Abstract
“Live High-Train Low” (LHTL) training can alter oxidative status of athletes. This study compared prooxidant/antioxidant balance responses following two LHTL protocols of the same duration and at the same living altitude of 2250 m in either normobaric (NH) or hypobaric (HH) hypoxia. Twenty-four well-trained triathletes underwent the following two 18-day LHTL protocols in a cross-over and randomized manner: Living altitude (PIO2 = 111.9 ± 0.6 vs. 111.6 ± 0.6 mmHg in NH and HH, respectively); training “natural” altitude (~1000–1100 m) and training loads were precisely matched between both LHTL protocols. Plasma levels of oxidative stress [advanced oxidation protein products (AOPP) and nitrotyrosine] and antioxidant markers [ferric-reducing antioxidant power (FRAP), superoxide dismutase (SOD) and catalase], NO metabolism end-products (NOx) and uric acid (UA) were determined before (Pre) and after (Post) the LHTL. Cumulative hypoxic exposure was lower during the NH (229 ± 6 hrs.) compared to the HH (310 ± 4 hrs.; P<0.01) protocol. Following the LHTL, the concentration of AOPP decreased (-27%; P<0.01) and nitrotyrosine increased (+67%; P<0.05) in HH only. FRAP was decreased (-27%; P<0.05) after the NH while was SOD and UA were only increased following the HH (SOD: +54%; P<0.01 and UA: +15%; P<0.01). Catalase activity was increased in the NH only (+20%; P<0.05). These data suggest that 18-days of LHTL performed in either NH or HH differentially affect oxidative status of athletes. Higher oxidative stress levels following the HH LHTL might be explained by the higher overall hypoxic dose and different physiological responses between the NH and HH.
Highlights
It is well established that both, hypoxia [1, 2] and exercise [3, 4] elicit prooxidant/antioxidant perturbations
The present study focused on comparing prooxidant/antioxidant responses following 18-day Live High Train Low” (LHTL) protocols in either normobaric hypoxia (NH) or hypobaric hypoxia (HH) within a cross-over designed framework
The average pressure of inspired O2 (PIO2) was identical between the NH (111.9 ± 0.6 mmHg) and the HH (111.6 ± 0.6 mmHg) LHTL protocol
Summary
It is well established that both, hypoxia [1, 2] and exercise [3, 4] elicit prooxidant/antioxidant perturbations. Exercise mainly augments oxidative stress through increased production of superoxide anion (O2°-) and oxygen-derived intermediates [8] within the mitochondria as a result of activity-induced O2 flux increase. 18-days of LHTL training has been shown to augment oxidative stress and decrease antioxidant capacity in elite runners [13]. Authors speculated that the lower hypoxic dose and the lower training intensity during the latter study [14] might explain the lack of significant differences in oxidative stress. These data suggest that during a LHTL protocol, both hypoxia and exercise training modulate oxidative status in a dose-dependent manner
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