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...

Patients with RHD hospitalized in sub-Saharan Africa are young, socially disadvantaged, with a high mortality rate and extremely low access to surgery. Poverty, as quantified by GDP and educational level, affects RHD-related severity, NYHA class and left ventricular dysfunction.

The aim of this study was to characterize the time course of maximal oxygen consumption VO2(max) changes during bedrests longer than 30 days, on the hypothesis that the decrease in VO2(max) tends to asymptote. On a total of 26 subjects who participated in one of three bedrest campaigns without countermeasures, lasting 14, 42 and 90 days, respectively, VO2(max) maximal cardiac output (Qmax) and maximal systemic O2 delivery (QaO2max) were measured. After all periods of HDT, VO2max, Qmax, and QaO2max were significantly lower than before. The VO2max decreased less than qmax after the two shortest bedrests, but its per cent decay was about 10% larger than that of Qmax after 90-day bedrest. The VO2max decrease after 90-day bedrest was larger than after 42- and 14-day bedrests, where it was similar. The Qmax and QaO2max declines after 90-day bedrest was equal to those after 14- and 42-day bedrest. The average daily rates of the VO2max, Qmax, and QaO2max decay during bedrest were less if the bedrest duration were longer, with the exception of that of VO2max in the longest bedrest. The asymptotic VO2max decay demonstrates the possibility that humans could keep working effectively even after an extremely long time in microgravity. Two components in the VO2max decrease were identified, which we postulate were related to cardiovascular deconditioning and to impairment of peripheral gas exchanges due to a possible muscle function deterioration.

The beat-by-beat non-invasive assessment of cardiac output (Q litre x min(-1)) based on the arterial pulse pressure analysis called Modelflow can be a very useful tool for quantifying the cardiovascular adjustments occurring in exercising humans. Q was measured in nine young subjects at rest and during steady-state cycling exercise performed at 50, 100, 150 and 200 W by using Modelflow applied to the Portapres non-invasive pulse wave (Q(Modelflow)) and by means of the open-circuit acetylene uptake (Q(C2H2)). Q values were correlated linearly ( r = 0.784), but Bland-Altman analysis revealed that mean Q(Modelflow) - Q(C2H2) difference (bias) was equal to 1.83 litre x min(-1) with an S.D. (precision) of 4.11 litre x min(-1), and 95% limits of agreement were relatively large, i.e. from -6.23 to +9.89 litre x min(-1). Q(Modelflow) values were then multiplied by individual calibrating factors obtained by dividing Q(C2H2) by Q(Modelflow) for each subject measured at 150 W to obtain corrected Q(Modelflow) (Qcorrected) values. Qcorrected values were compared with the corresponding Q(C2H2) values, with values at 150 W ignored. Data were correlated linearly ( r = 0.931) and were not significantly different. The bias and precision were found to be 0.24 litre x min(-1) and 3.48 litre x min(-1) respectively, and 95% limits of agreement ranged from -6.58 to +7.05 litre x min(-1). In conclusion, after correction by an independent method, Modelflow was found to be a reliable and accurate procedure for measuring Q in humans at rest and exercise, and it can be proposed for routine purposes.

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6 Ϯ 3.4 yr, 82.1 Ϯ 13.7 kg, maximal aerobic power 330 Ϯ 67 W), we determined beat-by-beat cardiac output (Q ), oxygen delivery (Q a O 2 ), and breathby-breath lung oxygen uptake (V O2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O 2 ϭ 0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Q st, by model flow) and heart rate (fH, electrocardiography), and Q a O 2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state f H and Q were higher, and Qst and V O2 were unchanged. Q a O 2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A 1) for V O2 was unchanged. For fH, Q and Q a O 2 , A1 was lower. Phase I time constant (1) for Q a O 2 and V O2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Q st kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A 1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Q st. Thus the dual origin of the phase I of Q and Q a O 2 , neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed. cardiovascular response ALTHOUGH OUR KNOWLEDGE of the central (neural) control of the cardiovascular system at the exercise steady state is quite well established (19,42,57), how the circulatory readjustments upon exercise onset occur and match the increase in pulmonary oxygen uptake (V O 2 ) is less understood, as are the mechanisms underlying this matching. The kinetics of V O 2 at exercise onset were seen for a long time as reflecting essentially the metabolic adaptations in the working muscles (15,31,33). Some authors, however, soon identified two components of the V O 2 kinetics: 1) a rapid, almost immediate phase (phase I) (5, 54, 55), which they attributed to an immediate increase in cardiac output (Q ) at exercise start; and 2) a subsequent slower phase (phase II), to which they restricted the influence of muscle metabolic adjustments. The strongest support to this view came from the demonstration that the kinetics of Q (12, 13, 16, 60) and arterial O 2 flow (Q a O 2 ) (27) are very rapid.The concept of a close correspondence between V O 2 and muscle O 2 consumption was further undermined by the recent demonstration that, upon the onset of light exercise, the V O 2 kinetics are faster than the kinetics of muscle O 2 consumption estimated from the monoexponential decrease in phosphocreatine concentration (7,14,43). This would imply dissociation of the kinetics of V O 2 and muscle O 2 consumption, which should respond to different control mechanisms.Our postulate is that the V O 2 kinetics are dictated by ...