REPOSITORY > RESULTS

Abstract

The present thesis assesses the theory of cross-adaptation, whereby the adaptation to one stressor (i.e. exercise, heat, hypoxia) could benefit performance during exposure to another stressor. We investigated the independent and combined effects of training, heat and hypoxic acclimation on selected cardiorespiratory, thermoregulatory, hematological and cellular responses during exercise in normoxic (NOR), hypoxic (HYP) and hot (HE) ambient conditions.
Participants conducted 10-d adaptations to I: training, II: hypoxia, III: heat, and IV: combined heat and hypoxic acclimation. Before and after each 10-d adaptation period, participants completed three cycle ergometer exercise tests in NOR, HYP and HE conditions. The first 30-min phase of each test comprised steady-state exercise at 40% NOR Wpeak followed by incremental exercise to exhaustion. The acclimation protocols were:
I. Participants with higher and lower (V̇O2max: 57.9 ± 6.2 and 41.7 ± 5.0 mL·kg-1·min-1, respectively) maximal aerobic power conducted daily 60min exercise at 50% NOR Wpeak).
II. Participants were confined to a normobaric hypoxic environment (partial pressure of oxygen in the inspired air, PiO2 = 87 ± 3 mmHg) and completed daily exercise in hypoxia at a heart rate corresponding to 50%Wpeak.
III. Participants conducted daily 90-min controlled-hyperthermia (target rectal temperature, Tre = 38.5℃) exercise on a cycle ergometer.
IV. Participants were confined to a hypoxic environment (II) and conducted daily 90-min controlled-hyperthermia exercise in a hot environment (III).
V. Following the NOR maximal exercise test conducted before and after heat acclimation (III) we immersed participants in water maintained at 28°C for 60 min.
Results of the above acclimation procedures were as follows:
I. V̇O2max increased by +9.2 ± 8.5% and +10.2 ± 15.4% in the untrained group in NOR and HE, respectively. Increases in Wpeak were correlated with baseline values in NOR (r=-0.6) and HYP (r=-0.5). Peak sweat rate increased in both groups in HE, and was activated at a lower rectal temperature (Tre) in the trained group.
II. V̇O2max increased by 10.7% and 7.9% in NOR and HE, respectively, whereas no differences were found in HYP. Increases in V̇O2max did not translate into increases in Wpeak in either NOR or HE.
III. V̇O2max and maximal cardiac output (COmax) were not affected. Wpeak was increased in NOR and HE by 41±21 and 26±22 W, respectively, but not in HYP. GME was higher whereas resting Tre and sweating thresholds were lower across environmental conditions. The gain of the sweating response decreased in HYP.
IV. V̇O2max and the anaerobic threshold were not modified in any of the environments. Wpeak increased by 6.3 ± 3.4% in NOR and 4.0 ± 4.9% in HE, respectively. Forehead sweating (magnitude and gain) was augmented in HE. Time to exhaustion in hot hypoxic conditions increased by 12.9 ± 10.6%.
V. Baseline pre-immersion Tre was similar pre- and post-heat acclimation, as was Tre cooling rate, the vasomotor response and shivering.
A training effect was observed in the untrained participants (I). Hypoxic acclimation combined with moderate-intensity exercise training improved V̇O2max in NOR and HE, but did not affect exercise performance or thermoregulatory responses in any of the environmental conditions (II). Our data do not support a beneficial cross-over effect of heat acclimation on V̇O2max in NOR or HYP conditions (III). A 10-day combined heat and hypoxic acclimation conferred minor benefits in aerobic performance in NOR or HE conditions (IV). Heat production and heat loss responses in a high heat loss environment remained unaltered following heat acclimation (V). The results of the present thesis do not confirm the theory of cross-adaptation in humans.