钙过负荷与延迟性肌肉损伤

CALCIUM OVERLOAD IN EXERCISE INDUCED DELAYED ONSET MUSCLE DAMAGE

不习惯运动,特别是大强度离心运动结束一段时间后,运动的肌肉组织常出现一系列的炎性或退行性变化,我们将这种运动结束后出现的肌肉损伤变化定义为延迟性肌肉损伤。本文对这一类型的肌肉损伤的发生特点以及与细胞内钙不可逆增加的关系进行了研究,结果表明:细胞内钙过负荷在细胞损伤的早期即已出现,研究首次提供了延迟性肌肉损伤过程中细胞内钙过负荷的直接证据,并发现肌肉损伤过程中肌细胞变性坏死呈明显的阶段性。

Experiments were designed to study the role of calcium in delayed onset muscle damage resulting fromeccentric-based exercise in rats. The effects on both superficial white (WQ) and deep red quadricepes (RQ)muscle of running on a treadmill down a 16° incline at 16m. min^(-1) for 90 min were assessed by studyingpostexercise changes in 1. Histological appearance; 2. ATP ase NADH and SDH (succinate dehydrognase)activities in muscle; 3. Calcium in muscle cells (Alizarin red S method: ARS). The data indicated that:1. Muscle histology demonstrated localized disruption of normal binding patterns of some fibers immediatelyafter running and accumulation of mononuclear cells around some blood vessel by 3h postexercise and moreaccumulations of macrophages in interstitium and in some degenerated and necrosis (some fibers presentsegmental necrosis) muscle fibers by 24h and 48h postexercise in RQ. The damage was more serious by 48hthan 24h. The sarcoplasm of a few affected muscle fibers was removed, leaving the sarcolemma intact whichresult in the myocytes' 'ghost' appearance by 48h. But no distinct changes were detected in WQ; 2. Serialcross sections that were stained for ATPase, NADH and SDH activities showed marked decrease of enzymeactivities in some degenerated muscle fibers. It was very difficult to identify the affected muscle fibers byATPase and NADH activities by 24h and 48h postexercise. The enzyme activities of affected fibers weresimilar to slowtwitch fibers as indicated by myofibrillar ATPase activities after acid preincubation andsimilarto fasttwitch fibers as indicated by myofibrillar ATPase activity after alkaline preincubation and byNADH activity; 3. No calcium was unreversibly increased in the cross section of muscles immediately afterexercise by ARS staining. However, the calcium was unreversibly increased in some slight degenerated musclefiber by 3h and more fibers were affected by 24h and 48h postexercise in RQ. The slight positive stainingof calcium by ARS occurred before the decrease of enzymes activities and the invasion of macrophages inmuscle fibers. A clear correlation between degeneration and calcium overload was found in damaged musclefibers before accumulation of macrophages in these fibers. Our research indicated that calcium overload maybe one of the causative factors of eccentric exercise induced delayed onset muscle damage.