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ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY

Simultaneous determination of the kinetics of cardiac output, systemic O₂ delivery, and lung O₂ uptake at exercise onset in men

¹Département de Physiologie, Centre Médical Universitaire, Genève, Switzerland; ²Département d'Anesthésiologie, Pharmacologie et Soins Intensifs Chirurgicaux, Hôpital Cantonal Universitaire, Bâtiment Opéra, Genève, Switzerland; ³Laboratorio di Fisiologia, Dipartimento di Scienze e Tecnologie Biomediche, Università di Udine, Udine, Italy; and ⁴Sezione di Fisiologia Umana, Dipartimento di Scienze Biomediche e Biotecnologie, Università di Brescia, Brescia, Italy

Submitted 24 May 2005 ; accepted in final form 8 October 2005

We tested whether the kinetics of systemic O₂ delivery (aO₂) at exercise start was faster than that of lung O₂ uptake (O₂), being dictated by that of cardiac output (), and whether changes in would explain the postulated rapid phase of the O₂ increase. Simultaneous determinations of beat-by-beat (BBB) and aO₂, and breath-by-breath O₂ 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). O₂ was determined using Grønlund's algorithm. 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 O₂ saturation (infrared oximetry) allowed computation of BBB aO₂. The , aO₂ and O₂ kinetics were analyzed with single and double exponential models. f_H, Q_st, , and O₂ increased upon exercise onset to reach a new steady state. The kinetics of aO₂ had the same time constants as that of . The latter was twofold faster than that of O₂. The O₂ 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 changes fully explained the phase I of O₂ increase. We suggest that in unsteady states, lung O₂ is dissociated from muscle O₂ consumption. The two components of and aO₂ kinetics may reflect vagal withdrawal and sympathetic activation.

cardiovascular response

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