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骨骼肌记忆中的核固着:一项针对人体和动物研究的系统回顾和荟萃分析。

Myonuclear permanence in skeletal muscle memory: a systematic review and meta-analysis of human and animal studies.

机构信息

Department of Physical Education and Sport Sciences, Faculty of Literature and Human Sciences, Lorestan University, Khorramabad, Iran.

Department of Physiology, University of Kentucky, Lexington, KY, USA.

出版信息

J Cachexia Sarcopenia Muscle. 2022 Oct;13(5):2276-2297. doi: 10.1002/jcsm.13043. Epub 2022 Aug 12.

DOI:10.1002/jcsm.13043
PMID:35961635
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9530508/
Abstract

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.

摘要

骨骼肌记忆的一个方面是,在经过一段时间的停训后,之前受过训练的肌肉能够更快地进行肥大。尽管肌肉记忆的分子基础仍有待充分阐明,但人们认为一种潜在的机制可能是在最初的肥大生长阶段永久保留获得的肌核。然而,肌核的永久性仍存在争议,需要进行荟萃分析来阐明这一重要方面的领域现状,即骨骼肌可塑性。本研究的目的是进行荟萃分析,以评估与体力活动和衰老相关的肌核的永久性。如果有可用的卫星细胞(SCs)丰度数据,也会考虑到它们对肌核丰度变化的潜在影响。共确定了 147 篇经过同行评审的文章,分为五个单独的荟萃分析;(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。骨骼肌肥大与较高的肌核含量相关,这些含量在啮齿动物中是保留的,但在人类中不是,与萎缩(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)相关。在人类中,萎缩后肌核和 SC 含量均降低(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。然而,无论萎缩方式如何,啮齿动物的肌核都被发现更持久,而萎缩≥30%则与肌核含量的减少相关(SMD = -1.02,95%CI -1.53 至 -0.51,P = 0.0001)。在人类中,少肌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 至 1.19,P = 0.0002;分别)。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永久性的骨骼肌记忆概念,并表明其他机制,如表观遗传学,可能在介导骨骼肌可塑性的这一方面发挥更重要的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d119/9530508/f5253c68ccc2/JCSM-13-2276-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d119/9530508/f5253c68ccc2/JCSM-13-2276-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d119/9530508/f5253c68ccc2/JCSM-13-2276-g001.jpg

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