Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.


Date of Graduation


Document Type


Degree Name

Master of Science (MS)


Department of Graduate Kinesiology


Nicholas Luden

Michael Saunders

Christopher Womack


Purpose: The aim of this study was to determine the effect of creatine supplementation (CrS) on repeated sprint performance in both normoxia and normobaric hypoxia (simulated altitude ~3,000 m). Methods: Nineteen recreationally trained cyclists were randomly assigned to one of two groups; one received six days of either CrS (n = 12; 0.3 g/kg of body mass of creatine monohydrate) and the other received six days of placebo (PLA; n = 7; 0.3 g/kg of maltodextrin). All subjects completed separate trials in normoxia (inspired O2 = 20.93%) and hypoxia (O2 = 15%) before and after the supplementation phase. Body water content was estimated with bioelectrical impedance before and after supplementation. This was used as an affirming metric for anticipated water retention resulting from CrS. The repeated sprint protocol consisted of 6 x 10-second maximal cycling sprints (separated by 20-second recovery intervals), two minutes of rest, and a final 30-second sprint, on a cycle ergometer. Peak power (W) and average power (W) during each sprint interval, as well as fatigue index (W/s) during the 30-second Wingate, were compared using a series of repeated measures ANOVAs with two within-subject factors [time (pre- and post-supplementation) and condition (normoxia and hypoxia) and one between-subject factor (treatment). Results: Body water content increased with CrS (p<0.05), but not PLA. Hypoxia impaired mean power and %O2 saturation in both CrS and PLA. However, there was no treatment x time interaction for peak or average power output and fatigue index during any of the sprints, in either normoxia or hypoxia. Conclusions: Despite the increase in body water content following CrS, crudely indicating an increase in skeletal muscle creatine content, CrS had no impact on sprint performance in normoxia or hypoxia. Similarly, there was no change in sprint performance following PLA in either condition. The lack of CrS efficacy in the current study is surprising. Though speculative, we did not screen subjects for high dietary protein (and associated creatine) intake and therefore may have disproportionately recruited subjects with high protein diets. This has been shown to attenuate the increase in skeletal muscle creatine following CrS. Regardless, the inefficacy of CrS in normoxia prevented us from determining if CrS imparts similar benefits in different environmental conditions. As such, recommendations for CrS for repeated sprint performance in hypoxia cannot be made based on the current data.

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