中国组织工程研究 ›› 2025, Vol. 29 ›› Issue (30): 6499-6508.doi: 10.12307/2025.949

• 组织构建综述 tissue construction review • 上一篇    下一篇

运动促进骨骼肌线粒体生物合成的调控机制

张子寒1,王加新1,杨文意2,朱  磊1   

  1. 1曲阜师范大学体育科学学院,山东省济宁市  273100;2滨州市体育总会办公室,山东省滨州市  256600
  • 收稿日期:2024-11-02 接受日期:2024-12-17 出版日期:2025-10-28 发布日期:2025-03-28
  • 通讯作者: 王加新,硕士,副教授,曲阜师范大学体育科学学院,山东省济宁市 273100
  • 作者简介:张子寒,女,1999年生,山东省东营市人,汉族,曲阜师范大学在读硕士,主要从事运动训练及相关生理生化机制方面的研究。

Regulatory mechanism of exercise promoting mitochondrial biogenesis in skeletal muscle

Zhang Zihan¹, Wang Jiaxin¹, Yang Wenyi², Zhu Lei¹   

  1. ¹School of Sports Science, Qufu Normal University, Jining 273100, Shandong Province, China; ²Binzhou Sports Bureau, Binzhou 256600, Shandong Province, China 
  • Received:2024-11-02 Accepted:2024-12-17 Online:2025-10-28 Published:2025-03-28
  • Contact: Wang Jiaxin, MS, Associate professor, School of Sports Science, Qufu Normal University, Jining 273100, Shandong Province, China
  • About author:Zhang Zihan, Master candidate, School of Sports Science, Qufu Normal University, Jining 273100, Shandong Province, China

摘要:




文题释义:
骨骼肌线粒体生物合成:于骨骼肌内,经系列复杂分子信号传导与调控程序,促使线粒体数量攀升、功能进阶的生物学过程。此过程涉及多信号通路协同,如腺苷酸活化蛋白激酶通路感知能量变动激活过氧化物酶体增殖物激活受体γ共激活因子1α、丝裂原活化蛋白激酶响应机械应激或代谢变化调控基因表达,以适配肌肉能量需求,对维持肌肉代谢、提升运动耐力、抵御氧化损伤意义深远,是运动提升肌肉健康的关键机制,为改善肌肉功能提供靶点。
运动诱导调控:运动时肌肉能量代谢与应激状态更迭,成为激活线粒体生物合成信号通路的关键驱动力。如有氧运动提升AMP/ATP比值激活腺苷酸活化蛋白激酶,抗阻训练施予机械负荷刺激丝裂原活化蛋白激酶,进而精准调控线粒体生物合成各环节,优化其数量、结构与功能,实现肌肉代谢效能跃升、抗疲劳潜能激活及对代谢应激的良好适应,为制定个性化运动方案筑牢理论根基,推动运动健康效益最大化。

背景:骨骼肌线粒体生物合成及其运动调控机制是目前的研究焦点。腺苷酸活化蛋白激酶、过氧化物酶体增殖物激活受体 γ 共激活因子1α、丝裂原活化蛋白激酶、钙调信号等通路于运动诱导的线粒体生物合成意义深远,关乎肌肉代谢优化、运动表现提升与代谢病预防。然而,各通路的相互作用、调控机制及其在运动对骨骼肌线粒体生物合成的综合效应尚不清楚。
目的:探讨骨骼肌线粒体生物合成相关信号通路,精准解析运动在其中的诱导及调控细节,阐释运动激活信号通路促进线粒体生成与功能强化的原理,为改善肌肉代谢、提升运动效能、预防代谢疾病筑牢理论根基。
方法:通过检索中国知网(CNKI)、万方、维普等中文数据库,以及PubMed、Web of Science等英文数据库,收集自建库至2024年8月发表的与骨骼肌线粒体生物合成及其调控机制相关的最新文献。结合多条信号通路的研究结果,系统梳理了运动对线粒体生物合成的调控机制,重点关注腺苷酸活化蛋白激酶、过氧化物酶体增殖物激活受体 γ 共激活因子1α、蛋白激酶A、丝裂原活化蛋白激酶、钙调信号通路的相互作用和协同机制。
结果与结论:①骨骼肌线粒体生物合成是一个复杂的生物学过程,涉及多条信号通路的协同调控,旨在根据能量需求和外界应激的变化,优化骨骼肌的代谢能力、抗疲劳性以及整体运动表现,其核心机制包括腺苷酸活化蛋白激酶、过氧化物酶体增殖物激活受体 γ 共激活因子1α、丝裂原活化蛋白激酶等关键因子的相互作用和调节。②腺苷酸活化蛋白激酶通过感知细胞能量状态,激活过氧化物酶体增殖物激活受体 γ 共激活因子1α,促进线粒体生物合成。而过氧化物酶体增殖物激活受体 γ 共激活因子1α作为骨骼肌线粒体生物合成的主要调控因子,能够调节线粒体蛋白和DNA的合成,增强抗氧化应激反应,提升线粒体功能。③丝裂原活化蛋白激酶信号通路,特别是丝裂原活化蛋白激酶 p38,在应激反应中通过激活过氧化物酶体增殖物激活受体 γ 共激活因子1α进一步促进线粒体生成。④此外,钙调信号通路和PKA信号通路亦在骨骼肌的代谢调节中扮演着重要角色。⑤运动能够通过激活上述多条信号通路,显著提高骨骼肌的线粒体生物合成能力,优化细胞的代谢效率,增强肌肉耐力,改善运动表现。⑥未来研究可聚焦于深入探讨腺苷酸活化蛋白激酶、过氧化物酶体增殖物激活受体 γ 共激活因子1α、丝裂原活化蛋白激酶和钙调信号在不同运动强度和模式下的交互机制;加强对不同年龄、性别及健康状况群体的研究;验证研究成果的普适性与群体特异性;挖掘新兴调控因子如 FNIP1、PERM1的精细机制及其在运动干预中的潜力;以及推动运动健康研究成果向临床应用转化等。
https://orcid.org/0009-0007-9418-5606(张子寒);https://orcid.org/0009-0008-8453-2659(王加新)

