BACKGROUND: Creatine supplementation (CrS) elevates phosphocreatine (PCr) levels and expedites PCr replenishment following exercise. Furthermore, hypoxic environments increase the reliance on anaerobic metabolism and impairs PCr replenishment during recovery, which could potentially enhance the efficacy of CrS under these conditions. The aim of this study was to determine the effect of CrS on repeated sprint performance in both normoxia (N) and normobaric hypoxia (NH) (simulated altitude ~3,000 m). METHODS: 19 recreationally trained cyclists (VO2max = 40.6 ± 5.0 mL/kg/min) were randomly assigned to either six days of CrS (n = 12; 0.3 g/kg of body mass of creatine monohydrate) or placebo (PLA; n = 7; 0.3 g/kg of maltodextrin). All subjects completed separate trials in normoxia (inspired O2 = 20.9%) and hypoxia (O2 = 15.0%) before and after the supplementation phase. Body water content was estimated via bioelectrical impedance before and after supplementation. The repeated sprint protocol consisted of 6 x 10 s maximal cycling sprints (separated by 20 s recovery intervals), two minutes of rest, and a final 30 s sprint, on a cycle ergometer. RESULTS: Body water content increased by 1.24 ± 2.03% with CrS (p < 0.05), but not PLA. Compared to N, NH impaired mean power (pwr) and O2 saturation in both CrS (Npwr: 432.7 ± 128.8 W, NHpwr: 413.2 ± 114.1 W; N O2 saturation 97.4 ± 0.7%: NH O2 saturation 86.7 ± 2.5%) and PLA (Npwr: 465.3 ± 139.0 W, NHpwr: 450.2 ± 128.1 W; N O2 saturation 97.3 ± 1.7%: NH O2 saturation 86.3 ± 3.0%). However, there was no treatment x time interaction for peak or mean power output and fatigue index during any of the sprints, in either normoxia or hypoxia. CONCLUSIONS: CrS had no impact on sprint performance in normoxia or hypoxia. Similarly, there was no change in sprint performance following PLA in either condition.

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