Long Yu-Feng, Chow Simon Kwoon-Ho, Cui Can, Wong Ronald Man Yeung, Qin Ling, Law Sheung-Wai, Cheung Wing-Hoi
Musculoskeletal Research Laboratory, Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China.
Bone Quality and Health Centre, Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China.
J Orthop Translat. 2022 Aug 22;35:37-52. doi: 10.1016/j.jot.2022.06.003. eCollection 2022 Jul.
Sarcopenia is a hallmark of the ageing process, which is characterized by the decline in muscle mass and strength. Growing evidence indicates that mitochondria dysfunction play core roles in this process. Meanwhile, physical exercise is regarded as one of the efficiency therapies to attenuate sarcopenia via regulating mitochondrial function during ageing. However, the specific mechanisms among exercise, mitochondrial function and sarcopenia are still unclear. The aim of this systematic review is to delineate the effects of physical exercise on mitochondria during ageing in order to explore potential target for rescuing sarcopenia.
A systematic literature search was performed in PubMed, Embase and Web of Science. Information was extracted from the included studies for review.
In this review, 16 pre-clinical studies were included and 105 clinical studies that were not mechanistic research were excluded. 16 pre-clinical studies provided evidence that physical exercise could affect mitochondrial quality control to attenuate sarcopenia. Most of the included studies described the important role of mitochondrial dynamic equilibrium in sarcopenia and showed that effective physical exercise could influence mitochondrial biogenesis, fusion, fission and mitophagy to attenuate sarcopenia in aged animal.
This systematic review provides an up-to-date sequential overview and highlights the link in the potential mitochondria-related target and physical exercise in aged animal.
Currently, there is no standard treatment method for sarcopenia. This systematic review revealed the underlying mechanisms for how physical exercise improved muscle performance via regulating mitochondrial dynamic equilibrium, which could provide scientific support for using exercise as a timely intervention for sarcopenia. Additionally, this systematic review allows a better understanding of mitochondrial dynamic equilibrium and exercise for future development of new therapeutic interventions to attenuate sarcopenia.
肌肉减少症是衰老过程的一个标志，其特征是肌肉质量和力量下降。越来越多的证据表明，线粒体功能障碍在这一过程中起核心作用。同时，体育锻炼被认为是通过调节衰老过程中的线粒体功能来减轻肌肉减少症的有效疗法之一。然而，运动、线粒体功能和肌肉减少症之间的具体机制仍不清楚。本系统综述的目的是描述体育锻炼对衰老过程中线粒体的影响，以探索挽救肌肉减少症的潜在靶点。
在PubMed、Embase和Web of Science中进行了系统的文献检索。从纳入的研究中提取信息进行综述。
在本综述中，纳入了16项临床前研究，排除了105项非机制性研究的临床研究。16项临床前研究提供了证据，表明体育锻炼可以影响线粒体质量控制以减轻肌肉减少症。大多数纳入研究描述了线粒体动态平衡在肌肉减少症中的重要作用，并表明有效的体育锻炼可以影响线粒体生物发生、融合、裂变和线粒体自噬，以减轻老年动物的肌肉减少症。
本系统综述提供了最新的序列概述，并突出了老年动物潜在的线粒体相关靶点与体育锻炼之间的联系。
目前，肌肉减少症尚无标准治疗方法。本系统综述揭示了体育锻炼如何通过调节线粒体动态平衡改善肌肉性能的潜在机制，这可为将运动作为肌肉减少症的及时干预措施提供科学支持。此外，本系统综述有助于更好地理解线粒体动态平衡和运动，以促进未来开发减轻肌肉减少症的新治疗干预措施。
