Abstract

The objective of this study is to investigate the effectiveness of novel repeated-sprint training in hypoxia (RSH) protocol, likely maximizing hypoxic stimulus (higher than commonly used) while preserving training quality (interset rest in normoxia). Twenty-three world-class female rugby sevens players performed four repeated-sprint training sessions (4 sets of 5 × 5-s cycle sprints-25-s intersprint recovery and 3-min interset rest) under normobaric hypoxia (RSH, exercise and interset rest at FiO 2 of 10.6% and 20.9%, respectively; n = 12) or normoxia (repeated-sprint training in normoxia; exercise and interset rest at FiO 2 of 20.9%; n = 11) during a 9-d training camp before international competition. Repeated-sprint ability (8 × 5-s treadmill sprints-25-s recovery), on-field aerobic capacity, and brachial endothelial function were assessed pre- and postintervention. Arterial oxygen saturation (pooled data: 87.0% ± 3.1% vs 96.7% ± 2.9%, P < 0.001) and peak and mean power outputs (sets 1 to 4 average decrease: -21.7% ± 7.2% vs -12.0% ± 3.8% and -24.9% ± 8.1% vs -14.9% ± 3.5%; both P < 0.001) were lower in RSH versus repeated-sprint training in normoxia. The cumulated repeated-sprint distance covered significantly increased from pre- to postintervention (+1.9% ± 3.0%, P = 0.019), irrespective of the condition ( P = 0.149). On-field aerobic capacity did not change (all P > 0.45). There was no significant interaction (all P > 0.240) or condition main effect (all P > 0.074) for any brachial artery endothelial function variable. Only peak diameter increased ( P = 0.026), whereas baseline and peak shear stress decreased ( P = 0.014 and 0.019, respectively), from pre- to postintervention. In world-class female rugby sevens players, only four additional repeated-sprint sessions before competition improve repeated-sprint ability and brachial endothelial function. However, adding severe hypoxic stress during sets of repeated sprints only did not provide supplementary benefits.

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