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

Abstract

Simultaneous determination of the kinetics of cardiac output, systemic O 2 delivery, and lung O2 uptake at exercise onset in men. Am J Physiol Regul Integr Comp Physiol 290: R1071-R1079, 2006. First published October 20, 2005 doi:10.1152/ajpregu.00366.2005.-We tested whether the kinetics of systemic O 2 delivery (Q aO2) at exercise start was faster than that of lung O 2 uptake (V O2), being dictated by that of cardiac output (Q ), and whether changes in Q would explain the postulated rapid phase of the V O2 increase. Simultaneous determinations of beat-by-beat (BBB) Q and Q aO 2, and breath-by-breath V O2 at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 Ϯ 3.2 years, maximal aerobic power 333 Ϯ 61 W). V O2 was determined using Grønlund'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 steadystate method. This, along with the time course of hemoglobin concentration and arterial O 2 saturation (infrared oximetry) allowed computation of BBB Q aO 2. The Q , Q aO2 and V O2 kinetics were analyzed with single and double exponential models. f H, Qst, Q , and V O2 increased upon exercise onset to reach a new steady state. The kinetics of Q aO 2 had the same time constants as that of Q . The latter was twofold faster than that of V O2. The V 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 Q changes fully explained the phase I of V O2 increase. We suggest that in unsteady states, lung V O2 is dissociated from muscle O 2 consumption. The two components of Q and Q aO2 kinetics may reflect vagal withdrawal and sympathetic activation. cardiovascular response AT THE ONSET OF SQUARE-WAVE light aerobic exercise, O 2 consumption increases to attain a steady level, proportional to the exerted mechanical power. Its increase rises at a finite rate in response to the step increase in power, so that an O 2 deficit is incurred in the first minutes of exercise. The O 2 deficit reflects the decrease in high-energy phosphate concentration that is necessary to accelerate aerobic metabolic pathways (5,19,35,37). Analogous to the charge of a single capacitance, the increase in O 2 consumption was described by monoexponential equations (5,15,19). The monoexponential decrease in phosphocreatine concentration upon square-wave exercise onset (6, 46) is perhaps the strongest evidence provided so far in favor of this single capacitance model for O 2 consumption. Assuming close correspondence between O 2 consumption by the working muscles and O 2 uptake at the lungs (V O 2 ), the V O 2 was investigated to gain information on O 2 consumption (15, 16).This correspondence, however, was questioned. In fact, the kinetics of O 2 consumption requires that it be sustained by adequate O 2 transfer from ambient air to mitochondria. Thus, concomitant with the increase in O 2 consumption, th...

Non-invasive haemodynamic assessments using Innocor™ during standard graded exercise tests

“…2) lends further credence to earlier studies investigating the haemodynamic response to rest-to-exercise transitions. In these studies, it was shown that a steady state for cardiac output is attained between 30 (Lador et al 2006(Lador et al , 2008 and 60 s (De Cort et al 1991). Also, Davies et al (1972) found a rapid adjustment of cardiac output after increasing power (i.e.…”

“…Evidence for quick adjustments of cardiac output to increased power comes from the examination of haemodynamics during rest-to-exercise transitions in healthy participants by determining cardiac function on a beat-by-beat basis, using Doppler ultrasound (De Cort et al 1991) or the model flow method (Lador et al 2006(Lador et al , 2008. These studies showed that when increasing power from rest to 50, 80, or 100 W (i.e., "rest-to-exercise" transitions), a steady state for cardiac output is quickly reached (e.g., within the first minute).…”

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“…It is also noteworthy that the correction factor is independent of exercise intensity and thus of the ongoing blood flow and TPR. As a consequence, the method can conveniently be used for the analysis of dynamic states (Lador et al, 2006).…”

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