Hypoxia causes pulmonary vasoconstriction. Regional hypoxic vasoconstriction improves the matching of perfusion to alveolar ventilation. Global hypoxic vasoconstriction increases right ventricular afterload. The hypoxic pulmonary pressor response is universal in mammals and in birds, but with considerable inter-species and inter-individual variability. Chronic hypoxia induces pulmonary hypertension in proportion to initial vasoconstriction. Chronic hypoxia also is associated with an increase in red blood cell mass, which aggravates pulmonary hypertension by an increased blood viscosity. Hypoxic vasoconstriction is a quasi-immediate response followed by vascular remodeling after a as soon as after 6-8 hours to become largely irreversible with supplemental oxygen after 24 to 48 hours of hypoxic exposure. Hypoxic pulmonary hypertension in humans is usually mild to moderate, but pulmonary vascular pressure-flow relationships are steep, which corresponds to a substantial afterload on the right ventricle during exercise. This limits aerobic exercise capacity be a decrease in maximum right ventricular flow output. A partial recovery of maximum oxygen uptake has been reported with intake specific pulmonary vasodilating interventions in hypoxic subjects. While there are very few reported measurements of cardiac function during exercise, resting echocardiographic examinations disclose subtle deteriorations in both systolic and diastolic function, with right ventricular predominance. These findings are more pronounced in patients with chronic mountain sickness, but their clinical significance remains incompletely understood.