Affiliation:
1. Department of Sports Sciences The University of Tokyo Meguro Toyko Japan
2. Graduated School of Sport Sciences Waseda University Saitama Japan
3. School of Human Sciences (Exercise and Sport Science) University of Western Australia Perth Western Australia Australia
Abstract
AbstractHypoxic exercise, which can induce arterial and tissue deoxygenation, promotes physiological adaptations. However, reduced oxygen availability can lower the absolute training intensity (i.e., mechanical stress). Adding normoxic recovery to sprint interval exercise (SIE) is one potential approach to strike a balance between providing a hypoxic stimulus and maintaining the absolute training intensity. However, the effects of adding normoxic recovery to SIE on performance and physiological responses are uncertain. We tested the hypothesis that hypoxic SIE with normoxic recovery enhances arterial deoxygenation and muscle deoxygenation levels without impeding performance compared to an entirely normoxic condition. On separate days, seven male sprinters performed 4 × 30‐s ‘all‐out’ cycle sprints with 4.5‐min recovery with hypoxic exposure (FiO2: 12.7%O2) applied continuously (hypoxia, HYP), intermittently during sprint periods only (intermittent, INT), or not at all (normoxia, NOR). Power output, oxygen saturation, muscle oxygenation, surface electromyography (EMG) activity, heart rate, blood lactate concentration, and ratings of perceived exertion were measured. The total work significantly decreased in HYP than NOR (p < 0.05) and INT (p < 0.01). The aTrterial oxygen saturation was lower during HYP than NOR (∼86% vs. ∼97%; p < 0.001), while lower values were also obtained for INT than NOR during sprint periods (∼85% vs. ∼97%; p < 0.001) but not during recovery periods (∼96% vs. ∼97%). The heart rate differed (p < 0.05) between conditions (NOR: ∼164 bpm; INT: ∼160 bpm; HYP: ∼156 bpm). No other variables demonstrated significant differences between conditions. Adding hypoxia during exercise while recovering in normoxia did not compromise exercise capacity during SIE, despite inducing larger arterial deoxygenation levels compared to normoxia.