Effects of the ‘live high–train low’ method on prooxidant/antioxidant balance on elite athletes

Abstract

Background/Objectives: We previously demonstrated that acute exposure to hypoxia (3 h at 3000 m) increased oxidative stress markers. Thus, by using the 'living high-training low' (LHTL) method, we further hypothesized that intermittent hypoxia associated with endurance training alters the prooxidant/antioxidant balance. Subjects/Methods: Twelve elite athletes from the Athletic French Federation were subjected to 18-day endurance training. They were divided into two groups: one group (control group) trained at 1200 m and lived in hypoxia (2500-3000 m simulated altitude) and the second group trained and lived at 1200 m. The subjects performed an acute hypoxic test (10 min at 4800 m) before and immediately after the training. Plasma levels of advanced oxidation protein products (AOPP), malondialdehydes (MDA), ferric-reducing antioxidant power (FRAP), lipid-soluble antioxidants normalized for triacylglycerols, and cholesterol and retinol were measured before and after the 4800 m tests. Results: After the training, MDA and AOPP concentrations were decreased in response to the 4800 m test only for the control group. Eighteen days of LHTL induced a significant decrease of all antioxidant markers (FRAP, P ¼ 0.01; a-tocopherol, P ¼ 0.04; b-carotene, P ¼ 0.01 and lycopene, P ¼ 0.02) for the runners. This imbalance between antioxidant and prooxidant might result from insufficient intakes in vitamins A and E. Conclusions: The LHTL model characterized by the association of aerobic exercises and intermittent resting hypoxia exposures decreased the antioxidant status whereas the normoxic endurance training induced preconditioning mechanisms in response to the 4800 m test.

Thirteen days of “live high–train low” does not affect prooxidant/antioxidant balance in elite swimmers

“…On the other hand, we also described that 13 days of LHTL were not sufficient to improve aerobic performances in elite swimmers suggesting a lower physiological stimulus, probably explained by a shorter duration of hypoxic exposure at 3,000 m (7 vs. 12 days for swimmers and runners, respectively) and a lower intensity of training (Robach et al 2006). Thus, based on the evidence that oxidative stress is increased in a dose-dependent manner with exercise (Palazzetti et al 2003) and hypoxia (Pialoux et al 2008a), we can reasonably hypothesize that 13 days of LHTL may induce less oxidative stress than 18 days of LHTL (Pialoux et al 2008b) because of a likely lower physiological stimulus. Therefore, we investigated the impact of 13 days of LHTL described in the companion article (Robach et al 2006) on the antioxidant/prooxidant balance in elite endurance swimmers.…”

“…To our knowledge only one study described the effect of normoxic endurance training associated with intermittent hypoxic exposure on oxidative stress and antioxidant status (Pialoux et al 2008b). We previously reported that 18-days of ''living high-training low'' in elite runners weakened the antioxidant status and induced an increase in oxidative stress responses to an acute hypoxic test, whereas the same training without hypoxic exposure did not affect these parameters.…”

“…We previously reported a decrease in plasmatic antioxidant markers after 18 days of LHTL in elite runners (Pialoux et al 2008b). Although, aerobic performance was improved (Brugniaux et al 2006b), we concluded that the repetition of aerobic training sessions in normoxia associated with the resting exposure to hypoxia was responsible for a drop in plasma antioxidant, probably enhanced by low intakes of lipid-soluble antioxidants.…”

Vitamin C Supplementation Does not Improve Hypoxia-Induced Erythropoiesis

“…It has been shown that hypoxia exposure increases oxidative stress, increasing ROS production ( Radak et al, 1997;Pialoux et al, 2009;Pialoux et al, 2010). Furthermore, it has been suggested that ROS are involved in Epo-mediated erythroid differentiation and that antioxidants could attenuate erythropoiesis (Nagata et al, 2007).…”

“…Hypoxia increases oxidative stress both in humans and in rodents (Radak et al, 1997;Asha Devi et al, 2005;Devi et al, 2007;Pialoux et al, 2009). It has been shown that supplements with antioxidant mixtures can compensate for the decline in membrane stability following intermittent hypobaric hypoxia as a consequence of decreased lipid peroxidation (LPO) and protein oxidation (Devi et al, 2007;Vani et al, 2010).…”