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针对“筋痿”气血失于濡筋的核心病机，构建以线粒体为关键环节的力学-生物学响应框架，阐述经筋病位向气血病机传导的现代科学内涵。力学加载作为作用于机体的物理应力刺激，主要表现为推拿等外部施力形成的被动加载，以及导引等肌肉自主收缩形成的主动加载。力学加载可通过机械力信号转导与代谢需求驱动两条路径调控线粒体功能。将骨骼肌线粒体功能障碍视为筋痿“气”失调的核心微观基础，聚焦“气”与线粒体能量代谢、“血”与微循环效率的内在联系。在此基础上，阐明不同力学加载的调节规律，即气滞致痿或为“线粒体网络碎片化”，治宜调气，可通过推拿等外部施力的被动加载修复线粒体动力学；气虚致痿则因“线粒体生物发生不足”，治宜补气，应借助导引等自主运动的主动加载促进生物发生实现补益之效。该理论框架可揭示不同力学加载方式调控线粒体的生物学差异，为筋痿“同病异治”提供基于微观机制的解释。
Abstract：This study focuses on the core pathology of sinew wei (痿), which is mainly characterized by the failure of qi and blood to nourish the sinews. A mechanical-biological response framework is constructed with mitochondria as a key component, explaining the modern interpretation of the disease location of sinew transmitting to qi and blood pathology. Mechanical loading, as a physical stress stimulus applied to the body, manifests primarily as passive loading formed by external forces such as massage, and active loading resulting from voluntary muscle contractions, such as dao yin (导引). Mechanical loading can regulate mitochondrial function through two pathways, mechanical signal transduction and metabolic demand-driven regulation. Skeletal muscle mitochondrial dysfunction is regarded as the core microscopic basis of qi imbalance in sinew wei, highlighting the intrinsic connection between qi and mitochondrial energy metabolism, as well as between blood and microcirculatory efficiency. Accordingly, distinct regulatory patterns of mechanical loading are identified. Wei associated with qi stagnation may correspond to mitochondrial network fragmentation and can be treated by regulating qi through passive loading, such as tuina, to restore mitochondrial dynamics. In contrast, wei caused by qi deficiency is attributed to insufficient mitochondrial biogenesis and may be treated by tonifying qi through active loading, such as dao yin, to promote mitochondrial biogenesis. This framework reveals the biological differences in mitochondrial regulation induced by distinct mechanical loading modalities and provides a microscopic mechanism-based explanation for the principle of "treating the same disease with different methods" in sinew wei.
[1]李元浩，陈彦飞，秦伟凯，等.中医“筋”的解剖实质探析[J].陕西中医，2019,40(3):374-377.
[2]林星星，董宝强.论经筋理论的整体观[J].北京中医药大学学报，2017,40(10):808-812.
[3]付夜平，杨芳，孙鑫，等.从脾-线粒体理论探析肌少症机理及其防治[J].辽宁中医杂志，2025,52(12):84-88.
[4]戴娜，何兰，胡晶，等.“脾主肌肉”的理论探讨及其临床意义[J].中医杂志，2018,59(2):95-99.
[5]黄于婷，杨岚菲，方燕平，等.推拿手法治疗经筋病的原理探析[J].时珍国医国药，2018,29(6):1414-1415.
[6]CHEN H,VERMULST M,WANG YE,et al. Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations[J]. Cell,2010,141(2):280-289.
[7]CHANG YW,SONG ZH,CHEN CC. FAK regulates cardiomyocyte mitochondrial fission and function through Drp1[J]. FEBS J,2022,289(7):1897-1910.
[8]GROMAKOVSKIS V. Exploring fascia in myofascial pain syndrome:an integrative model of mechanisms[J]. Front Pain Res(Lausanne),2025,6:1712242. doi:10. 3389/fpain. 2025. 1712242.
[9]KHAN M, ALI S, AL AZZAWI TNI,et al. The key roles of ROS and RNS as a signaling molecule in plant-microbe interactions[J]. Antioxidants(Basel),2023,12(2):268.
[10]GERWIN RD. A new unified theory of trigger point formation:failure of pre-and post-synaptic feedback control mechanisms[J]. Int J Mol Sci,2023,24(9):8142.
[11]VAN DER ZWAARD S,BROCHERIE F,JASPERS RT.Under the hood:skeletal muscle determinants of endurance performance[J]. Front Sports Act Living,2021,3:719434. doi:10. 3389/fspor. 2021. 719434.
[12]FERNANDO R,SHINDYAPINA AV,OST M,et al.Downregulation of mitochondrial metabolism is a driver for fast skeletal muscle loss during mouse aging[J].Commun Biol,2023,6(1):1240.
[13]SCANDALIS L, KITZMAN DW, NICKLAS BJ, et al.Skeletal muscle mitochondrial respiration and exercise intolerance in patients with heart failure with preserved ejection fraction[J]. JAMA Cardiol, 2023,8(6):575-584.
[14]NYBERG M,JONES AM. Matching of o2 utilization and o2 delivery in contracting skeletal muscle in health,aging,and heart failure[J]. Front Physiol,2022,13:898395. doi:10. 3389/fphys. 2022. 898395.
[15]MCDERMOTT MM,FERRUCCI L,GONZALEZ-FREIRE M,et al. Skeletal muscle pathology in peripheral artery disease:a brief review[J]. Arterioscler Thromb Vasc Biol,2020,40(11):2577-2585.
[16]BOUVIERE J,FORTUNATO RS,DUPUY C,et al.Exercise-stimulated ROS sensitive signaling pathways in skeletal muscle[J]. Antioxidants,2021,10(4):537.
