Human endurance performance is often evaluated on the basis of the maximal rate of oxygen uptake during exercise (V(O(2)max)). Methods for overcoming limits to V(O(2)max) are touted as means for increasing athletic endurance performance. Here, we argue that the respiratory system is well designed for delivering O(2) to meet O(2) demands and that no single factor is rate-determining for O(2) uptake. We show that V(O(2)max) can vary 5000-fold among mammals, while any limitation to O(2) delivery by a single component of the respiratory system affects V(O(2)max) by 10% or less. Attempts to increase O(2) delivery by enhancing one step in the respiratory system are shown to have little effect. Blood doping, hyperoxia and O(2) supplementation of high-altitude natives all raise O(2) availability substantially to the working muscles, but these treatments increase V(O(2)max) only minimally. Finally, we argue that O(2) uptake is only one of a number of properties important to human aerobic performance.