Publications by authors named "Michela Cautero"

We hypothesised that phase II time constant (τ2) of alveolar O2 uptake ( [Formula: see text] ) is longer in hypoxia than in normoxia as a consequence of a parallel deceleration of the kinetics of O2 delivery ( [Formula: see text] ). To test this hypothesis, breath-by-breath [Formula: see text] and beat-by-beat [Formula: see text] were measured in eight male subjects (25.4±3.

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This article summarises the pros and cons of different algorithms developed for estimating breath-by-breath (B-by-B) alveolar O(2) transfer (VO 2A) in humans. VO 2A is the difference between O(2) uptake at the mouth and changes in alveolar O(2) stores (∆ VO(2s)), which for any given breath, are equal to the alveolar volume change at constant FAO2/FAiO2 ∆VAi plus the O(2) alveolar fraction change at constant volume [V Ai-1(F Ai - F Ai-1) O2, where V (Ai-1) is the alveolar volume at the beginning of a breath. Therefore, VO 2A can be determined B-by-B provided that V (Ai-1) is: (a) set equal to the subject's functional residual capacity (algorithm of Auchincloss, A) or to zero; (b) measured (optoelectronic plethysmography, OEP); (c) selected according to a procedure that minimises B-by-B variability (algorithm of Busso and Robbins, BR).

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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.

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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.

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To evaluate if changes in athletes' physical fitness due to seasonal training are associated with changes in cardiovascular autonomic control, nine swimmers (three males and six females; aged 14-18 years) were evaluated before and after 5 months of training and competitions. Maximal oxygen consumption (VO2max) and ventilatory threshold were determined during a maximal test; heart rate (HR) and blood pressure (BP) variabilities' power spectra were calculated at rest (supine and sitting positions) and in the recovery of two exercises at 25 and 80% pre-training VO2max. At the end of the season: (a) VO2max and ventilatory threshold increased respectively by 12 and 34% (P<0.

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We tested whether the kinetics of systemic O(2) delivery (QaO(2)) at exercise start was faster than that of lung O(2) uptake (Vo(2)), being dictated by that of cardiac output (Q), and whether changes in Q would explain the postulated rapid phase of the Vo(2) increase. Simultaneous determinations of beat-by-beat (BBB) Q and QaO(2), and breath-by-breath Vo(2) at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/- 3.

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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.

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