Influence of exercise intensity on systemic oxidative stress and antioxidant capacity

Abstract

The aim of the current study was to examine the influence of exercise intensity on systemic oxidative stress (OS) and endogenous antioxidant capacity. Non-smoking, sedentary healthy adult males (n = 14) participated in two exercise sessions using an electronically braked cycle ergometer. The first session consisted of a graded exercise test to determine maximal power output and oxygen consumption (VO(2max)). One week later, participants undertook 5-min cycling bouts at 40%, 55%, 70%, 85% and 100% of VO(2max), with passive 12-min rest between stages. Measures of systemic OS reactive oxygen metabolites (dROM), biological antioxidant potential (BAP), heart rate (HR), VO(2), blood lactate and rating of perceived exertion were assessed at rest and immediately following each exercise stage. Significant (P<0·05) differences between exercise bouts were examined via repeated measures ANOVA and post hoc pairwise comparisons with Bonferroni correction. Increasing exercise intensity significantly augmented HR (P<0·001), VO(2) (P<0·001), blood lactate (P<0·001) and perceived exertion (P<0·001) with no significant effect on dROM levels compared with resting values. In contrast, increasing exercise intensity resulted in significantly (P<0·01) greater BAP at 70% (2427 ± 106), 85% (2625 ± 121) and 100% (2651 ± 92) of VO(2max) compared with resting levels (2105 ± 57 μmol Fe(2+)/L). The current results indicate that brief, moderate-to-high-intensity exercise significantly elevates endogenous antioxidant defences, possibly to counteract increased levels of exercise-induced reactive oxygen species. Regular moderate-to-high-intensity exercise may protect against chronic OS associated diseases via activation, and subsequent upregulation of the endogenous antioxidant defence system.

Redox Mechanism of Reactive Oxygen Species in Exercise

“…However, the overproduction of ROS induced by exhaustive exercise training or other stresses, along with compromised antioxidant defenses, can lead to oxidative stress and related tissue damage (Powers et al, 2011b; Zuo et al, 2012). Interestingly, proper exercise (moderate to high intensity exercise) stimulates the adaptive responses and strengthens the endogenous antioxidant defense systems to combat excessive ROS thereby maintaining muscle redox balance (Parker et al, 2014; Zuo et al, 2015b). …”

Exercise intensity, redox homeostasis and inflammation in type 2 diabetes mellitus

“…5,6 However, the intensity of exercise needed to produce the most favourable changes in redox homeostasis, the balance between RS and antioxidants, is still under debate. 7,8,9 High-intensity interval training (HIIT) is a time efficient way of increasing cardiorespiratory fitness with double the improvements in VO2peak in a shorter exercise time. 10 It has been suggested that HIIT may provide greater improvements in redox homeostasis regulation than traditional moderate-intensity continuous training (MICT).…”

Acute Low-Volume High-Intensity Interval Exercise and Continuous Moderate-Intensity Exercise Elicit a Similar Improvement in 24-h Glycemic Control in Overweight and Obese Adults

“…A single session of low to moderate-intensity exercise in healthy males attenuates the postprandial oxidative stress response to a meal ingested 2 h before (Mc Clean et al, 2007) and 24 h after exercise (Takahashi et al, 2015). Furthermore, high-intensity exercise which elicits greater oxidative stress and antioxidant activity compared to low to moderate intensity exercise (Schneider et al, 2005; Fisher-Wellman and Bloomer, 2009; Parker et al, 2014), may also attenuate postprandial oxidative stress (Tyldum et al, 2009; Gabriel et al, 2012). Considering the impact of HIIE on postprandial oxidative stress are equivocal (Canale et al, 2014), and overweight and inactive population's exhibit greater basal and postprandial oxidative stress than healthy controls (Tucker et al, 2008; Fisher-Wellman et al, 2009), further research is warranted.…”