Cardiorespiratory responses of humans at rest and during submaximal exercise in acute normobaric (NH) and hypobaric hypoxia (HH) have been reported repeatedly. Greater hypoxemia, hypocapnia, and blood alkalosis have been observed in HH compared to NH. However, such responses to maximal exercise have barely been considered in the past. We analyzed data from 16 studies (168 well-trained subjects; average baseline VO2max: 62.5 mL/min/kg). Nine studies were performed in acute NH and 7 in HH. Altitudes corresponding to the used hypobaria or FiO2 varied between 2286 and 5400 m. The decreases of VO2max ( - 7.0% vs. - 6.0%), HRmax ( - 0.8% vs. - 1.2%), and SaO2 ( - 5.2 vs. - 5.6%) per 1000m gain in altitude did not differ between NH and HH. However, VEmax (BTPS) increased in HH compared to NH (2.0% vs. - 1.8%; P < 0.01), mainly resulting from higher breathing frequencies. In the overall group (NH + HH) altitude-dependent changes in VO2max were related to changes in SaO2 (r = 0.9; P < 0.01) and changes in VEmax to changes in HRmax (r = 0.8; P < 0.01). The relationship between changes in HRmax and VEmax indicates close coupling between cardiac and respiratory responses. In contrast to the observations at rest and during submaximal exercise, VEmax is higher in HH compared to NH. Since the higher VEmax in HH did not result in improved SaO2 it may primarily be due to enhanced dead space ventilation. It is suspected that acclimatization to HH (not NH) is necessary to improve ventilatory efficiency and climbing performance at very high real altitudes.
© Copyright 2014 High Altitude Medicine & Biology. Mary Ann Liebert. Alle Rechte vorbehalten.