Cardiorespiratory response to progressive leg exercise under acute normobaric hypoxia.

There is no clear evidence that the cardiorespiratory response to progressive 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, containing 15% or 10% O2 in N2 (rest PaO2 = 60 +/- 3 and 45 +/- 1 mmHg, respectively), performed leg exercise until exhaustion above the ventilatory threshold, determined from the changes in the ventilatory equivalent for oxygen (VO2VEAT). Acute hypoxemia potentiated the increase in minute ventilation (VE) in response to exercise, but this effect was only 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 effects of hypoxemia on VE and HR were not proportional to the fall in PaO2. In addition, severe hypoxemia depressed the pressor vascular response to exercise. By contrast, VO2max and VO2VEAT decreased in proportion to hypoxemia and VO2VEAT was also negatively correlated with the peak lactate concentration. It was concluded that severe hypoxemia attenuated the cardiorespiratory response to exercise, whereas its consequences on the metabolic components of exercise (VO2max, VO2VEAT, lactic acid production) seem proportional to the reduced muscle oxygen supply.