Why is V˙o 2 max after altitude acclimatization still reduced despite normalization of arterial O2 content?

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Abstract
Acute hypoxia (AH) reduces maximal O2 consumption (V˙o 2 max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O2 saturation that can normalize arterial O2 concentration ([O2]),V˙o 2 max remains low. To determine why, seven lowlanders were studied at V˙o 2 max(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 (Fi O2 = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by ∼15% in both AH and CH ( P < 0.05). At maximal exercise, arterial [O2] 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. O2extraction 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%. PulmonaryV˙o 2 max (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 recoverV˙o 2 max after acclimatization despite normalization of arterial [O2] 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.