Pulmonary hemodynamics responses to hypoxia and/or CO2 inhalation during moderate exercise in humans

Abstract

In this study, we hypothesized that adding CO₂ 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% O₂), inhaled CO₂ (4.5% CO₂), and combination of hypoxia and inhaled CO₂. 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 CO₂ inhalation and combined conditions showed acidosis. sPAP increases from rest in ambient air to exercise ranged as follows: ambient + 110%, CO₂ inhalation + 135%, combined + 184%, hypoxia + 217% (p < 0.001). CO was higher when inhaling O₂-poor gas mixtures with or without CO₂ (~ 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 CO₂ inhalation and combined condition (- 29%). We conclude that (1) acute CO₂ inhalation did not significantly modify pulmonary hemodynamics during moderate exercise. (2) CO₂ adjunction to hypoxic gas mixture did not modify CO, despite a higher CaO₂ in combined condition than in hypoxia. (3) TPR was lower in combined than in hypoxia condition, limiting sPAP increase in combined condition.

Keywords: CO2 inhalation; Cardiac output; Exercise; Human; Hypoxia; Pulmonary artery pressure.