Acute Effects of the Wim Hof Breathing Method on Repeated Sprint Ability: A Pilot Study

The Wim Hof breathing method (WHBM) combines periods of hyperventilation (HV) followed by voluntary breath-holds (BH) at low lung volume. It has been increasingly adopted by coaches and their athletes to improve performance, but there was no published research on its effects. We determined the feasibility of implementing a single WHBM session before repeated sprinting performance and evaluated any acute ergogenic effects. Fifteen amateur runners performed a single WHBM session prior to a Repeated Ability Sprint Test (RAST) in comparison to voluntary HV or spontaneous breathing (SB) (control) in a randomized cross-over design. Gas exchange, heart rate, and finger pulse oxygen saturation (SpO2) were monitored. Despite large physiological effects in the SpO2 and expired carbon dioxide (VCO2) levels of both HV and WHBM, no significant positive or negative condition effects were found on RAST peak power, average power, or fatigue index. Finger SpO2 dropped to 60 ± 12% at the end of the BHs. Upon the last HV in the WHBM and HV conditions, end-tidal CO2 partial pressure (PETCO2) values were 19 ± 3 and 17 ± 3 mmHg, indicative of respiratory alkalosis with estimated arterial pH increases of +0.171 and of +0.181, respectively. Upon completion of RAST, 8 min cumulated expired carbon dioxide volumes in the WHBM and HV were greater than in SB, suggesting lingering carbon dioxide stores depletion. These findings indicate that despite large physiological effects, a single WHBM session does not improve anaerobic performance in repeated sprinting exercise

