Simultaneous determination of the kinetics of cardiac output, systemic O sub(2) delivery, and lung O sub(2) uptake at exercise onset in men

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