Why is Vo2max after altitude acclimatization still reduced despite normalization of arterial O2 content?

Acute hypoxia (AH) reduces maximal O-2 consumption ((V) over dot O-2max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O-2 saturation that can normalize arterial O-2 concentration ([O-2]), (V) over dot O-2max remains low. To determine why, seven lowlanders were studied at (V) over dot O-2max (cycle ergometry) at sea level (SL), after 9-10 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (FIO2 = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O-2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by similar to15% in both AH and CH (P < 0.05). At maximal exercise, arterial [O-2] in AH was 31% lower than at SL (P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O-2 extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76% of the cardiac output perfused the legs, in CH the legs received only 67%. Pulmonary (V) over dot O-2max (4.1 +/- 0.3 l/min at SL) fell to 2.2 +/- 0.1 l/min in AH (P < 0.05) and was only 2.4 +/- 0.2 l/min in CH (P < 0.05). These data suggest that the failure to recover (V) over dot O-2max after acclimatization despite normalization of arterial [O-2] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH.