Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/6569
Title: Why is VO2 max after altitude acclimatization still reduced despite normalization of arterial O2 content?
Authors: Calbet, José A.L. 
Boushel, R.
Radegran, Goran
Sondergaard, H.
Wagner, P.D.
Saltin, Bengt
UNESCO Clasification: 241106 Fisiología del ejercicio
Keywords: Hypoxia
Altitude
Cardiac output
Issue Date: 2002
Publisher: 0363-6119
Journal: American Journal of Physiology - Regulatory Integrative and Comparative Physiology 
Abstract: Acute hypoxia (AH) reduces maximal O2 consumption (VO2 max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O2 saturation that can normalize arterial O2 concentration ([O2]), VO2 max remains low. To determine why, seven lowlanders were studied at VO2 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 (FiO2 = 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 approximately 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. O2 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 VO2 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 recover VO2 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.
URI: http://hdl.handle.net/10553/6569
ISSN: 0363-6119
DOI: 10.1152/ajpregu.00156.2002
Source: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology (2003 Feb) [ISSN 0363-6119], v. 284(2), p. R304-R316
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