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1 Physiology, University Medical Center, 1211 Geneva 4, Switzerland
2 Biomedical Science and Technology, University of Udine, 33100 Udine, Italy
3 Anesthesiology, Cantonal University Hospital, 1211 Geneva 4, Switzerland
4 Physiology, University Medical Center, 1211 Geneva 4, Switzerland; Biomedical Science and Biotechnology, University of Brescia, 25100 Brescia, Italy
* To whom correspondence should be addressed. E-mail: guido.ferretti{at}medecine.unige.ch.
We tested whether the kinetics of systemic O2 delivery (QaO2) at exercise start was faster than that of lung O2 uptake (VO2), being dictated by that of cardiac output (Q), and whether changes in Q would explain the postulated rapid phase of the VO2 increase. Simultaneous determinations of beat-by-beat (BBB) Q and QaO2, and breath-by-breath VO2 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). VO2 was determined using Gronlund's algorithm. Q was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate (fH, electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB QaO2. The Q, QaO2 and VO2 kinetics were analysed with single and double exponential models. fH, Qst, Q and VO2 increased upon exercise onset to reach a new steady state. The kinetics of QaO2 had the same time constants (N.S.) as that of Q. The latter was twofold faster than that of VO2. The VO2 kinetics was 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 VO2 increase. We conclude that in unsteady states lung VO2 is dissociated from muscle O2 consumption. The two components of Q and QaO2 kinetics may reflect vagal withdrawal and sympathetic activation.
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