The effect of exercise-induced hypoxemia on blood redox status in well-trained rowers

Abstract

Exercise-induced arterial hypoxemia (EIAH), characterized by decline in arterial oxyhemoglobin saturation (SaO(2)), is a common phenomenon in endurance athletes. Acute intensive exercise is associated with the generation of reactive species that may result in redox status disturbances and oxidation of cell macromolecules. The purpose of the present study was to investigate whether EIAH augments oxidative stress as determined in blood plasma and erythrocytes in well-trained male rowers after a 2,000-m rowing ergometer race. Initially, athletes were assigned into either the normoxemic (n = 9, SaO(2) >92%, [Formula: see text]: 62.0 ± 1.9 ml kg(-1) min(-1)) or hypoxemic (n = 12, SaO(2) <92%, [Formula: see text]: 60.5 ± 2.2 ml kg(-1 )min(-1), mean ± SEM) group, following an incremental [Formula: see text] test on a wind resistance braked rowing ergometer. On a separate day the rowers performed a 2,000-m all-out effort on the same rowing ergometer. Following an overnight fast, blood samples were drawn from an antecubital vein before and immediately after the termination of the 2,000-m all-out effort and analyzed for selective oxidative stress markers. In both the normoxemic (SaO(2): 94.1 ± 0.9%) and hypoxemic (SaO(2): 88.6 ± 2.4%) rowers similar and significant exercise increase in serum thiobarbituric acid-reactive substances, protein carbonyls, catalase and total antioxidant capacity concentration were observed post-2,000 m all-out effort. Exercise significantly increased the oxidized glutathione concentration and decreased the ratio of reduced (GSH)-to-oxidized (GSSG) glutathione in the normoxemic group only, whereas the reduced form of glutathione remained unaffected in either groups. The increased oxidation of GSH to GSSG in erythrocytes of normoxemic individuals suggest that erythrocyte redox status may be affected by the oxygen saturation degree of hemoglobin. Our findings indicate that exercise-induced hypoxemia did not further affect the increased blood oxidative damage of lipids and proteins observed after a 2,000-m rowing ergometer race in highly-trained male rowers. The present data do not support any potential link between exercise-induced hypoxemia, oxidative stress increase and exercise performance.

Effects of exercise on alterations in redox homeostasis in elite male and female endurance athletes using a clinical point-of-care test

“…Indeed, some of the largest reported changes in redox homeostasis occurred in the general preparation phases of periodised training programs, such as when athletes are returning to training after a transition period of minimal training and detraining (Kyparos et al 2009;Kyparos et al 2011).…”

Alterations in Redox Homeostasis in the Elite Endurance Athlete

“…The exercise protocols used to assess ARH were sport-specific and ranged from 2,000 m simulated rowing races, maximal treadmill and cycling tests, multiple Wingate tests, and an interval swim test. Only two studies reported the analytical variability of the assays used [25,107], and only the cycling study of Cuevas et al [109], and the two rowing studies of Kyparos et al [25,107] controlled for changes in plasma volume (PV). Biomarkers of lipid peroxidation either increased or did not change pre-to post-exercise challenge, with large increases (45-100 %) for thiobarbituric acid reactive substances (TBARS) pre-to post-simulated 2,000 m rowing races [24,25,107], a modest increase (16 %) in swimmers pre-to post-interval swimming (8 9 100 m) [110], and no change reported in one cycling study utilising multiple Wingate tests [109].…”

“…Only two studies reported the analytical variability of the assays used [25,107], and only the cycling study of Cuevas et al [109], and the two rowing studies of Kyparos et al [25,107] controlled for changes in plasma volume (PV). Biomarkers of lipid peroxidation either increased or did not change pre-to post-exercise challenge, with large increases (45-100 %) for thiobarbituric acid reactive substances (TBARS) pre-to post-simulated 2,000 m rowing races [24,25,107], a modest increase (16 %) in swimmers pre-to post-interval swimming (8 9 100 m) [110], and no change reported in one cycling study utilising multiple Wingate tests [109]. Two other assays were used to assess lipid peroxidation, conjugated dienes (CD) and RBC malondialdehyde (MDA) as follows: Pittaluga et al [108] reported a small increase pre-to post-maximal exercise in professional road cyclists for CD, and in distance runners, Dane et al [111] reported no change for RBC MDA pre-to post-maximal exercise.…”

“…Three studies measured biomarkers of protein oxidation (protein carbonyls, PC; advanced oxidation protein products, AOPP), with two studies in rowers showing the largest increase for PC (*70 %) pre-to-post a simulated 2,000 m race [25,107], and a decrease (15 %) for AOPP in swimmers following an interval swim test [110]. The biomarker of oxidative DNA (deoxyribonucleic acid) damage, 8-oxo-2 0 -deoxyguanosine (8-OHdG), was measured in lymphocytes, increasing 29 and 35 % in the lymphocytes of cyclists 24 hours after a single and multiple Wingate tests, respectively [109].…”

“…Only three studies referenced the training phase within the athlete's macrocycle at the time of the study. Two rowing studies were undertaken within the general preparation phase [25,107], and one cycling study in the competition season [108]. The exercise protocols used to assess ARH were sport-specific and ranged from 2,000 m simulated rowing races, maximal treadmill and cycling tests, multiple Wingate tests, and an interval swim test.…”