Effectiveness of voluntary isocapnic hyperpnoea for mitigating hypoxemia and acute mountain sickness in normobaric...

This study aimed to examine the physiological mechanisms associated with Voluntary Isocapnic Hyperpnoea (VIH) in severe hypoxia and evaluated whether such respiratory modulation may attenuate hypoxemia and Acute Mountain Sickness (AMS). Eighteen healthy participants (8 females) completed two 2-hour sessions in a normobaric hypoxic chamber simulating 4200 m above sea level, in randomized order: an experimental session including a 5-minute VIH intervention after 1 h, and a control session without VIH. AMS symptoms, arterial oxygen saturation (SpO₂), heart rate, blood pressure and gases were monitored before and during the hypoxic exposure. Separate repeated-measures ANOVAs were employed to analyze the effects of VIH and differences between the sessions. VIH decreased clinical hypoxemia (from 83.3% to 22.2%) and reduced AMS incidence (from 11.1% to 5.5%). This was associated with an increase in SpO₂ (p = 0.011, ηp² = 0.341, ω² = 0.159) and blood oxygen partial pressure (p = 0.027, ηp² = 0.271, ω² = 0.112). SpO₂ kinetics differed between sessions (p = 0.011, ηp² = 0.132, ω² = 0.061), with higher values during the experimental session. This benefit was acute as differences in SpO₂ were not noted at the final timepoint. Substantial intra-individual variability and no sex-related interactions were observed. These preliminary findings suggest that VIH is a feasible method for transiently improving blood oxygen saturation under hypoxia, and has the potential to attenuate AMS. Further research is nevertheless warranted to clarify the role of VIH within the framework of altitude medicine and address potential mechanistic explanations. Methodological insights from the present study should inform future investigations.