Effect of three weeks of repeated-sprint training in hypoxia induced by voluntary hypoventilation at low lung volume (RSH-VHL) versus repeated-sprint training with normal breathing (RSN) on the cardiorespiratory response to acute normobaric hypoxia in youth elite mogul skiers.

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Training with voluntary hypoventilation at low lung volume (VHL), that is, exhaling to functional residual capacity and then performing short, high-intensity efforts with breath-holding, induces transient arterial desaturation, hypercapnia and respiratory acidosis without requiring a hypoxic chamber. Mechanistically, repeated bouts of arterial desaturation, hypercapnia and breath-holding may stimulate peripheral chemoreceptors and the ventilatory drive, potentially improving cardiorespiratory responses under hypoxia. The effects of RSH-VHL training on the acute ventilatory and cardiac response to a hypoxic exercise challenge have, to our knowledge, not been investigated in athletes that practice sport at altitude or in winter sports athletes. Here we investigate whether a 3-week RSH-VHL programme (2 sessions/week) modify the ventilatory, cardiac and oxygen-saturation response to a hypoxia sensitivity test in youth elite mogul skiers, more than the same volume of repeated-sprint training performed with normal breathing (RSN). We also want to evaluate if the change in hypoxic ventilatory response (HVR; ΔVE between hypoxia and normoxia) is greater in RSH-VHL than in RSN, and if it is associated with smaller falls in arterial saturation (SpO₂) and smaller increases in heart rate (HR) during hypoxic exercise. In a two-arm parallel-group, randomized controlled trial with pre/post measurements, athletes will be randomized in control and intervention groups. Both groups will perform 3 weeks × 2 sessions·week⁻¹. Sessions will consist of a warm-up, then 2 sets × 8 running sprints of 50 m all-out (~8 s) on flat terrain, 30 s of active recovery between sprints, and 3 min of recovery between sets. Testing session will consist of a test for hypoxia sensitivity inspired by the Richalet protocol (4 subsequent stages: rest normoxia [RN], rest hypoxia [RH], exercise hypoxia [EH] at 100 W men / 80 W women, exercise normoxia [EN]; FiO₂ ≈ 0.115, equivalent to ~4,800 m, on a cycle ergometer with a Hypoxico generator and Cortex MetaMax 3B gas analyser). We hypothesize that, from pre to post, the change in ventilatory response to hypoxia (ΔVE = VE in hypoxia − VE in normoxia) increases more in RSH-VHL than in RSN. Secondary hypotheses are: i) The change in cardiac response to hypoxia (ΔHR) decreases more in RSH-VHL than in RSN; and ii) the change in saturation response to hypoxia (ΔSpO₂ = SpO₂ hypoxia − SpO₂ normoxia) becomes less negative (smaller desaturation) in RSH-VHL than in RSN.

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