During constant-load exercise of moderate intensity, pulmonary O2 uptake (VO2) is characterized by two temporal response components. The first occurs during the transit delay from the exercising limbs and is mediated predominantly by increased pulmonary blood flow. Thereafter, this response is supplemented by the influence of increased O2 extraction, causing VO2 to increase monoexponentially to its steady state, with a time constant that does not vary appreciably with work rate, at this intensity. At work rates that engender a lactic acidosis, however, an additional slow phase of VO2 is superimposed upon the underlying kinetics: this is of delayed onset and prolongs the time to steady state over the range within which the increases in blood lactate and [H+] stabilize or even decrease (heavy exercise). At higher work rates (severe exercise) a steady state is unattainable, with the VO2 trajectory resulting in VO2max progressively earlier the higher the work rate: it is therefore a fundamental determinant of exercise tolerance. Although the kinetic features of this slow VO2 component (other than its delay) remain to be determined, current evidence suggests that it is manifest predominantly in the exercising limbs, with the recruitment profile and metabolic features of fast-twitch fiber activation being the major contributor.