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...

The energy cost of front-crawl swimming (Cs, kJ x m(-1)) at maximal voluntary speeds over distances of 50, 100, 200 and 400 m, and the underwater torque (T') were assessed in nine young swimmers (three males and six females; 12-17 years old). Cs was calculated from the ratio of the total metabolic energy (Es, kJ) spent to the distance covered. Es was estimated as the sum of the energy derived from alactic (AnA1), lactic (AnL) and aerobic (Aer) processes. In turn, AnL was obtained from the net increase of lactate concentration after exercise, AnA1 was assumed to amount to 0.393 kJ x kg(-1) of body mass, and Aer was estimated from the maximal aerobic power of the subject. Maximal oxygen consumption was calculated by means of the back-extrapolation technique from the oxygen consumption kinetics recorded during recovery after a 400-m maximal trial. Underwater torque (T' x N x m), defined as the product of the force with which the feet of a subject lying horizontally in water tends to sink times the distance from the feet to the center of volume of the lungs, was determined by means of an underwater balance. Cs (kJ x m(-1)) turned out to be a continuous function of the speed (v, m x s(-1)) in both males (Cs = 0.603 x 10(0.228v), r2 =0.991; n = 12) and females (Cs = 0.360 x 10(0.339r), r2 = 0.919; n = 24). A significant relationship was found between T' and Cs at 1.2 m x s(-1); Cs = 0.042T' + 0.594, r = 0.839, n = 10, P<0.05. On the contrary, no significant relationships were found between Cs and T' at faster speeds (1.4 and 1.6 m x s(-1)). This suggests that T' is a determinant of Cs only at speeds comparable to that maintained by the subjects over the longest, 400-m distance [mean (SD) 1.20 (0.07) m x s(-1)].

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.

Alveolar gas transfer over a given breath (i) was determined in ten subjects at rest and during steady-state cycling at 60, 90 or 120 W as the sum of volume of gas transferred at the mouth plus the changes of the alveolar gas stores. This is given by the gas fraction (FA) change at constant volume plus the volume change (deltaVAi) at constant fraction i.e. VAi-1(FAi-FAi-1)+FAi x deltaVAi, where VAi-1 is the end-expiratory volume at the beginning of the breath. These quantities, except for VAi-1, can be measured on a single-breath (breath-by-breath) basis and VAi-1 set equal to the subject's functional residual capacity (FRC, Auchincloss model). Alternatively, the respiratory cycle can be defined as the interval elapsing between two equal expiratory gas fractions in two successive breaths (Grønlund model G). In this case, Ft1 = Ft2 and thus the term VAi-1 (FAi-FAi-1) vanishes. In the present study, average alveolar O2 uptake (VO2,A) and CO2 output (VCO2,A) were equal in both approaches whereby the mean signal-to-noise ratio (S/N) was 40% larger in G. Other approaches yield steady state S/N values equal to that obtained in G, although they are based on the questionable assumption that the inter-breath variability of alveolar gas transfer is minimal. It is concluded that the only promising approach for assessing "true" single-breath alveolar gas transfer is that originally proposed by Grønlund.

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.