assessed muscle response to hypertrophy; (3–4) human and rodent studies assessed muscle response to atrophy; and (5) human studies assessed muscle response with ageing. Skeletal muscle hypertrophy was associated with higher myonuclear content that was retained in rodents, but not humans, with atrophy (SMD = −0.60, 95% CI −1.71 to 0.51, P = 0.29, and MD = 83.46, 95% CI −649.41 to 816.32, P = 0.82; respectively). Myonuclear and SC content were both lower following atrophy in humans (MD = −11, 95% CI −0.19 to −0.03, P = 0.005, and SMD = −0.49, 95% CI −0.77 to −0.22, P = 0.0005; respectively), although the response in rodents was affected by the type of muscle under consideration and the mode of atrophy. Whereas rodent myonuclei were found to be more permanent regardless of the mode of atrophy, atrophy of ≥30% was associated with a reduction in myonuclear content (SMD = −1.02, 95% CI −1.53 to −0.51, P = 0.0001). In humans, sarcopenia was accompanied by a lower myonuclear and SC content (MD = 0.47, 95% CI 0.09 to 0.85, P = 0.02, and SMD = 0.78, 95% CI 0.37–1.19, P = 0.0002; respectively). The major finding from the present meta-analysis is that myonuclei are not permanent but are lost during periods of atrophy and with ageing. These findings do not support the concept of skeletal muscle memory based on the permanence of myonuclei and suggest other mechanisms, such as epigenetics, may have a more important role in mediating this aspect of skeletal muscle plasticity.

中文翻译：

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骨骼肌记忆中的肌核持久性：人类和动物研究的系统回顾和荟萃分析

骨骼肌记忆的一个方面是先前训练过的肌肉在一段时间的停止训练后更快地肥大的能力。尽管肌肉记忆的分子基础仍有待完全阐明，但被认为介导肌肉记忆的一种潜在机制是在肥大生长的初始阶段获得的肌核的永久保留。然而，肌核持久性仍存在争议，并且可以从荟萃分析中受益，以阐明骨骼肌可塑性这一重要方面领域的当前状态。本研究的目的是进行荟萃分析，以评估与体力活动和衰老变化相关的肌核的持久性。如果可用，考虑到卫星细胞（SC）对肌核丰度变化的潜在影响，也考虑其丰度。确定了 147 篇经过同行评审的文章纳入五项独立的荟萃分析中；(1-2) 人类和啮齿动物研究评估了肌肉对肥大的反应；(3-4) 人类和啮齿动物研究评估了肌肉对萎缩的反应；(5) 人体研究评估了衰老过程中的肌肉反应。骨骼肌肥大与啮齿动物而非人类中保留的较高肌核含量相关，并伴有萎缩（SMD = -0.60，95% CI -1.71至0.51，P = 0.29，MD = 83.46，95% CI -649.41 至816.32，P  = 0.82；分别）。人类萎缩后肌核和 SC 含量均较低（MD = -11，95% CI -0.19 至 -0.03，P  = 0.005，SMD = -0.49，95% CI -0.77 至 -0.22，P  = 0.0005； ），尽管啮齿动物的反应受到所考虑的肌肉类型和萎缩模式的影响。然而，无论萎缩模式如何，啮齿动物的肌核都更持久，萎缩≥30%与肌核含量减少相关（SMD = -1.02，95% CI -1.53​​至-0.51，P = 0.0001 ）  。在人类中，肌肉减少症伴随着较低的肌核和 SC 含量（MD = 0.47，95% CI 0.09 至 0.85，P  = 0.02，SMD = 0.78，95% CI 0.37-1.19，P  = 0.0002；分别）。目前荟萃分析的主要发现是，肌核不是永久性的，而是在萎缩和衰老过程中丢失的。这些发现并不支持基于肌核永久性的骨骼肌记忆概念，并表明其他机制（例如表观遗传学）可能在调节骨骼肌可塑性的这一方面发挥更重要的作用。