Effects of acute exposure to moderate hypoxia during different phases of repeated-sprint cycling on fatigue and anaerobic power reserve

Abstract

The purpose of this study was to investigate the effects of acute moderate hypoxia (14.5% inspired oxygen fraction) on the magnitude of fatigue development during the different phases (work, recovery, and both) of a repeated-sprint test (10 x 6-s sprints interspersed with 30-s recovery) in healthy, trained males. This study also sought to investigate the relationship between anaerobic power reserve and fatigue during the aforementioned repeated-sprint test. Fourteen exercise-trained males completed four trials of the repeated-sprint test under each of the following conditions: (a) normoxia (20.93% inspired oxygen fraction), (b) acute hypoxia during the work intervals only, (c) acute hypoxia during the recovery intervals only, and (d) acute hypoxia during both the work and recovery intervals. The order of the experimental conditions was systematically balanced. Fatigue scores were not different between experimental conditions, despite the fact that arterial oxygen saturation values from the acute hypoxia during recovery condition and the acute hypoxia during both work and recovery condition differed significantly from the normoxia and acute hypoxia during work intervals only conditions (p < .001). There was no relationship between anaerobic power reserve and fatigue in any experimental condition. The results of the present study indicate that although the participants experienced different levels of hypoxia during the experimental trials, the degree of hypoxia was insufficient to alter mechanical performance during a repeated-sprint test. The lack of an effect on mechanical performance does not appear to be influenced by an individual's anaerobic power reserve. It may be inferred that the degree of hypoxia employed was neither severe enough as to impair levels of muscle oxygenation beyond what was experienced in normoxia, nor as to induce further fatigue related to central mechanisms.