Michela Cautero

Correction of cardiac output obtained by Modelflow from finger pulse pressure profiles with a respiratory method in humans

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.

Energy cost of front-crawl swimming at supra-maximal speeds and underwater torque in young swimmers.

Abstract The energy cost of front-crawl swimming (Cs, kJ · 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 (AnAl), lactic (AnL) and aerobic (Aer) processes. In turn, AnL was obtained from the net increase of lactate concentration after exercise, AnAl was assumed to amount to 0.393 kJ · 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′, N · 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 · m−1) turned out to be a continuous function of the speed (v, m · s−1) in both males (Cs=0.603 · 100.228v, r2=0.991; n=12) and females (Cs=0.360 · 100.339v, r2=0.919; n=24). A significant relationship was found between T′ and Cs at 1.2 m · 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 · 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 · s−1].

PHASE I DYNAMICS OF CARDIAC OUTPUT, SYSTEMIC O2 DELIVERY AND LUNG O2 UPTAKE AT EXERCISE ONSET IN MEN IN ACUTE NORMOBARIC HYPOXIA

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+/-3.4 yr, 82.1+/-13.7 kg, maximal aerobic power 330+/-67 W), we determined beat-by-beat cardiac output (Q), oxygen delivery (QaO2), and breath-by-breath lung oxygen uptake (VO2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2=0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Qst, by model flow) and heart rate (fH, electrocardiography), and QaO2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q were higher, and Qst and VO2 were unchanged. QaO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for VO2 was unchanged. For fH, Q and QaO2, A1 was lower. Phase I time constant (tau1) for QaO2 and VO2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Qst 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 A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q and QaO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.

Identification of vascular responses to exercise and orthostatic stress in bed rest-induced cardiovascular deconditioning

In this paper, the effects of bed rest-induced cardiovascular deconditioning were investigated by means of a previously developed multivariate model for the assessment of arterial control of circulation. The vascular response to exercise and tilt, before and after a 14-day head down tilt bed rest, was identified and disentangled from the main mechanisms due to global, neural control of circulation. Results of the decomposition of diastolic pressure and pulse pressure beat-by-beat series and the relevant spectral analysis suggested that the autoregulation-related response is not affected by prolonged exposition to microgravity. As to the complex regulation of arterial blood pressure, a maintained responsiveness to sympathetic stimuli was found, even in presence of indications of the cardiovascular deconditioning, such as tachycardia, reset of baroreflex, cardiopulmonary unloading. These preliminary results emphasized the necessity for more complex analyses of the main alterations and compensatory mechanisms elicited by microgravity-induced-cardiovascular deconditioning, in order to develop more effective long term strategies to prevent it.