Reductions in systemic and locomotor limb muscle blood flow and O2 delivery limit aerobic capacity in humans. To examine whether O2 delivery limits both aerobic power and capacity, we first measured systemic haemodynamics, O2 transport and O2 uptake during incremental and constant (372 +/- 11 W; 85% of peak power; mean +/- S.E.M.) cycling exercise to exhaustion (n = 8) and then measured systemic and leg haemodynamics and during incremental cycling and knee-extensor exercise in male subjects (n = 10). During incremental cycling, cardiac output and systemic O2 delivery increased linearly to 80% of peak power (r2 = 0.998, P < 0.001) and then plateaued in parallel to a decline in stroke volume (SV) and an increase in central venous and mean arterial pressures (P < 0.05). In contrast, heart rate and increased linearly until exhaustion (r2 = 0.993; P < 0.001) accompanying a rise in systemic O2 extraction to 84 +/- 2%. In the exercising legs, blood flow and O2 delivery levelled off at 73-88% of peak power, blunting leg per unit of work despite increasing O2 extraction. When blood flow increased linearly during one-legged knee-extensor exercise, per unit of work was unaltered on fatigue. During constant cycling, , SV, systemic O2 delivery and reached maximal values within approximately 5 min, but dropped before exhaustion (P < 0.05) despite increasing or stable central venous and mean arterial pressures. In both types of maximal cycling, the impaired systemic O2 delivery was due to the decline or plateau in because arterial O2 content continued to increase. These results indicate that an inability of the circulatory system to sustain a linear increase in O2 delivery to the locomotor muscles restrains aerobic power. The similar impairment in SV and O2 delivery during incremental and constant load cycling provides evidence for a central limitation to aerobic power and capacity in humans.