Exercise Physiology and Biochemistry Laboratory, Department of Physical Education and Sports Science at Serres, Aristotle University of Thessaloniki, 62110 Serres, Greece.
J Exp Biol. 2012 May 15;215(Pt 10):1615-25. doi: 10.1242/jeb.067470.
The central aim of this review is to address the highly multidisciplinary topic of redox biology as related to exercise using an integrative and comparative approach rather than focusing on blood, skeletal muscle or humans. An attempt is also made to re-define 'oxidative stress' as well as to introduce the term 'alterations in redox homeostasis' to describe changes in redox homeostasis indicating oxidative stress, reductive stress or both. The literature analysis shows that the effects of non-muscle-damaging exercise and muscle-damaging exercise on redox homeostasis are completely different. Non-muscle-damaging exercise induces alterations in redox homeostasis that last a few hours post exercise, whereas muscle-damaging exercise causes alterations in redox homeostasis that may persist for and/or appear several days post exercise. Both exhaustive maximal exercise lasting only 30 s and isometric exercise lasting 1-3 min (the latter activating in addition a small muscle mass) induce systemic oxidative stress. With the necessary modifications, exercise is capable of inducing redox homeostasis alterations in all fluids, cells, tissues and organs studied so far, irrespective of strains and species. More importantly, 'exercise-induced oxidative stress' is not an 'oddity' associated with a particular type of exercise, tissue or species. Rather, oxidative stress constitutes a ubiquitous fundamental biological response to the alteration of redox homeostasis imposed by exercise. The hormesis concept could provide an interpretative framework to reconcile differences that emerge among studies in the field of exercise redox biology. Integrative and comparative approaches can help determine the interactions of key redox responses at multiple levels of biological organization.
本篇综述的核心目的是采用整合与比较的方法，探讨与运动相关的氧化还原生物学这一多学科主题，而不是集中于血液、骨骼肌或人类。本文还尝试重新定义“氧化应激”，并引入“氧化还原稳态改变”这一术语，以描述指示氧化应激、还原应激或两者兼有的氧化还原稳态改变。文献分析表明，非肌肉损伤性运动和肌肉损伤性运动对氧化还原稳态的影响完全不同。非肌肉损伤性运动引起的氧化还原稳态改变仅持续数小时，而肌肉损伤性运动引起的氧化还原稳态改变可能持续数天甚至数天。持续仅 30 秒的耗竭性最大运动和持续 1-3 分钟的等长运动（后者除了激活少量肌肉外）都会引起全身氧化应激。通过必要的修改，运动能够引起迄今为止研究的所有液体、细胞、组织和器官的氧化还原稳态改变，而与品系和物种无关。更重要的是，“运动引起的氧化应激”不是与特定运动类型、组织或物种相关的“异常”。相反，氧化应激构成了对运动引起的氧化还原稳态改变的普遍基本生物学反应。适应现象的概念可以提供一个解释框架，以调和运动氧化还原生物学领域研究中出现的差异。整合与比较方法可以帮助确定关键氧化还原反应在多个生物学组织层次上的相互作用。
