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 vs 7.9 ± 1.0 l.min^-1) and femoral arterial oxygen delivery (1.2 ± 0.2 vs 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 vs 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 a-vO₂ difference was decreased (p<0.05) from 140.8 ± 8.7 to 111.3 ± 21.6 ml.l^-1 and leg VO₂peak was 10% lower compared to the control trial (1.1 ± 0.2 vs 1.0 ± 0.2 l.min^-1), (p=0.069). In summary, at altitude, some degree of vasoconstriction is needed to mach O₂ delivery with O₂ demand. Peak cardiac output at altitude is not limited by excessive mean arterial pressure. Exercising leg VO₂peak is not limited by restricted vasodilation in the altitude acclimatised human.