Choi Seung Jun
Division of Sports and Health Science, Kyungsung University, Busan, Korea.
J Exerc Rehabil. 2014 Aug 31;10(4):200-4. doi: 10.12965/jer.140139. eCollection 2014 Aug.
Activity-induced muscle injury and dysfunction have been identified as key components of musculoskeletal injuries. These injuries often occur following eccentric contractions, when the muscle is under tension and stretched by a force that is greater than the force generated by the muscle. Many daily activities require muscles to perform eccentric contractions, including walking (or running) downhill or down stairs, lowering heavy objects, and landing from a jump. Injuries often occur when these activities are performed at high intensity or for prolonged periods of time. General features of eccentric-induced muscle injury are well documented and include disruption of intracellular muscle structure, prolonged muscle weakness and dysfunction, a delayed-onset muscle soreness, and inflammation. Several weeks are required for the affected tissue to fully regenerate and recover from eccentric-induced muscle injury. Possible mechanisms responsible for eccentric-induced muscle injury are activation impairment and structural disruption of the sarcomere. These two factors seem to be the main sources of eccentric-induced muscle injury. Rather than being separate mechanisms they may be complimentary and interact with each other. Therefore, in this review we will focus on the two main cellular mechanism of muscle cell injury following accustomed eccentric contraction.
运动诱发的肌肉损伤和功能障碍已被确认为肌肉骨骼损伤的关键组成部分。这些损伤通常发生在离心收缩之后，即当肌肉处于张力下并被大于肌肉产生的力的外力拉伸时。许多日常活动都需要肌肉进行离心收缩，包括下坡行走（或跑步）、下楼梯、放下重物以及从跳跃中落地。当这些活动高强度进行或持续较长时间时，损伤往往就会发生。离心诱发的肌肉损伤的一般特征已有充分记录，包括细胞内肌肉结构的破坏、肌肉长期无力和功能障碍、延迟性肌肉酸痛以及炎症。受影响的组织需要数周时间才能从离心诱发的肌肉损伤中完全再生和恢复。导致离心诱发肌肉损伤的可能机制是肌节的激活受损和结构破坏。这两个因素似乎是离心诱发肌肉损伤的主要来源。它们并非相互独立的机制，而是可能相互补充并相互作用。因此，在本综述中，我们将重点关注习惯性离心收缩后肌肉细胞损伤的两种主要细胞机制。
