Cardiac Limitation To Exercise Capacity At High Altitudes

Exposure to high altitude is associated with a decrease in aerobic exercise capacity. This is explained by a decrease in oxygen delivery to the tissues or the product of cardiac output by arterial oxygen content. Arterial oxygen content is decreased at altitude because of a reduced inspired partial pressure of oxygen. However, this limited by the hypoxic chemoreflex, which increases ventilation and decreases alveolar partial pressure of carbon dioxide, thereby improving alveolar partial pressure of oxygen. In addition, there is a renal synthesis and release of erythropoietin, which increases the hemoglobin content of the blood. Both adaptations bring arterial oxygen content back to its pre-hypoxic exposure sea-level value in 2 to 3 weeks at altitudes up to 5000 m, without, however, restoring exercise capacity. Altitude is also associated with a decrease in maximum cardiac output. The mechanisms of hypoxia-induced decrease in maximum cardiac output remain incompletely understood. Previously proposed explanations have been a decreased peripheral demand due to altered matching of diffusional and convectional oxygen delivery processes, a decrease in the chronotropic reserve or a decreased central nervous system output to the heart. Pharmacological studies in hypoxic volunteers suggest that at least part of the limitation of cardiac output at high altitude might be related to hypoxic pulmonary hypertension, as a cause of excessive right ventricular afterload. This notion has recently been confirmed by Doppler echocardiographic studies, which suggest that high altitude-induced right heart failure (HARHF) might be more common than previously assumed.

Keywords: altitude, exercise; heart; pulmonary hypertension; hypoxic pulmonary vasoconstriction; right heart failure