With increasing altitude, air pressure and O2 partial pressure (PO2) in the ambient air decrease, so that oxygen can no longer be absorbed as well by the hemoglobin. The result is a lower partial pressure of oxygen in the blood as well as a lower oxygen saturation. Via peripheral chemoreceptors, this reduced oxygen saturation is perceived in the body and hyperventilation is triggered. This slightly increases the alveolar PO2 and activates the sympathetic nervous system. The resulting increased heart rate compensates for the lower O2 content per heartbeat. However, this so-called acute adaptation cannot prevent the maximum oxygen transport and thus the maximum aerobic capacity (VO2max) from being restricted. Thus, an untrained person loses about 1% of his VO2max per 100m at an altitude of 1,500m, resulting in a power loss of 10% at 2,500m, 25% at 4,000m, and 65% at 8,000m.
Systemic blood pressure does not change significantly during acute adaptation at altitude because sympathetic activation and the direct vasodilatory effect of hypoxia neutralize in the peripheral circulation.
Endurance training at altitude can be used specifically to increase performance. The lower blood oxygen saturation at altitude causes a variety of adaptation reactions over a longer period of time:
- The number of erythrocytes increases (erythropoiesis) due to the release of the hormone EPO.
- The hemoglobin concentration increases, resulting in better oxygen transport.
- The respiratory and cardiac output increases.
- The capillaries also increase (capillarization), which enables better gas exchange.
Thus, altitude training increases aerobic performance. Gas exchange becomes more economical in the long run, as oxygen can be better absorbed and transported further. However, this altitude acclimatization takes time (about three weeks of continuous stay at high altitudes).