Take a trip to any food retail store, find yourself in the health section and you are immediately struck by the vast quantity of available supplements all posing various remedies. Concerning the active person wishing to aid their recovery from exercise to enable them to work-out without the feeling of muscle weakness, lethargy, delayed onset muscle soreness etc., one is often attracted to this range of products, in particular the shelf stacked and labelled ‘antioxidants’.

Antioxidants have received a plethora of attention within both the media and scientific domains. Many reasons have been established within the literature to support the use of antioxidant supplementation for the athletic population including; their use in protecting muscle fibers against oxidative damage (Schroder et al 2001), their role in delaying muscular fatigue resulting in increased endurance performance capacity (Reid 2008) and their potential to be beneficial to the overall health of an individual (Powers et al 2011a). In addition, antioxidant supplementation can result in a balanced diet where nutrition intake is inadequate (Powers et al 2011a). However, are antioxidants really a necessity in overcoming oxidative stress induced by exercise? The purpose of this article is to explore the topic of oxidative stress, its’ source, the body’s mechanism in coping with this stress and its effect on training adaptations.

What is oxidative stress?

Briefly, within the cell mitochondria, during normal metabolism, oxygen is used for the production of energy. During the process of oxidative phosphorylation, the vast majority of oxygen consumed is bound to hydrogen to form water. At time points where a small percentage of this water is not completely reduced, oxygen intermediates known as reactive oxygen species (ROS) are produced. Cumulatively these species are referred to as oxidative stress. It occurs as a consequence of an imbalance between oxidant capacity and antioxidant capacity (Williams et al 2006).

Beneficial Role of Oxidative Stress

Despite the fact that ROS is mostly associated with being detrimental to health, oxidative stress is in fact an essential part of cellular development and its’ optimal function (Thannickal and Fanburg 2000). Cells utilize oxidative stress as a biological stimulus as it acts as a sub-cellular messenger necessary for important signalling process, which modulate enzyme and gene action. It is an important factor in the growth, proliferation and initiating the death of cells. Within the immune system, oxidative stress is incorporated in the biosynthesis of other molecules including the immune response to cells and detoxifying drugs (Thannickal and Fanburg 2000). Oxidative stress is a requisite of vasodilatation (Wagner et al 2000) and is considered essential for muscular function and metabolism (Jackson 2008). Recently it has been stated that redox signalling (the alteration of a biological system in response to a change in the level of a particular reactive oxygen species) in contracting muscle is one of the basic elements in exercise biology (Powers and Jackson 2008).

The body’s defence mechanism

The body is naturally equipped with highly effective antioxidant defence systems. These can be present in an enzymatic form (superoxide dismutase (SOD), catalase, glutathione peroxidase (GPX) and glutathione reductase) and non-enzymatic forms (glutathione, uric acid, lipoic acid, bilrubin and co-enzyme Q10. Of course, with the use of supplementation, this endogenous store can be further boosted with the use of antioxidants including vitamin C, E and β-carotene. In addition, it has been reported that the endogenous antioxidant systems respond rapidly to an increased production of ROS. Gene expression can be modulated by cells along with the capacity of antioxidant enzymes to cope with various degrees of oxidative stress (Peternelj and Coombes 2011). But surely if I exercise, that means increased levels of oxidative stress, then, I need antioxidants…right?

Exercise-Induced Oxidative Stress

Exercise increases oxygen consumption by up to 20 times above resting values resulting a 200-fold greater oxygen usage in mitochondria, so yes a greater level of ROS are produced during exercise and muscular contraction (Peternelj and Coombes 2011). However, cells are capable of adapting to increased ROS production to become more resistant to the adverse effects of oxidative stress. In order for this adaptation to be present though, exercise must be regular in order for the body to accustom to these increased oxidant levels. The adaptation to increased oxidant levels for the individual who conducts periods of acute exercise is minimal as it is not sufficient enough to replenish the state of oxidant-antioxidant homeostasis (Ji 2008). In order to ensure long term stimulation of an endogenous antioxidant system, regular physiological stimuli are required to be present such as those activated by exercise, aiding in the maintenance of a pro-oxidative environment which effectively overloads the antioxidant system. With regular exercise, ROS positively affects the remodelling of skeletal muscle post injury (Radak et al 2008). While moderate levels of ROS are evidently necessary for physiological processes, where excess levels are present, this becomes inhibitory to muscle function as is illustrated by Reid’s model for the role of the redox state on muscle force production, in response to ROS (Reid et al 1993; Reid 2001).

Many areas are discussed within the literature regarding sports nutrition and antioxidants including its effect on exercise, its use as an ergogenic aid, its relationship with muscle damage and also as a recovery aid. The focus point here however is the interference that antioxidants have on what should be the benefits of exercise training. When consumed in high amounts it has been reported that antioxidants have been shown to increase markers of exercise-induced oxidative stress. Malm et al (1996) saw that where coenzyme Q10 was administered after high intensity exercise, creatine kinase (CK), a marker of oxidative stress increased. This study however was of low quality due to the lack of methodological details. Childs et al (2001) using a dose combination of vitamin C and N-acetylcysteine supplementation also saw a rise in oxidative stress level following eccentric arm exercise. 2 months supplementation of vitamin E use among ironman triathletes (Nieman et al 2004) was associated with an increase in inflammation and lipid peroxidation. These few studies presented here have many limitations including lack of individual redox states reported prior to supplementation. The focus of many of these studies is centred on vitamin E, C and coenzyme Q10. Where null findings are reported, this may be due to insufficient dosages, treatment duration variation and the lack of detection techniques.


To conclude, the multifunctional role of reactive species, their benefits and consequences alongside the use of antioxidant supplementation demonstrate the complexity of exercise-induced oxidative stress. The relationship between antioxidants and ROS should be carefully considered as the redox state will dictate cell functioning. It is important not to undermine the natural ability the body has when coping with stress induced by exercise. While antioxidants have their place in certain circumstances, more specifically within the subject of disease onset and recovery, a balanced diet including a variety of fruits and vegetables remains the best nutritional approach to maintain optimal antioxidant status to inhibit the blunting of training adaptations by interrupting important signalling to muscles and cells. Consistent research is required to allow clear conclusions to be drawn on specific sporting disciplines, specific antioxidant components and time-dose-responses.

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