骨骼肌记忆的一个方面是先前训练过的肌肉在一段时间后更快地肥大的能力。虽然肌肉记忆的分子基础还有待完全阐明,认为介导肌肉记忆的一个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,肌核持久性存在争议,将受益于荟萃分析,以阐明骨骼肌可塑性这一重要方面的领域现状。这项研究的目的是进行荟萃分析,以评估与身体活动和衰老变化相关的肌核持久性。如果可用,考虑到卫星细胞(SC)对肌核丰度变化的潜在影响,也考虑了它们的丰度.在五个单独的荟萃分析中确定了一百四十七篇同行评审的文章;(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)人类研究评估了肌肉对衰老的反应。骨骼肌肥大与啮齿动物保留的较高的肌核含量有关,但不是人类,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;)。人萎缩后肌核和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;分别),尽管啮齿动物的反应受到所考虑的肌肉类型和萎缩方式的影响。而无论萎缩的方式如何,啮齿动物的肌核被发现更持久,≥30%的萎缩与肌核含量降低相关(SMD=-1.02,95%CI-1.53至-0.51,P=0.0001).在人类中,肌肉减少症伴有较低的肌核和SC含量(分别为MD=0.47,95%CI0.09至0.85,P=0.02,SMD=0.78,95%CI0.37-1.19,P=0.0002)。本荟萃分析的主要发现是,肌核不是永久性的,而是在萎缩和衰老期间丢失的。这些发现不支持基于肌核持久性的骨骼肌记忆的概念,并提出了其他机制,比如表观遗传学,在调节骨骼肌可塑性方面可能有更重要的作用。
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.