During constant-load exercise of moderate intensity, pulmonary O2uptake (&OV0312;O2) 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 O2extraction, causing &OV0312;O2to 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 &OV0312;O2is 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 &OV0312;O2trajectory resulting in &OV0312;O2maxprogressively earlier the higher the work rate: it is therefore a fundamental determinant of exercise tolerance. Although the kinetic features of this slow &OV0312;O2component (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.