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运动诱导的肌肉损伤与炎症:综述

Exercise-induced muscle damage and inflammation: a review.

作者信息

Pyne D B

机构信息

Division of Biochemistry and Molecular Biology, Australian National University, Canberra.

出版信息

Aust J Sci Med Sport. 1994 Sep-Dec;26(3-4):49-58.

PMID:8665277
Abstract

Unaccustomed exercise may result in significant damage to skeletal muscle and cause delayed onset muscle soreness (DOMS) in both recreational and elite athletes. Two basic mechanisms-'metabolic' and 'mechanical' stress--have been proposed to explain how exercise initiates damage to skeletal muscle fibres. The extent of damage, particularly after eccentrically-biased exercise, has been assessed by histological and ultrastructural examination, and the measurement of the efflux of cytosolic enzymes into the circulation. The role of reactive oxygen species in the mediation of exercise-induced oxidative damage to muscle and the protection offered by anti-oxidant defence systems have been well studied. Free radical generation is normally estimated by indirect methods such as chemiluminescence, spectrophotometry, flow cytometry, or the measurement of products of lipid peroxidation such as malondialdehyde (MDA) and thiobarbituric acid reactive substances (TBARS). Although several theories have been proposed to account for the DOMS phenomenon, the underlying mechanisms are still to be elucidated. A group of proteins known collectively as cytokines regulate inflammatory and immunological processes involved in the repair of damaged tissue.

摘要

不习惯的运动可能会对骨骼肌造成严重损伤,并在业余和精英运动员中引发延迟性肌肉酸痛(DOMS)。人们提出了两种基本机制——“代谢”和“机械”应激——来解释运动如何引发骨骼肌纤维损伤。损伤程度,尤其是在以离心为主的运动后,已通过组织学和超微结构检查以及测量胞质酶向循环中的外流来评估。活性氧在介导运动诱导的肌肉氧化损伤中的作用以及抗氧化防御系统提供的保护已得到充分研究。自由基生成通常通过间接方法估计,如化学发光、分光光度法、流式细胞术,或测量脂质过氧化产物,如丙二醛(MDA)和硫代巴比妥酸反应性物质(TBARS)。尽管已经提出了几种理论来解释DOMS现象,但其潜在机制仍有待阐明。一组统称为细胞因子的蛋白质调节参与受损组织修复的炎症和免疫过程。

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