Peake Jonathan M, Neubauer Oliver, Della Gatta Paul A, Nosaka Kazunori
Tissue Repair and Translational Physiology Group, School of Biomedical Sciences, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia;
Center of Excellence for Applied Sport Science Research, Queensland Academy of Sport, Brisbane, Queensland, Australia.
J Appl Physiol (1985). 2017 Mar 1;122(3):559-570. doi: 10.1152/japplphysiol.00971.2016. Epub 2016 Dec 29.
Unaccustomed exercise consisting of eccentric (i.e., lengthening) muscle contractions often results in muscle damage characterized by ultrastructural alterations in muscle tissue, clinical signs, and symptoms (e.g., reduced muscle strength and range of motion, increased muscle soreness and swelling, efflux of myocellular proteins). The time course of recovery following exercise-induced muscle damage depends on the extent of initial muscle damage, which in turn is influenced by the intensity and duration of exercise, joint angle/muscle length, and muscle groups used during exercise. The effects of these factors on muscle strength, soreness, and swelling are well characterized. By contrast, much less is known about how they affect intramuscular inflammation and molecular aspects of muscle adaptation/remodeling. Although inflammation has historically been viewed as detrimental for recovery from exercise, it is now generally accepted that inflammatory responses, if tightly regulated, are integral to muscle repair and regeneration. Animal studies have revealed that various cell types, including neutrophils, macrophages, mast cells, eosinophils, CD8 and T-regulatory lymphocytes, fibro-adipogenic progenitors, and pericytes help to facilitate muscle tissue regeneration. However, more research is required to determine whether these cells respond to exercise-induced muscle damage. A large body of research has investigated the efficacy of physicotherapeutic, pharmacological, and nutritional interventions for reducing the signs and symptoms of exercise-induced muscle damage, with mixed results. More research is needed to examine if/how these treatments influence inflammation and muscle remodeling during recovery from exercise.
由离心(即拉长)肌肉收缩组成的不习惯运动通常会导致肌肉损伤,其特征为肌肉组织的超微结构改变、临床体征和症状(如肌肉力量和活动范围降低、肌肉酸痛和肿胀加剧、肌细胞蛋白质外流)。运动诱导的肌肉损伤后的恢复时间进程取决于初始肌肉损伤的程度,而这又反过来受运动强度和持续时间、关节角度/肌肉长度以及运动期间使用的肌肉群影响。这些因素对肌肉力量、酸痛和肿胀的影响已得到充分表征。相比之下,关于它们如何影响肌肉内炎症以及肌肉适应/重塑的分子方面则知之甚少。尽管炎症在历史上一直被视为不利于运动恢复,但现在人们普遍认为,炎症反应如果受到严格调节,对于肌肉修复和再生是不可或缺的。动物研究表明,包括中性粒细胞、巨噬细胞、肥大细胞、嗜酸性粒细胞、CD8和调节性T淋巴细胞、成纤维脂肪生成祖细胞和周细胞在内 的各种细胞类型有助于促进肌肉组织再生。然而,需要更多研究来确定这些细胞是否对运动诱导的肌肉损伤做出反应。大量研究调查了物理治疗、药物治疗和营养干预对减轻运动诱导的肌肉损伤体征和症状的疗效,结果不一。需要更多研究来检验这些治疗是否以及如何在运动恢复期间影响炎症和肌肉重塑。