LOW CHEMORESPONSIVENESS AND INADEQUATE HYPERVENTILATION CONTRIBUTE TO EXERCISE-INDUCED HYPOXEMIA

Is inadequate hyperventilation a cause of the exercise-induced hypoxemia observed in some athletes during intense exercise? If so, is this related to low chemoresponsiveness? To test the hypothesis that exercise-induced hypoxemia, inadequate hyperventilation, and chemoresponsiveness are related, 36 nonsmoking healthy men were divided into hypoxemic (Hyp; n = 13) or normoxemic (Nor; n = 15) groups based on arterial oxygen saturation (Sa(O2); Hyp less than or equal to 90%, Nor > 92%) observed during maximum O-2 uptake (VO2max). Men with intermediate Sa(O2) values (n = 8) were only included in correlation analysis. Ventilatory parameters were collected at rest, during a treadmill maximal oxygen consumption (VO2max) test, and during a 5-min run at 90% VO2max. Chemoresponsiveness at rest was assessed via hypoxic ventilatory response (HVR) and hypercapnic ventilatory response (HCVR). VO2max was not significantly different between Nor and Hyp. Sa(O2) was 93.8 +/- 0.9% (Nor) and 87.7 +/- 2.0% (Hyp) at VO2max. End-tidal PO2 and the ratio of minute ventilation to oxygen consumption (VE/VO2) were lower while PET(CO2) was higher for Hyp (P less than or equal to 0.01). End-tidal PO2, end-tidal PCO2, and VE/VO2 correlated (P less than or equal to 0.05) to Sa(O2) (r = 0.84, r = -0.70, r = 0.72, respectively), suggesting that differences in oxygenation were due to differences in ventilation. HVR and HCVR were significantly lower for Hyp. HVR was related to VE/VO2 (r = 0.43), and HCVR was related to the ratio VE to CO2 production at VO2max (r = 0.61). In summary, the results suggest that inadequate hyperventilation, related to low hypoxic and hypercapnic drive is a significant mechanism in the hypoxemia experienced by some athletes during intense exercise.