Exercise-Induced Oxidative Stress

 

Dr.  Chen Chee Keong,

Head, Sports Science Unit, School of Medical Sciences,

Universiti Sains Malayasia, Kubang Kerian

 

Free radicals (FR) are reactive compounds that are produced naturally in the human body. They are molecules or molecule fragments with one or more unpaired electrons in their outer orbits. Hence, they are very unstable and reactive since they tend to ‘snatch’ an electron from other molecules. Free radicals include reactive oxygen species (ROS) and reactive nitrogen species. Examples of free radicals related to exercise commonly cited in the literature are superoxide ion, hydrogen peroxide, peroxyl, nitric oxide and hydroxyl.

 

 

 

Cells in our body are protected against free radical-mediated injury by enzymatic and non-enzymatic antioxidants. Antioxidants are substances that help to reduce the severity of oxidative stress either by forming a less reactive radical or by quenching the damaging FR chain reaction. Endogenous enzymatic antioxidants that are active in the body include superoxide dismutase, catalase and gluthathione peroxidase while non-enzymatic antioxidants include vitamin A, vitamin C, vitamin E, flavanoids, thiols, uric acid, bilirubin and micronutrients (iron, copper, zinc, selenium, manganese) that act as enzymatic cofactors. However, these antioxidant defenses can be overwhelmed if there is an imbalance between FR production and its antioxidant capacity in favour of the former. This will result in oxidative stress. Oxidative stress is implicated in virtually every known disease and there is increasing evidence linking free radical production to the process of aging.

  

 

There is adequate credible evidence indicating that there is an increased generation of free radicals during and after exercise, resulting in a substantial degree of oxidative modifications to various molecules. These include free radical-induced damage to lipids, proteins and DNA.  Dillard et al. (1978) were the first investigators to provide evidence that physical exercise can lead to increased lipid peroxidation. Davies et al. (198) confirmed this finding of exercise-induced oxidative stress by demonstrating a 2- to 3- fold increase in free radical production during exhaustive exercise in rats. Consequently, data from numerous studies seem to support the occurrence of exercise-induced oxidative stress, but it remains unclear what causes the increase in FR production. It is possible that different types of exercise (aerobic. anaerobic or combination/mixed) involve different mechanisms of FR generation.

 

 

FRs has also been shown to lead to muscular fatigue and therefore limit performance. Numerous factors seem to be implicated in FR-induced muscular fatigue. The alteration of the mitochondrial functions with exposure to ROS is considered a major factor of muscular fatigue. FRs can also induce alterations to the respiratory complexes, with a consequent decrease of electron transfer and ATP formation. Hence, aerobic pathways become less efficient under these circumstances. Contractile proteins (actin and myosin) and calcium pump are muscular compounds that are sensitive to redox status. Thus, ROS have a negative effect on muscular contraction (contractile property) and muscular contraction control (calcium pump) which can lead to muscular fatigue. Furthermore, it has been demonstrated that action potential for muscle contraction can be modified by ROS.

 

In summary, there is growing evidence in the literature demonstrating the production of FRs during and after physical activity. However, it must be highlighted that only exercise of sufficient intensity or duration appears to lead to a large enough increase in FR production to overwhelm the antioxidant defence. Thus, individuals following the standard exercise prescription for health promotion and maintenance should not be deterred from practising a healthy lifestyle provided that they have adequate intake of nutrients and vitamins from a balance diet. In my next article, I will discuss the various antioxidants in further detail and what the recent literature says regarding antioxidant supplementation on athletic performance

 

 

References:

 

Dekkers, JC, van Doornen LJ, & Kemper HC. (1996). The role of antioxidant vitamins and enzymes in the prevention of exercised-induced muscle damage. Sports Med.       21(3):231-38

 

Finaud, J, Lac, G & Filaire, E. (2006). Oxidative Stress: Relationship with Exercise andTraining. Sports Med. 36(4):327-58.

 

Halliwell, B. & Chiricao. (1993). Lipid peroxidation: its mechanism, measurement, and significanc. Am J Clin Nutr. 57(Suppl): 715S-24S.

 

Ji, L.L. (1995a). Exercise and oxidative stress: Role of cellular antioxidant  systems. Exerc. Sport. Sci. Rev. 23, 135-166.

 

Reid, M.B., Hack, K.E., Franchek, K.M., Valberg, P.A., Kobzik, L. & West, M.S. (1992a). Reactive oxygen in skeletal muscle. I. Intracellular oxidant kinetics and fatigue in vitro. J. Appl. Physiol. 73(5), 1797-1804.

 

Reid, M.B., Shoji, T., Moody, M.R. & Entman, M.L. (1992b).  Reactive oxygen in skeletal    muscle. II. Extracellular release of free radicals. J. Appl. Physiol. 73(5), 1805-1809

 

Vollaard, NBJ, Shearman, JP & Cooper, CE. (2005). Exercise-Induced Oxidative Stress: Myths, Realities and Physiological Relevance. Sports Med. 35(2):1045-62.