CARDIORESPIRATORY RESPONSE TO PROGRESSIVE LEG EXERCISE UNDER ACUTE NORMOBARIC HYPOXIA

There is no clear evidence that the cardiorespiratory response to prog ressive maximal leg exercise was affected in proportion to the fall in PaO2 as measured from arterialized ear lobe blood. Subjects inhaling room air (rest PaO2 = 81 +/- 1 mmHg) or hypoxic gas mixtures, containi ng 15% or 10% O-2 in N-2 (rest PaO2 = 60 +/- 3 and 45 +/- 1 mmHg, resp ectively), performed leg exercise until exhaustion above the ventilato ry threshold, determined from the changes in the ventilatory equivalen t for oxygen (VO(2)VEAT). Acute hypoxemia potentiated the increase in minute ventilation (VE) in response to exercise, but this effect was o nly found when VE changes were expressed in percent of data collected during the 0 W work load cycling period preceding exercise. Hypoxemia always potentiated the heart rate (HR) response to exercise. These eff ects of hypoxemia on VE and HR were not proportional to the fall in Pa O2. In addition, severe hypoxemia depressed the pressor vascular respo nse to exercise. By contrast, VO(2)max and VO(2)VEAT decreased in prop ortion to hypoxemia and VO(2)VEAT was also negatively correlated with the peak lactate concentration. It was concluded that severe hypoxemia attenuated the cardiorespiratory response to exercise, whereas its co nsequences on the metabolic components of exercise (VO(2)max, VO(2)VEA T, lactic acid production) seem proportional to the reduced muscle oxy gen supply.