We tested whether the kinetics of systemic O(2) delivery (QaO(2)) at exercise start was faster than that of lung O(2) uptake (Vo(2)), being dictated by that of cardiac output (Q), and whether changes in Q would explain the postulated rapid phase of the Vo(2) increase. Simultaneous determinations of beat-by-beat (BBB) Q and QaO(2), and breath-by-breath Vo(2) at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/- 3.2 years, maximal aerobic power 333 +/- 61 W). Vo(2) was determined using Gronlund's algorithm. Q was computed from BBB stroke volume (Q(st), from arterial pulse pressure profiles) and heart rate (f(h), electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O(2) saturation (infrared oximetry) allowed computation of BBB QaO(2). The Q, QaO(2) and Vo(2) kinetics were analyzed with single and double exponential models. f(h), Q(st), Q, and Vo(2) increased upon exercise onset to reach a new steady state. The kinetics of QaO(2) had the same time constants as that of Q. The latter was twofold faster than that of Vo(2). The Vo(2) kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q changes fully explained the phase I of Vo(2) increase. We suggest that in unsteady states, lung Vo(2) is dissociated from muscle O(2) consumption. The two components of Q and QaO(2) kinetics may reflect vagal withdrawal and sympathetic activation.