Abstract
Physical activity may benefit health by modulating oxidative stress and inflammation. However, the selection of suitable exercise-induced oxidative stress biomarkers is still challenging. This study aimed at systematically summarizing the available evidence on exercise-induced oxidative stress measured in urine and/or saliva. Two meta-analyses including the most frequently quantified biomarkers of oxidative stress, namely, urinary isoprostane and DNA oxidation products, were performed. Three electronic databases (PubMed, EMBASE and Cochrane CENTRAL) were interrogated. Among 4479 records, 43 original articles were included in the systematic review and 11 articles were included in meta-analysis I and II, respectively. We observed a pooled trend of increase of urinary isoprostanes in response to physical activity (+0.95, 95% CI: −0.18; 2.09). In comparison with aerobic exercise, anaerobic training determined a greater induction of isoprostanes (+5.21, 95% CI: 2.76; 7.66, p < 0.0001), which were markedly increased after vigorous physical activity (+6.01, 95% CI: 1.18; 10.84, p < 0.001) and slightly decreased in response to exercise interventions protracted over time (e.g., months) (−1.19, 95% CI: −2.25; −0.12, p < 0.001). We recommend the most integrative approach of oxidative stress multi-marker panels in response to physical activity instead of selecting one preferential biomarker to quantify physical activity-induced oxidative stress in humans.
Highlights
In the last few decades, the scientific interest in physical activity-induced oxidative stress has been fuelled by three complementary concepts
The main reasons texts, original data not adequately reported
Despite the wide heterogeneity among a large set of oxidative stress biomarkers quantified in both urine and saliva, the present meta-analysis concluded that urinary isoprostanes seem more prone to physical activity modulation
Summary
In the last few decades, the scientific interest in physical activity-induced oxidative stress has been fuelled by three complementary concepts. Oxidative stress is involved in the pathogenesis [2] or represents a downstream consequence of several diseases [3]. Since the pioneering discovery that lipid peroxidation biomarkers increase in subjects following acute exercise [5,6], the understanding of the exercise-induced oxidative stress was further extended by the introduction of some key scientific discoveries including (1) the involvement of pro-oxidants species in the production and modulation of muscles force [7]; (2) the dose-response effect of training on primary antioxidant levels in cardiac and skeletal muscle [8]; (3) the contribution of nitric oxide in muscle vasodilatation [9]. Its production in contracting muscles [10] Overall, this body of evidence laid the foundations for applying the theory of hormesis to exercise-induced oxidative stress [11]
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