Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High Altitude

BACKGROUND The hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA), HVR at SL may not predict PASP at HA. We hypothesized that resting oxygen saturation as measured by pulse oximetry (Sp o 2 ) at HA would correlate better than HVR at SL with PASP at HA. METHODS In 20 participants at SL, we measured normobaric, isocapnic HVR (L/min · −%Sp o 2 −1 ) and resting PASP using echocardiography. Both resting Sp o 2 and PASP measures were repeated on day 2 (n = 10), days 4 to 8 (n = 12), and 2 to 3 weeks (n = 8) after arrival at 5,050 m. These data were also collected at 5,050 m in life-long HA residents (ie, Sherpa [n = 21]). RESULTS Compared with SL, Sp o 2 decreased from 98.6% to 80.5% ( P P o 2 or PASP at any time point at 5,050 m (all P > .05). Sherpa had lower PASP ( P o 2 . Upon correction for hematocrit, Sherpa PASP was not different from lowlanders at SL but was lower than lowlanders at all HA time points. At 5,050 m, although Sp o 2 was not related to PASP in lowlanders at any point (all R 2 ≤ 0.05, P > .50), there was a weak relationship in the Sherpa ( R 2 = 0.16, P = .07). CONCLUSIONS We conclude that neither HVR at SL nor resting Sp o 2 at HA correlates with elevations in PASP at HA.