Abstract
We sought to determine the effects of prolonged moderate hypobaric hypoxia (HH) on cardiac baroreflex sensitivity (cBRS) in young women, and whether these effects are a consequence of the reduced arterial oxygen (O2) tension and/or increased pulmonary ventilation in HH. We hypothesised that HH would reduce cBRS and that this effect would be counteracted by acute restoration of the inspiratory partial pressure of O2 (PiO2) and/or voluntary attenuation of pulmonary ventilation. Twelve healthy women (24.0±4.2 years) were studied before (DAY 0) and twice during a sojourn in a hypobaric chamber (~8 hours, DAY 1; 4 days, DAY 4) where barometric pressure corresponded to ~3,500 m altitude. Minute ventilation (V̇E; pneumotachometer), heart rate (electrocardiogram), and arterial pressure (finger volume clamp method) were recorded. cBRS was calculated using transfer function analysis between systolic pressure and RR interval. Assessments were made during i. spontaneous breathing, and (in HH only) ii. controlled breathing (reducing V̇E by ~1 L·min-1), and iii. breathing a hyperoxic gas mixture that normalized PiO2. During spontaneous breathing HH decreased cBRS (12.5±7.1, 8.9±4.4 and 7.4±3.0 ms·mmHg-1 on DAY 0, DAY 1 and DAY 4, respectively; P=0.018). The normalization of PiO2 increased cBRS (10.6±3.3 and 10.7±6.1 ms·mmHg-1 on DAY 1 and DAY 4) in HH compared to values observed during spontaneous breathing (P<0.001), whereas controlled breathing had no effect on cBRS (P=0.708). These findings indicate that ongoing arterial chemoreflex activation by the reduced arterial O2 tension, independently of the hypoxic ventilatory response, reduces cBRS in young women exposed to extended HH.