Abstract

We read with great interest an article by Knez et al. (4) published in the February 2007 issue of Medicine & Science in Sports & Exercise , measuring the oxidative stress response to endurance exercise in half and full Ironman triathletes. Interestingly, Knez et al. (4) found that those athletes taking antioxidant supplementation exhibited a greater oxidative stress response to endurance exercise than nonusers. Although the authors (4) were able to support their results by referencing previous research that suggests the prooxidant effect of antioxidant supplementation (vitamin E) in Ironman triathletes (5), we believe that Knez et al. (4) failed to consider more recently reported findings that suggest other mechanisms to explain the differential oxidative response between the antioxidant supplementing and nonsupplementing athletes. Based on the classical physiological concept of hormesis (3), which refers to a generally favorable biological response to exposures of toxins or stressors, recurring episodes of exercise-induced oxidative stress may increase the tolerance of the organism to withstand higher doses; however, this protective long-term effect may be ablated when exercise training is combined with antioxidant supplementation. In this context, and contrary to the general credence that oxidative stress associated with strenuous exercise causes cellular damage, the role of exerciseinduced production of free radicals in cell signaling should be considered (2). Particularly, the redox-sensitive transcription factor nuclear factor (NF)-kappa (J)B is activated with exercise, leading to increased expression of antioxidant enzymes (1). There is sufficient evidence to suggest that reactive oxygen or nitrogen species (RONS) are crucial in generating signals that are imperative for cell adaptation to exercise training. In a recent study using rats, GomezCabrera and colleagues (1) eloquently demonstrated that decreasing the exercise-induced RONS formation (via xanthine oxidase inhibition) prevented activation of important signaling pathways, predominantly the mitogenactivated protein kinase–NFJB pathway, and, as a result, antioxidant enzyme expression was reduced. When considering Gomez-Cabrera et al._s (1) findings, it is reasonable to speculate that athletes taking antioxidant supplementation throughout an exercise training period may develop inappropriate antioxidant adaptations. Consequently, under exposure to an extreme oxidative exercise challenge such as an ultraendurance race, users of antioxidant supplementation may well display an increased oxidative stress compared with nonusers. Therefore, the findings of Gomez-Cabrera et al. (1) and Knez et al. (4) raise an important question: Does antioxidant supplementation prevent favorable adaptations to exercise training? We believe that the recommendation that physically active individuals should supplement with antioxidants needs to be revised, as exogenous antioxidants may prevent useful and protective adaptations to habitual exercise.

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