Evans W J, Cannon J G
Exerc Sport Sci Rev. 1991;19:99-125.
Exercise-induced skeletal muscle damage results in a remarkable number of localized and systemic changes, including release of intracellular proteins, delayed onset muscle soreness, the acute-phase response, and an increase in skeletal muscle protein turnover. These exercise-induced adaptations appear to be integral to the repair of the damaged muscle and may be essential for hypertrophy. Chronic exercise produces adaptations in skeletal muscle, resulting in increased capacity of oxidative metabolism; the repair of damaged muscle resulting in hypertrophy may be an important mechanism for protection against further exercise-induced damage. Although the release of CK from skeletal muscle following damage is a commonly observed phenomenon, circulating CK activity is not a quantitative and, in some cases, even a qualitative indicator of skeletal muscle damage. Eccentric exercise-induced skeletal muscle damage offers an opportunity to investigate the signals and modulators of the repair of muscle damage, a process that may be central to the adaptations in muscle as a result of chronic activity.
运动诱导的骨骼肌损伤会导致大量局部和全身变化,包括细胞内蛋白质释放、延迟性肌肉酸痛、急性期反应以及骨骼肌蛋白质周转增加。这些运动诱导的适应性变化似乎是受损肌肉修复所必需的,可能对肌肉肥大至关重要。长期运动可使骨骼肌产生适应性变化,导致氧化代谢能力增强;受损肌肉修复导致的肥大可能是预防进一步运动诱导损伤的重要机制。虽然损伤后骨骼肌中肌酸激酶(CK)的释放是一种常见现象,但循环中的CK活性并非骨骼肌损伤的定量指标,在某些情况下甚至不是定性指标。离心运动诱导的骨骼肌损伤为研究肌肉损伤修复的信号和调节因子提供了契机,这一过程可能是长期运动导致肌肉适应性变化的核心。