[17]FAN P,XIE XH,CHEN CH,et al. Molecular regulation mechanisms and interactions between reactive oxygen species and mitophagy[J]. DNA Cell Biol,2019,38(1):10-22.
[18]LI X, ZHANG W, CAO Q, et al. Mitochondrial dysfunction in fibrotic diseases[J]. Cell Death Discov,2020,6:80. doi:10. 1038/s41420-020-00316-9.
[19]KECHAGIA JZ,IVASKA J,ROCA-CUSACHS P. Integrins as biomechanical sensors of the microenvironment[J]. Nat Rev Mol Cell Biol,2019,20(8):457-473.
[20]黄博，阮磊，王兰兰，等.推拿法介导机械敏感性离子通道Piezo1对骨骼肌损伤模型大鼠细胞凋亡的影响[J].湖南中医药大学学报，2023,43(12):2249-2255.
[21]周可林，董硕，国生，等.振腹推拿手法对CUMS抑郁症模型大鼠骨骼肌线粒体能量代谢障碍的干预作用机制[J].环球中医药，2022,15(2):197-204.
[22]HUNG CM,LOMBARDO PS,MALIK N,et al. AMPK/ULK1-mediated phosphorylation of Parkin ACT domain mediates an early step in mitophagy[J]. Sci Adv,2021,7(15):eabg4544.
[23]PARK JM,LEE DH,KIM DH. Redefining the role of AMPK in autophagy and the energy stress response[J].Nat Commun,2023,14(1):2994.
[24]匡小霞.基于AMPK调节骨骼肌能量代谢研究按法对激痛点去活化效应机制[D].长沙：湖南中医药大学，2023.
[25]蒋全睿，吴琼，朱晓晴，等.按压对慢性激痛点模型大鼠线粒体自噬水平及PINK1/Parkin通路的影响[J].中国康复医学杂志，2022,37(12):1593-1598.
[26]余艳，陈雪吟，杨丽虹，等.基于“痿病治宜导引”的导引适应症的现代思考[J].中医杂志，2024,65(11):1170-1173.
[27]SAITO Y, CHIKENJI TS, MATSUMURA T, et al.Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors[J].Nat Commun,2020,11(1):889.
[28]TOKUMITSU H,SAKAGAMI H. Molecular mechanisms underlying Ca2+/calmodulin-dependent protein kinase kinase signal transduction[J]. Int J Mol Sci,2022,23(19):11025.
[29]JÄGER S, HANDSCHIN C, ST-PIERRE J,et al. AMPactivated protein kinase(AMPK)action in skeletal muscle via direct phosphorylation of PGC-1α[J]. Proc Natl Acad Sci,2007,104(29):12017-12022.
[30]南淞华，彭超杰，崔应麟. PGC-1α对线粒体功能的调控作用及机制[J].生理学报，2025,77(2):300-308.
[31]MOORE TM,ZHOU Z,COHN W,et al. The impact of exercise on mitochondrial dynamics and the role of Drp1in exercise performance and training adaptations in skeletal muscle[J]. Mol Metab,2019,21:51-67. doi:10. 1016/j.molmet. 2018. 11. 012.
[32]甘丽祯，吴霞，陈沛，等.功法静力性训练通过PINK1/Parkin通路调控T2DM小鼠骨骼肌线粒体自噬的作用机制[J].南京中医药大学学报，2025,41(2):151-159.
[33]HONG J,PARK Y. Microvascular function and exercise training:functional implication of nitric oxide signaling and ion channels[J]. Pulse,2024,12(1):27-33.
[34]FUKAI T, USHIO-FUKAI M. Cross-talk between NADPH oxidase and mitochondria:role in ROS signaling and angiogenesis[J]. Cells,2020,9(8):1849.
[35]薛惠天，王兰兰，孙梦龙，等.基于NF-κB信号通路探讨各时间点推拿㨰法对兔骨骼肌损伤修复的动态影响[J].中华中医药杂志，2024,39(3):1232-1237.
[36]尤成亨，刘超，石梦妮，等.推拿促进膝骨关节炎骨骼肌血管网络再生功能重塑[J].中国中西医结合杂志，2024,44(5):627-631.
[37]杨小慧，裴鑫，谭若彤，等.背部推法对慢性疲劳综合征大鼠运动能力和骨骼肌线粒体功能的影响[J].中国运动医学杂志，2025,44(4):291-297.
[38]李晓玲，何浈，王思诺，等.论中医康复学整体功能观[J].中医杂志，2025,66(5):437-442.
[39]黄思彭，姚小玲，王继先，等.基于“血管-神经”网络再生探讨推拿治疗骨骼肌损伤的作用机制[J].世界中医药，2025,20(5):785-790.
[40]ZHANG X,GAO F. Exercise improves vascular health:role of mitochondria[J]. Free Radic Biol Med,2021,177:347-359. doi:10. 1016/j. freeradbiomed. 2021. 11. 002.
基本信息:
DOI：10.13288/j.11-2166/r.2026.07.005
中图分类号:R255.6
引用信息:
[1]常稀莉,黄思彭,孙武权,等.力学加载调控线粒体功能对“筋痿”气血濡养作用初探[J].中医杂志,2026,67(07):725-729+735.DOI:10.13288/j.11-2166/r.2026.07.005.
基金信息:
国家自然科学基金（82274670,82474671,82575245）; 国家中医药管理局高水平中医药重点学科建设项目（ZYYZDXK-2023061）
2026-04-02
2026-04-02