Reliability of different blood indices to explore the oxidative stress in response to maximal cycling and static exercises

Abstract

This study compares the changes in four blood markers of exercise-induced oxidative stress in response to exercise protocols commonly used to explore the global muscle performance at work (maximal incremental cycle) and endurance to fatigue of selected muscles (static handgrip and thumb adduction). Cycling and static exercises allow the muscle to work in aerobic and anaerobic conditions, respectively. Healthy adults performed an incremental cycling exercise until volitional exhaustion and, on separated days, executed infra-maximal static thumb adduction and handgrip until exhaustion. Exercise-induced oxidative stress was assessed by the increased plasma concentration of thiobarbituric acid reactive substances (TBARS), the consumption of plasma reduced ascorbic acid (RAA), and erythrocyte reduced glutathione (GSH) antioxidants, and the changes in the total antioxidant status (TAS) of plasma. Five minutes after the end of the incremental cycling exercise, we measured a peak increase in TBARS level, maximal consumption of GSH and RAA, and a modest but significant decrease in TAS concentration. In response to both static thumb adduction and handgrip, significant variations of TBARS, GSH and RAA occurred but we did not measure any significant change in TAS level throughout the 20-min recovery period of both exercise bouts. The present study shows that only the changes in TBARS, GSH and RAA explore both dynamic and static exercises. In addition, TAS measurement does not seem to represent a reliable and unique tool to explore exercise-induced oxidative stress, at least during isometric efforts that allow the muscle to work under anaerobic condition.

The protective role of oral consumption of N-acetyl cysteine during a single session of exhaustive exercise in untrained subjects

“…It was found that the total antioxidant capacity decreased immediately after the exhaustive time in the treated group; this may be because of the antioxidant components used to quench the over production of harmful radicals at this particular time. This was supported by the investigation which shows that the antioxidant capacity may be temporarily reduced during and immediately post exercise (Teixeira, 2009;Kerksick and Willoughby, 2005;Steinberg et al, 2006). In our study, there was no change observed in the time to fatigue regarding the subjects treated with NAC as compared to the control.…”

Effect of short- and long-term strength exercise on cardiac oxidative stress and performance in rat

“…In acute strength exercises, ROS levels usually rise from their resting levels [30], and there is a close relationship between ROS production and the intensity of exercise [6]. These conditions are with oxidative stress probably caused by oxidizing materials produced in mitochondria or via reperfusion injury [26].…”

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

“…Moreover, other studies have reported increases in F 2 -isoprostanes (the reference biomarkers of lipid peroxidation) in plasma and decreases in reduced glutathione (GSH; a valid biomarker of the redox state) in erythrocytes after the same 30s cycling test (Groussard et al, 2003a;Groussard et al, 2003b; Cuevas et al, 2005; Cooke et al, 2008;Arent et al, 2010) (Fig.2). Similarly, several studies have reported increases in reactive species production determined by EPR in whole blood (Peters et al, 2006) and changes in the redox couple of reduced glutathione and oxidized glutathione (glutathione disulfide; GSSG) toward a more oxidized redox potential after isometric handgrip exercise (at 50% of maximal voluntary contraction to exhaustion) lasting from 84 to 170s (Matuszczak et al, 2005;Steinberg et al, 2006). Based on this evidence, it seems that even very short isometric exercise activating a relatively small muscle mass is able to increase reactive species production and induce oxidative stress systemically.…”