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This Article Full Text Full Text (PDF) All Versions of this Article: 586/1/123    most recent jphysiol.2007.146035v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lundby, C. Articles by Calbet, J. A. L. Search for Related Content PubMed PubMed Citation Articles by Lundby, C. Articles by Calbet, J. A. L. Related Collections Skeletal Muscle and Exercise

¹ Copenhagen Muscle Research Center, Rigshospitalet, section 7652, 2100 Copenhagen, Denmark
² Department of Sport Science, University of Århus, 8200 Århus, Denmark
³ Department of Biomedical Sciences, Panum Institute, University of Copenhagen, 2100 Copenhagen, Denmark
⁴ Department of Exercise Science, Concordia University, Montreal, Quebec, Canada
⁵ Ecole Nationale de Ski et d'Alpinisme, 74401 Chamonix, France
⁶ Department of Physical Education, University of Las Palmas de Gran Canaria, Spain

To test the hypothesis that the increased sympathetic tonus elicited by chronic hypoxia is needed to match O₂ delivery with O₂ demand at the microvascular level eight male subjects were investigated at 4559 m altitude during maximal exercise with and without infusion of ATP (80 µg (kg body mass)^–1 min^–1) into the right femoral artery. Compared to sea level peak leg vascular conductance was reduced by 39% at altitude. However, the infusion of ATP at altitude did not alter femoral vein blood flow (7.6 ± 1.0 versus 7.9 ± 1.0 l min^–1) and femoral arterial oxygen delivery (1.2 ± 0.2 versus 1.3 ± 0.2 l min^–1; control and ATP, respectively). Despite the fact that with ATP mean arterial blood pressure decreased (106.9 ± 14.2 versus 83.3 ± 16.0 mmHg, P < 0.05), peak cardiac output remained unchanged. Arterial oxygen extraction fraction was reduced from 85.9 ± 5.3 to 72.0 ± 10.2% (P < 0.05), and the corresponding venous O₂ content was increased from 25.5 ± 10.0 to 46.3 ± 18.5 ml l^–1 (control and ATP, respectively, P < 0.05). With ATP, leg arterial–venous O₂ difference was decreased (P < 0.05) from 139.3 ± 9.0 to 116.9 ± 8.4^–1 and leg was 20% lower compared to the control trial (1.1 ± 0.2 versus 0.9 ± 0.1 l min^–1) (P = 0.069). In summary, at altitude, some degree of vasoconstriction is needed to match O₂ delivery with O₂ demand. Peak cardiac output at altitude is not limited by excessive mean arterial pressure. Exercising leg is not limited by restricted vasodilatation in the altitude-acclimatized human.

(Received 2 October 2007; accepted after revision 9 October 2007; first published online 11 October 2007)
Corresponding author C. Lundby: Copenhagen Muscle Research Center, Rigshospitalet, section 7652, Blegdamsvej 9, 2100 Copenhagen Ø, Denmark. Email: lundby{at}idraet.au.dk