Pulmonary hemodynamics responses to hypoxia and/or CO 2 inhalation during moderate exercise in humans.

In this study, we hypothesized that adding CO ₂ to an inhaled hypoxic gas mixture will limit the rise of pulmonary artery pressure (PAP) induced by a moderate exercise. Eight 20-year-old males performed four constant-load exercise tests on cycle at 40% of maximal oxygen consumption in four conditions: ambient air, normobaric hypoxia (12.5% O ₂ ), inhaled CO ₂ (4.5% CO ₂ ), and combination of hypoxia and inhaled CO ₂ . Doppler echocardiography was used to measure systolic (s)PAP, cardiac output (CO). Total pulmonary resistance (TPR) was calculated. Arterialized blood pH was 7.40 at exercise in ambient and hypoxia conditions, whereas CO ₂ inhalation and combined conditions showed acidosis. sPAP increases from rest in ambient air to exercise ranged as follows: ambient + 110%, CO ₂ inhalation + 135%, combined + 184%, hypoxia + 217% (p < 0.001). CO was higher when inhaling O ₂ -poor gas mixtures with or without CO ₂ (~ 17 L min ^-1 ) than in the other conditions (~ 14 L min ^-1 , p < 0.001). Exercise induced a significant decrease in TPR in the four conditions (p < 0.05) but less marked in hypoxia (- 19% of the resting value in ambient air) than in ambient (- 33%) and in both CO ₂ inhalation and combined condition (- 29%). We conclude that (1) acute CO ₂ inhalation did not significantly modify pulmonary hemodynamics during moderate exercise. (2) CO ₂ adjunction to hypoxic gas mixture did not modify CO, despite a higher CaO ₂ in combined condition than in hypoxia. (3) TPR was lower in combined than in hypoxia condition, limiting sPAP increase in combined condition.