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Am J Physiol Regul Integr Comp Physiol (October 3, 2002). doi:10.1152/ajpregu.00156.2002
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Articles in PresS, published online ahead of print October 3, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00156.2002
Submitted on March 11, 2002
Accepted on September 27, 2002

WHY IS VO2max AFTER ALTITUDE ACCLIMATIZATION STILL REDUCED DESPITE NORMALIZATION OF ARTERIAL O2 CONTENT?

Jose A Calbet1*, Robert Boushel2, Goran Radegran3, Hans Sondergaard3, Peter D Wagner4, and Bengt Saltin3

1 Department of Physical Education, University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Canary Islands, Spain; The Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark
2 The Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark; Department of Exercise Science, Concordia University, Montreal, Quebec, Canada
3 The Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark
4 Department of Medicine, Section of Physiology, University of California San Diego, La Jolla, California, USA

* To whom correspondence should be addressed. E-mail: lopezcalbet{at}terra.es.

Acute hypoxia reduces VO2max, but after acclimatization, and despite increases in both [Hb] and arterial O2 saturation that can normalize arterial [O2], VO2max remains low. To determine why, 7 lowlanders were studied at VO2max (cycle ergometry) at sea level (SL), after 9-10 weeks at 5260m (CH), and 6 months later at sea level in acute hypoxia (AH) (FIO2 = 0.105) equivalent to 5260m. Pulmonary and leg indices of O2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by about 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), while in CH it was the same than at SL due to both polycythemia and hyperventilation. O2 extraction by the legs however remained at SL values in both AH and CH. While at both SL and in AH, 76% of the cardiac output perfused the legs, in CH the legs received only 67%. Pulmonary VO2max (4.1 ± 0.3 l.min-1 at SL) fell to 2.2 ± 0.1 l.min-1 in AH (P < 0.05) and was only 2.4 ± 0.2 l.min-1 in CH (P < 0.05). These data suggest that the failure to recover VO2max 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 non-exercising tissues. Oxygen transport from blood to muscle mitochondria on the other hand appears unaffected by CH.




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