Effect of supplemental oxygen on post-exercise inflammatory response and oxidative stress
School of Sport Science, Exercise and Health, The University of Western Australia, Crawley, Australia. Arbeitsphysiologie
(Impact Factor: 2.19).
10/2012; 113(4). DOI: 10.1007/s00421-012-2521-7
This investigation explored the influence of supplemental oxygen administered during the recovery periods of an interval-based running session on the post-exercise markers of reactive oxygen species (ROS) and inflammation. Ten well-trained male endurance athletes completed two sessions of 10 × 3 min running intervals at 85 % of the maximal oxygen consumption velocity (vVO(2peak)) on a motorised treadmill. A 90-s recovery period was given between each interval, during which time the participants were administered either a hyperoxic (HYP) (Fraction of Inspired Oxygen (F(I)O(2)) 99.5 %) or normoxic (NORM) (F(I)O(2) 21 %) gas, in a randomized, single-blind fashion. Pulse oximetry (S(p)O(2)), heart rate (HR), blood lactate (BLa), perceived exertion (RPE), and perceived recovery (TQRper) were recorded during each trial. Venous blood samples were taken pre-exercise, post-exercise and 1 h post-exercise to measure Interleukin-6 (IL-6) and Isoprostanes (F(2)-IsoP). The S(p)O(2) was significantly lower than baseline following all interval repetitions in both experimental trials (p < 0.05). The S(p)O(2) recovery time was significantly quicker in the HYP when compared to the NORM (p < 0.05), with a trend for improved perceptual recovery. The IL-6 and F(2)-IsoP were significantly elevated immediately post-exercise, but had significantly decreased by 1 h post-exercise in both trials (p < 0.05). There were no differences in IL-6 or F(2)-IsoP levels between trials. Supplemental oxygen provided during the recovery periods of interval based exercise improves the recovery time of S(P)O(2) but has no effect on post-exercise ROS or inflammatory responses.
Available from: Ernest Kuchar
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ABSTRACT: Elite athletes have a higher prevalence of exercise-induced bronchoconstriction than the general population. The pathogenesis of exercise-induced bronchoconstriction is not fully elucidated. Increasing evidence suggests that airway inflammation plays a major role in the immunopathogenesis of exercise-induced bronchoconstriction. The aim of our review is to discuss existing evidence and to present a new, modified inflammatory hypothesis of exercise-induced bronchoconstriction. Exercise alters the number and function of circulating immune cells. Episodes of upper respiratory symptoms in elite athletes do not follow the usual seasonal patterns. Moreover, they have an unusual short-term duration, which suggests a non-infectious etiology. If the pro-inflammatory response to exercise has the potential to induce symptoms that mimic respiratory tract infection, it definitely up-regulates pro-inflammatory cytokine expression in the airways. We can conclude that exercise up-regulates airway cytokine expression in a way that favors inflammation and allergic reactions in bronchi and lowers the threshold for bronchoconstriction to different stimuli like cool, dry air, allergens, and pollutants.
Available from: Martyn Binnie
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ABSTRACT: This study compared the effect of an 8-week pre-season conditioning program conducted on a sand (SAND) or grass (GRASS) surface on 20 m sprint performance. Twelve team sport athletes were required to attend three 1 h training sessions per week, including two surface-specific sessions (SAND, n=6 or GRASS, n=6), and one group session (conducted on grass). Throughout the training period, 20 m sprint times of all athletes were recorded on both sand and grass surfaces at the end of week 1, 4 and 8. Results showed a significant improvement in 20 m sand time in the SAND group only (p<0.05), whereas 20 m grass time improved equally in both training sub-groups (p<0.05). These results suggest that surface-specificity is essential for 20 m speed improvements on sand, and also that there is no detriment to grass speed gains when incorporating sand surfaces into a pre-season program.
Available from: David M. Bellar
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ABSTRACT: The purpose of this investigation was to examine the effects of a personal oxygen supplement (OS) on performance during exhaustive exercise, respiratory responses during exhaustive exercise, and cognitive function post exhaustive exercise. The participants for this blind, placebo-controlled experiment were apparently healthy college aged adults (n=20). First VO2 Max was assessed (47.6 ± 9.8mlO2/kg*min). Participants then ran two trials at 80% of VO2 Max speed to exhaustion, and received either a placebo (compressed air) or personal OS. Psychomotor Vigilance Testing was performed before and after each trial. Performance between treatments was evaluated via repeated measures analysis of variance (ANOVA) and was not found to be different (p=0.335, ηp=0.052), and order (Placebo First or Personal OS First) was not significant within the model (p=0.305, ηp=0.058). Mean times were 1057.6 ± 619.8 seconds for the oxygen trials and 992.5 ± 463.1 seconds for the placebo trials. Repeated measures ANOVAs were used to assess Minute Ventilation (Ve L/min), VCO2 (L O2/min) during exercise and recovery, mean heart rate during recovery, and Psychomotor Vigilance Testing results. Treatment was non-significant (p > 0.05) nor were any interaction effects (treatment*time, p > 0.05) for any variables. The results of this study suggest that a personal OS had no effect on performance and did not affect ventilation even at the time directly surrounding the application. The results of the study also suggest that personal OS do not enhance exercise recovery or cognition during exercise recovery.
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