Antioxidants and exercise: a tale of the complexities of relating signalling processes to physiological function?-猫眼课题宝

抗氧化剂和运动：信号过程与生理功能相关的复杂性？

DOI：

10.1113/jphysiol.2014.272294

发表时间：

2014

期刊：

The Journal of physiology

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(‘Vitamin C and E supplementation hampers cellular adaptation to endurance training in humans: a double-blind randomized controlled trial’Paulsen et al. 2014) is a useful addition to the debate that has raged in this area and provides some explanation of how the different parties may have come to their diametrically opposing views. In brief, the current study used a formal double-blind trial approach to address this issue and observed that vitamin E and C supplements blunted some cellular adaptations (training-induced increases in muscle mitochondrial proteins), but had no effect on physiological indicators of performance (VO2max etc.). Researchers have been attempting to suppress the assumed deleterious effects of reactive oxygen and nitrogen species that are generated during exercise since the first descriptions of their generation in such situations (eg Dillard et al. 1978) with little evidence that such interventions were beneficial. However, the realisation that these species play important roles in cell signalling (redox signalling) prompted a rethink of what the so-called ‘antioxidants’ were meant to achieve. Our group initially demonstrated that high doses of vitamin C could inhibit rapid stress responses to acute exercise (Khassaf et al. 2003) and this line was pursued by others who reported that high doses of antioxidants could reduce the training effects of exercise on muscle mitochondrial biogenesis, VO2max and improvements in insulin sensitivity (eg Gomez-Cabrera et al. 2008; Ristow et al. 2009). Although not overtly stated, such studies imply that reactive oxygen and nitrogen species must play a key and possibly unique role in regulating multiple training-induced adaptations to muscle in humans and animals. Unfortunately such findings could not be repeated by other eminent scientists who firmly reported normal adaptations to exercise training despite administration of high dose antioxidants (eg Higashida et al. 2011). This difference resulted in an intense head-to-head debate in the scientific literature from the groups reporting these differing results (eg Holloszy et al. 2012).So why do these studies (and their proponents) differ? It is easy to point out the multiple differences in experimental design that are likely to underlie the variability in reported outcome. These include: the use of animals or humans; trained or untrained subjects; the durations and protocols for the training; the choice of markers of oxidative stress (including some use of completely outdated assays, such as TBARS); the time points studied; the use of muscle versus blood markers; and many more potential factors. Consequently, we should not be surprised at the heterogeneity of the reported effects. It is also relevant to question the rationale behind using the particular antioxidant supplements given in these training experiments. Thus why did some investigators give vitamin E supplements for a period of time that does not allow sufficient time for tissue accretion, or why were excessively high vitamin C supplements used in both human and animal models despite widely acknowledged data describing vitamin C saturation kinetics in man and animals and the potential for non-redox effects at these high doses? It is also relevant to consider the current knowledge of redox signalling in muscle and other tissues, and what is clear from the basic biological research undertaken in this area is that these effects are highly site-specific and relatively subtle, such that reactive oxygen and nitrogen species are unlikely to represent a unique regulatory factor in multiple pathways associated with responses to exercise.