{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T02:20:56Z","timestamp":1793067656402,"version":"4.5.0"},"reference-count":50,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2003,2,1]]},"abstract":"<jats:p> Acute hypoxia (AH) reduces maximal O<jats:sub>2<\/jats:sub> consumption (V\u02d9o <jats:sub>2\u2009max<\/jats:sub>), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O<jats:sub>2<\/jats:sub> saturation that can normalize arterial O<jats:sub>2<\/jats:sub> concentration ([O<jats:sub>2<\/jats:sub>]),V\u02d9o <jats:sub>2\u2009max<\/jats:sub> remains low. To determine why, seven lowlanders were studied at V\u02d9o <jats:sub>2\u2009max<\/jats:sub>(cycle ergometry) at sea level (SL), after 9\u201310 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (Fi <jats:sub>O<jats:sub>2<\/jats:sub> <\/jats:sub> = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O<jats:sub>2<\/jats:sub> transport were measured in each condition. Both cardiac output and leg blood flow were reduced by \u223c15% in both AH and CH ( P &lt; 0.05). At maximal exercise, arterial [O<jats:sub>2<\/jats:sub>] in AH was 31% lower than at SL ( P &lt; 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O<jats:sub>2<\/jats:sub>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%. PulmonaryV\u02d9o <jats:sub>2\u2009max<\/jats:sub> (4.1 \u00b1 0.3 l\/min at SL) fell to 2.2 \u00b1 0.1 l\/min in AH ( P &lt; 0.05) and was only 2.4 \u00b1 0.2 l\/min in CH ( P &lt; 0.05). These data suggest that the failure to recoverV\u02d9o <jats:sub>2\u2009max<\/jats:sub> after acclimatization despite normalization of arterial [O<jats:sub>2<\/jats:sub>] 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. <\/jats:p>","DOI":"10.1152\/ajpregu.00156.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:27:39Z","timestamp":1425414459000},"page":"R304-R316","source":"Crossref","is-referenced-by-count":186,"title":["Why is V\u02d9<scp>o<\/scp> <sub>2\u2009max<\/sub> after altitude acclimatization still  reduced despite normalization of arterial O<sub>2<\/sub> content?"],"prefix":"10.1152","volume":"284","author":[{"given":"J. A. 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