Work capacity was studied at sea level and during 2 wk sojourn at 4300 m in 9 men. In comparison to the 1st day at altitude, after 2 wk sojourn maximal O2 consumption (.ovrhdot.VO2 max) and systemic O2 transport (.ovrhdot.TO2 max) increased 10% (P < 0.01). Increased .ovrhdot.TO2 max resulted from a 19% increase (P < 0.05) in arterial O2 content (CaO2), despite a 9% decrease (P < 0.05) in maximal cardiac output (.ovrhdot.Qmax). Increased CaO2 resulted from a 12% increase (P < 0.01) of O2 carrying capacity (O2 Cap) and a 6% increase (P < 0.05) of arterial O2 saturation (SaO2). Decreased .ovrhdot.Qmax resulted from a 9% reduction (P < 0.05) of maximal stroke volume (SVmax). Endurance time increased 60% (P < 0.01). After 3 wk at 4300 m, 450 ml of whole blood were removed from 5 volunteers to evaluate the role of relative polycythemia. Following blood removal, .ovrhdot.VO2 max and .ovrhdot.TO2 max were reduced 8 and 7%, respectively (P < 0.05). CaO2 fell 14% (P < 0.01) as the result of decreased O2 Cap. .ovrhdot.Qmax increased 8% (P < 0.05) as the result of increased SVmax. Endurance time was reduced 35% (P < 0.01). Apparently the effects of increased CaO2 during high-altitude hypoxia exceed those of reduced .ovrhdot.Qmax, resulting in increased work capacity. Relative polycythemia is a major contributor to increased work capacity.