Norwegian School of Sport Sciences, Department of Physical Performance, Oslo, Norway
Exerc Immunol Rev. 2012;18:42-97.
Exercise-induced muscle damage is an important topic in exercise physiology. However several aspects of our understanding of how muscles respond to highly stressful exercise remain unclear In the first section of this review we address the evidence that exercise can cause muscle damage and inflammation in otherwise healthy human skeletal muscles. We approach this concept by comparing changes in muscle function (i.e., the force-generating capacity) with the degree of leucocyte accumulation in muscle following exercise. In the second section, we explore the cytokine response to 'muscle-damaging exercise', primarily eccentric exercise. We review the evidence for the notion that the degree of muscle damage is related to the magnitude of the cytokine response. In the third and final section, we look at the satellite cell response to a single bout of eccentric exercise, as well as the role of the cyclooxygenase enzymes (COX1 and 2). In summary, we propose that muscle damage as evaluated by changes in muscle function is related to leucocyte accumulation in the exercised muscles. 'Extreme' exercise protocols, encompassing unaccustomed maximal eccentric exercise across a large range of motion, generally inflict severe muscle damage, inflammation and prolonged recovery (> 1 week). By contrast, exercise resembling regular athletic training (resistance exercise and downhill running) typically causes mild muscle damage (myofibrillar disruptions) and full recovery normally occurs within a few days. Large variation in individual responses to a given exercise should, however be expected. The link between cytokine and satellite cell responses and exercise-induced muscle damage is not so clear The systemic cytokine response may be linked more closely to the metabolic demands of exercise rather than muscle damage. With the exception of IL-6, the sources of systemic cytokines following exercise remain unclear The satellite cell response to severe muscle damage is related to regeneration, whereas the biological significance of satellite cell proliferation after mild damage or non-damaging exercise remains uncertain. The COX enzymes regulate satellite cell activity, as demonstrated in animal models; however the roles of the COX enzymes in human skeletal muscle need further investigation. We suggest using the term 'muscle damage' with care. Comparisons between studies and individuals must consider changes in and recovery of muscle force-generating capacity.
运动引起的肌肉损伤是运动生理学中的一个重要课题。然而，我们对肌肉如何对高应激运动做出反应的理解仍有许多方面不清楚。在这篇综述的第一部分，我们讨论了运动可以导致健康人类骨骼肌的肌肉损伤和炎症的证据。我们通过比较运动后肌肉功能（即产生力的能力）的变化与白细胞在肌肉中的积累程度来接近这个概念。在第二部分，我们探讨了细胞因子对“肌肉损伤运动”（主要是离心运动）的反应。我们回顾了这样一种观点，即肌肉损伤的程度与细胞因子反应的大小有关。在第三部分也是最后一部分，我们观察了单次离心运动对卫星细胞的反应，以及环氧化酶（COX1 和 2）的作用。总之，我们提出，肌肉功能的变化评估的肌肉损伤与运动肌肉中的白细胞积累有关。“极端”运动方案，包括不习惯的大范围运动的最大离心运动，通常会造成严重的肌肉损伤、炎症和长时间的恢复（>1 周）。相比之下，类似于常规运动训练（抗阻运动和下坡跑）的运动通常会导致轻度肌肉损伤（肌纤维断裂），并且通常在几天内就能完全恢复。然而，应该预期到个体对特定运动的反应会有很大的差异。细胞因子和卫星细胞反应与运动引起的肌肉损伤之间的联系并不那么明确。细胞因子的全身反应可能与运动的代谢需求更密切相关，而不是与肌肉损伤有关。除了 IL-6 之外，运动后全身细胞因子的来源仍不清楚。严重肌肉损伤后卫星细胞的反应与再生有关，而轻度损伤或非损伤性运动后卫星细胞增殖的生物学意义仍不确定。环氧化酶在动物模型中调节卫星细胞的活性；然而，环氧化酶在人类骨骼肌中的作用还需要进一步研究。我们建议谨慎使用“肌肉损伤”一词。在比较研究和个体时，必须考虑肌肉产生力的能力的变化和恢复。