中国组织工程研究杂志出版内容重点:组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程

关键词: 骨骼肌, 线粒体生物合成, 运动, 腺苷酸活化蛋白激酶, 过氧化物酶体增殖物激活受体 γ 共激活因子1α, 蛋白激酶A, MAPKs, 钙信号, 工程化组织构建

Abstract: BACKGROUND: Mitochondrial biogenesis in skeletal muscle and its regulatory mechanisms during exercise have become focal points of research. Pathways such as AMP-activated protein kinase, peroxisome proliferator-activated receptor γ coactivator 1α, mitogen-activated protein kinase, calcium-regulated signaling play profound roles in exercise-induced mitochondrial biogenesis, impacting muscle metabolic optimization, enhanced athletic performance, and the prevention of metabolic diseases. However, the interactions among these pathways, their regulatory mechanisms, and their comprehensive effects on exercise-induced mitochondrial biogenesis in skeletal muscle remain unclear.
OBJECTIVE: To explore the signaling pathways related to mitochondrial biogenesis in skeletal muscle, precisely analyze the induction and regulatory details of exercise within these pathways, and clearly elucidate the principles by which exercise-activated signaling pathways promote mitochondrial generation and functional enhancement. This will establish a theoretical foundation for improving muscle metabolism, enhancing exercise efficiency, and preventing metabolic diseases.
METHODS: An extensive literature search was conducted using China National Knowledge Infrastructure (CNKI), WanFang, VIP, PubMed, and Web of Science. The latest publications related to mitochondrial biogenesis in skeletal muscle and its regulatory mechanisms were collected from inception to August 2024. By integrating findings from multiple signaling pathways, the regulatory mechanisms of exercise on mitochondrial biogenesis were systematically reviewed, with a focus on the interactions and synergistic mechanisms of AMP-activated protein kinase, peroxisome proliferator-activated receptor γ coactivator 1α, protein kinase A, mitogen-activated protein kinase, calcium-regulated signaling pathways.
RESULTS AND CONCLUSION: (1) Mitochondrial biogenesis in skeletal muscle is a complex biological process involving the coordinated regulation of multiple signaling pathways. This process aims to optimize the metabolic capacity, fatigue resistance, and overall athletic performance of skeletal muscle in response to changes in energy demand and external stress. The core mechanisms include the interactions and regulation of key factors such as AMP-activated protein kinase, peroxisome proliferator-activated receptor gamma coactivator 1α, and mitogen-activated protein kinase. (2) AMP-activated protein kinase senses the cellular energy status and activates peroxisome proliferator-activated receptor gamma coactivator 1α, thereby promoting mitochondrial biogenesis. Peroxisome proliferator-activated receptor gamma coactivator 1α, as the main regulator of mitochondrial biogenesis in skeletal muscle, can modulate the synthesis of mitochondrial proteins and DNA, enhance the antioxidant stress response, and improve mitochondrial function. (3) The mitogen-activated protein kinase signaling pathway, particularly p38 mitogen-activated protein kinase, further promotes mitochondrial generation by activating peroxisome proliferator-activated receptor gamma coactivator 1α during stress responses. (4) Additionally, calcium signaling and protein kinase A pathways play significant roles in the metabolic regulation of skeletal muscle. (5) Exercise can significantly enhance mitochondrial biogenesis capacity in skeletal muscle by activating these multiple signaling pathways, optimizing cellular metabolic efficiency, increasing muscle endurance, and improving athletic performance. (6) Future research should focus on in-depth exploration of the interaction mechanisms among AMP-activated protein kinase, peroxisome proliferator-activated receptor gamma coactivator 1α, mitogen-activated protein kinases, and calcium signaling under different exercise intensities and modalities; strengthen studies across diverse age groups, genders, and health conditions; validate the universality and population-specificity of research findings; investigate the intricate mechanisms of emerging regulatory factors such as FNIP1 and PERM1 and their potential in exercise interventions; and promote the translation of exercise health research outcomes into clinical applications.

中国组织工程研究杂志出版内容重点:组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程

Key words: skeletal muscle, mitochondrial biogenesis, exercise, AMP-activated protein kinase, peroxisome proliferator-activated receptor gamma coactivator 1α, protein kinase A, mitogen-activated protein kinase, calcium signaling, engineered tissue construction

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