Faculty of Applied Health Sciences, Brock University, 1812 Sir Isaac Brock Way, St. Catharines, ON, L2S3A1, Canada.
Department of Kinesiology, Brock University, 1812 Sir Isaac Brock Way, St. Catharines, ON, L2S3A1, Canada.
Sports Med. 2022 Dec;52(12):2853-2869. doi: 10.1007/s40279-022-01733-9. Epub 2022 Jul 30.
Human menopause is widely associated with impaired skeletal muscle quality and significant metabolic dysfunction. These observations pose significant challenges to the quality of life and mobility of the aging population, and are of relevance when considering the significantly greater losses in muscle mass and force-generating capacity of muscle from post-menopausal females relative to age-matched males. In this regard, the influence of estrogen on skeletal muscle has become evident across human, animal, and cell-based studies. Beneficial effects of estrogen have become apparent in mitigation of muscle injury and enhanced post-damage repair via various mechanisms, including prophylactic effects on muscle satellite cell number and function, as well as membrane stability and potential antioxidant influences following injury, exercise, and/or mitochondrial stress. In addition to estrogen replacement in otherwise deficient states, exercise has been found to serve as a means of augmenting and/or mimicking the effects of estrogen on skeletal muscle function in recent literature. Detailed mechanisms behind the estrogenic effect on muscle mass, strength, as well as the injury response are beginning to be elucidated and point to estrogen-mediated molecular cross talk amongst signalling pathways, such as apoptotic signaling, contractile protein modifications, including myosin regulatory light chain phosphorylation, and the maintenance of muscle satellite cells. This review discusses current understandings and highlights new insights regarding the role of estrogen in skeletal muscle, with particular regard to muscle mass, mitochondrial function, the response to muscle damage, and the potential implications for human physiology and mobility.
绝经与骨骼肌质量受损和显著代谢功能障碍广泛相关。这些观察结果对老年人群的生活质量和移动能力提出了重大挑战，并且在考虑绝经后女性相对于同龄男性的肌肉质量和力量产生能力显著更大损失时具有相关性。在这方面，雌激素对骨骼肌的影响已在人体、动物和基于细胞的研究中得到证实。雌激素的有益作用已通过各种机制显现出来，包括通过预防性地影响肌肉卫星细胞数量和功能，以及通过损伤、运动和/或线粒体应激后的膜稳定性和潜在抗氧化影响，减轻肌肉损伤和增强损伤后的修复。除了在缺乏雌激素的情况下进行替代治疗外，运动已被发现是增强和/或模拟雌激素对骨骼肌功能影响的一种手段，这在最近的文献中已有报道。雌激素对肌肉质量、力量以及损伤反应的影响的详细机制开始被阐明，并指向雌激素介导的信号通路之间的分子串扰，如凋亡信号、收缩蛋白修饰，包括肌球蛋白调节轻链磷酸化，以及肌肉卫星细胞的维持。这篇综述讨论了目前对雌激素在骨骼肌中的作用的理解，并强调了新的见解，特别是关于肌肉质量、线粒体功能、对肌肉损伤的反应以及对人类生理学和移动能力的潜在影响。