Effects of age on hypoxic tolerance in women

Introduction The prevalence of acute mountain sickness (AMS) is increasing with altitude (i.e., 10-25% at 2,500 m and 50-85% at ~ 5,000 m; Bärtsch & Swenson, 2013). While there is no error-free test to predict its occurrence, several risk factors and tests have been proposed. For example, the hypoxic ventilatory response (HVR) measures the ratio between the increase in ventilation (VE) and the decrease in pulse saturation (SpO2) during hypoxic exposure. Some studies reported an increased (Lhuissier et al., 2012), no difference (Pokorski and Marczak, 2003), or a decreased HVR (Kronenberg and Drage, 1973) with age. The effect of sex remains also debated since women have been reported to have a higher (Richalet et al., 2012) or lower (Schneider et al. 2002; Vardy et al., 2006) AMS prevalence. Therefore, we aimed to compare measurements of HVR, VE and SpO2 between pre- (PreM) and post-menopausal (postM) women and to investigate if they are related to AMS. We hypothesized differences in hypoxic tolerance between age groups. Methods We screened pre-menopausal women (PreM; n = 13; age = 31.7 ± 7.8yr; weight = 63.5 ±9.6 kg; height = 167 ±10 cm) during three phases (early follicular, Fol1; late follicular, Fol2; luteal, Lut3) of their menstrual cycle and post-menopausal women (PostM; n = 15; age = 62.8 ±2.3 yr; weight = 56.1 ±8.3 kg; height 163 ±5 cm) on one occasion. They were evaluated with a pure nitrogen breathing test (N2T; Solaiman et al., 2014) for HVR and with a cycling exercise (5 min of rest followed by 5 min of cycling at 1.5 W/kg) in hypoxia (FiO2 = 14%; simulated altitude of 3,500 m) with measurement of SpO2 and VE. They were then exposed to one night in real altitude (3,375 m) with AMS assessment (Lake Louise Score; Roach et al., 2018). Results PreM had a higher resting VE in normoxia (9.95-10.07 vs 8.50 L/min; P < 0.05) and increased VE (7.49-8.78 vs 5.41 L/min; P < 0.05) during the N2T at the three measurements points than PostM. Moreover, only at Fol2, HVR (-0.43 vs -0.27 L/min/%; P = 0.023), VEpeak (18.9 vs 15.0 L/min; P = 0.025) during N2T and resting SpO2 in normoxia (95.9 vs 94.9, P = 0.093) were higher in PreM. The prevalence of AMS was similar between PreM and PostM (30.8 vs 40.0%). When AMS positive and AMS negative subgroups were compared, no difference in HVR was found while there were differences in SpO2 and VE. Discussion/Conclusion The main finding of the present study is that HVR was higher in PreM than in PostM only during the late follicular phase of the former. Since estrogen is known to have a stimulatory effect on both pulmonary ventilation and blood vessel vasodilation and peaks during this phase, this suggests that it is the main trigger of the observed differences in HVR. The prevalence of AMS was in line with the literature for a similar altitude (34% at 3,650m; Maggiorini et al., 1990). Contrary to Richalet et al. (2012), HVR did not diagnose AMS in any group nor was lower in the older age group. No other parameter showed to be a solid predictive metric for AMS. Given conflicting results in this study (i.e., HVR and AMS) and in the literature, there is no clear evidence of an effect of age on hypoxic tolerance and on AMS prediction. References Bärtsch, P., & Swenson, E. R. (2013). Acute high-altitude illnesses. New England Journal of Medicine, 368(24), 2294-2302. https://doi.org/10.1056/NEJMcp1214870 Kronenberg, R. S., & Drage, C. W. (1973). Attenuation of the ventilatory and heart rate responses to hypoxia and hypercapnia with aging in normal men. The Journal of Clinical Investigation, 52(8), 1812-1819. https://doi.org/10.1172/JCI107363 Lhuissier, F. J., Canouï‐Poitrine, F., & Richalet, J. P. (2012). Ageing and cardiorespiratory response to hypoxia. The Journal of Physiology, 590(21), 5461-5474. https://doi.org/10.1113/jphysiol.2012.238527 Maggiorini, M., Bühler, B., Walter, M., & Oelz, O. (1990). Prevalence of acute mountain sickness in the Swiss Alps. British Medical Journal, 301(6756), 853-855. https://doi.org/10.1136/bmj.301.6756.853 Pokorski, M., & Marczak, M. (2003). Ventilatory response to hypoxia in elderly women. Annals of Human Biology, 30(1), 53-64. https://doi.org/10.1080/03014460210162000 Richalet, J. P., Larmignat, P., Poitrine, E., Letournel, M., & Canouï-Poitrine, F. (2012). Physiological risk factors for severe high-altitude illness: A prospective cohort study. American Journal of Respiratory and Critical Care Medicine, 185(2), 192-198. https://doi.org/10.1164/rccm.201108-1396OC Roach, R. C., Hackett, P. H., Oelz, O., Bärtsch, P., Luks, A. M., MacInnis, M. J., ... & Lake Louise AMS Score Consensus Committee. (2018). The 2018 Lake Louise acute mountain sickness score. High Altitude Medicine & Biology, 19(1), 4-6. https://doi.org/10.1089/ham.2017.0164 Schneider, M., Bernasch, D., Weymann, J., Holle, R., & Bärtsch, P. (2002). Acute mountain sickness: influence of susceptibility, preexposure, and ascent rate. Medicine & Science in Sports & Exercise, 34(12), 1886-1891. Solaiman, A. Z., Feehan, R. P., Chabitnoy, A. M., Leuenberger, U. A., & Monahan, K. D. (2014). Ventilatory responses to chemoreflex stimulation are not enhanced by angiotensin II in healthy humans. Autonomic Neuroscience, 183, 72-79. https://doi.org/10.1016/j.autneu.2014.01.010 Vardy, J., Vardy, J., & Judge, K. (2006). Acute mountain sickness and ascent rates in trekkers above 2500 m in the Nepali Himalaya. Aviation, Space, and Environmental Medicine, 77(7), 742-744

Mechanisms underlying the health benefits of intermittent hypoxia conditioning

Intermittent hypoxia (IH) is commonly associated with pathological conditions, particularly obstructive sleep apnoea. However, IH is also increasingly used to enhance health and performance and is emerging as a potent non‐pharmacological intervention against numerous diseases. Whether IH is detrimental or beneficial for health is largely determined by the intensity, duration, number and frequency of the hypoxic exposures and by the specific responses they engender. Adaptive responses to hypoxia protect from future hypoxic or ischaemic insults, improve cellular resilience and functions, and boost mental and physical performance. The cellular and systemic mechanisms producing these benefits are highly complex, and the failure of different components can shift long‐term adaptation to maladaptation and the development of pathologies. Rather than discussing in detail the well‐characterized individual responses and adaptations to IH, we here aim to summarize and integrate hypoxia‐activated mechanisms into a holistic picture of the body's adaptive responses to hypoxia and specifically IH, and demonstrate how these mechanisms might be mobilized for their health benefits while minimizing the risks of hypoxia exposure