Nikolaidis Michalis G, Jamurtas Athanasios Z, Paschalis Vassilis, Fatouros Ioannis G, Koutedakis Yiannis, Kouretas Dimitris
Institute of Human Performance and Rehabilitation, Center for Research and Technology-Thessaly, Trikala, Greece.
Sports Med. 2008;38(7):579-606. doi: 10.2165/00007256-200838070-00005.
The aim of this article is to present the effects of acute muscle-damaging exercise on oxidative stress/damage of animal and human tissues using a quantitative approach and focusing on the time-course of exercise effects. The reviewed studies employed eccentric contractions on a dynamometer or downhill running. The statistical power of each study to detect a 20% or 40% post-exercise change compared with pre-exercise value in each oxidative stress/damage biomarker was calculated. Muscle-damaging exercise can increase free radical levels and augment oxidation of lipids, proteins, glutathione and possibly DNA in the blood. In contrast, the effect of muscle-damaging exercise on concentration of antioxidants in the blood, except for glutathione, was little. Muscle-damaging exercise induces oxidative stress/damage in skeletal muscle, even though this is not fully supported by the original statistical analysis of some studies. In contrast, muscle-damaging exercise does not appear to affect--at least to similar extent as the oxidative stress/damage markers--the levels of antioxidants in skeletal muscle. Based on the rather limited data available, the oxidative stress response of skeletal muscle to exercise was generally independent of muscle fibre type. Most of the changes in oxidative stress/damage appeared and were sustained for days after muscle-damaging exercise. The major part of the delayed oxidative stress/damage production that follows muscle-damaging exercise probably comes from phagocytic cells that are activated and recruited to the site of the initial damage. A point that emerged and potentially explains much of the lack of consensus among studies is the low statistical power of many of them. In summary, muscle-damaging exercise can increase oxidative stress/damage in blood and skeletal muscle of rats and humans that may persist for and/or appear several days after exercise.
本文旨在采用定量方法,重点关注运动效果的时间进程,呈现急性肌肉损伤运动对动物和人体组织氧化应激/损伤的影响。所综述的研究采用了测力计上的离心收缩或下坡跑。计算了每项研究检测每种氧化应激/损伤生物标志物运动后相对于运动前值变化20%或40%的统计功效。肌肉损伤运动可增加自由基水平,并增强血液中脂质、蛋白质、谷胱甘肽以及可能的DNA的氧化。相比之下,肌肉损伤运动对血液中除谷胱甘肽外的抗氧化剂浓度影响较小。肌肉损伤运动可诱导骨骼肌氧化应激/损伤,尽管一些研究的原始统计分析并未完全支持这一点。相比之下,肌肉损伤运动似乎不会影响——至少与氧化应激/损伤标志物的影响程度不同——骨骼肌中抗氧化剂的水平。基于现有相当有限的数据,骨骼肌对运动的氧化应激反应通常与肌纤维类型无关。氧化应激/损伤的大多数变化在肌肉损伤运动后出现并持续数天。肌肉损伤运动后延迟产生的氧化应激/损伤的主要部分可能来自被激活并募集到初始损伤部位的吞噬细胞。一个出现且可能解释了许多研究之间缺乏共识的问题是,其中许多研究的统计功效较低。总之,肌肉损伤运动可增加大鼠和人类血液及骨骼肌中的氧化应激/损伤,且这种情况可能在运动后持续和/或出现数天。