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Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery and lung O2 uptake at exercise onset in men.
No full textWe tested whether the kinetics of systemic O2 delivery (Q'aO2) at exercise start was faster than that of lung O2 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' aO2, 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 +/-3.2 years, maximal aerobic power 333 +/- 61 W). V'O2 was determined using Grønlund’s algorithm. Q' was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate (fH, electrocardiograpy) and calibrated against a steadystate method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB Q'aO2. The Q', Q'aO2 and V'O2 kinetics were analyzed with single and double exponential models. fH, Qst, Q', and V'O2 increased upon exercise onset to reach a new steady state. The
kinetics of Q'aO2 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
O2 consumption. The two components of Q' and Q'aO2 kinetics may reflect vagal withdrawal and sympathetic activation
Factors determining the kinetics of VO2max decay during bed-rest: implications for VO2max limitation
No full textThe aim of this study was to characterize the time course of maximal oxygen consumption (V'O2 max) changes during bedrests longer than 30 days, on the hypothesis that the decrease in V'O2 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, V'O2 max, maximal cardiac output (Qmax) and maximal systemic O2 delivery (QaO2max) were measured. After
all periods of HDT, V'O2 max; Qmax and QaO2max were significantly lower than before. The V'O2 max decreased less than Qmax after the two shortest bedrests, but its percent decay was about 10% larger than that of Qmax after 90-day bedrest. The V'O2 max decrease after 90-day bedrest was larger than after 42- and 14-day bedrests, where it was similar. The Qmax and QaO2max decline after 90-day bedrest was equal to those after 14- and 42-day bedrest. The average daily rates of the V'O2 max; Qmax and QaO2max decay during bedrest were less if the bedrest duration was longer, with the exception of that of V'O2 max in the longest bedrest. The asymptotic V'O2 max decay demonstrates the possibility that humans could keep working effectively even after an extremely long time in microgravity. Two components in the V'O2 max 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 time course of the decrease in maximal oxygen consumption during long-term bed rest in humans
No full textThe time course of the decrease in maximal oxygen consumption during long-term bed rest in human
Cardiac output, O2 delivery and V’O2 kinetics during step exercise in acute normobaric hypoxia.
No full textSimultaneous determination of kinetics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men.
No full textWe 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 +/- 3.2 years, maximal aerobic power 333 +/- 61 W). Vo(2) 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 steady-state method. This, along with the time course of hemoglobin concentration and arterial O(2) saturation (infrared oximetry) allowed computation of BBB QaO(2). The Q, QaO(2) and Vo(2) kinetics were analyzed with single and double exponential models. f(h), Q(st), Q, and Vo(2) increased upon exercise onset to reach a new steady state. The kinetics of QaO(2) had the same time constants as that of Q. The latter was twofold faster than that of Vo(2). The Vo(2) 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 Vo(2) increase. We suggest that in unsteady states, lung Vo(2) is dissociated from muscle O(2) consumption. The two components of Q and QaO(2) kinetics may reflect vagal withdrawal and sympathetic activation
Correction of cardiac output obtained by Modelflow from finger pulse pressure profiles with a respiratory method in humans
Get PDFThe beat-by-beat non-invasive assessment of cardiac output (Q’, litre·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 · min-1 with an S.D. (precision) of 4.11 litre · min-1, and 95 % limits of agreement were relatively large, i.e. from - 6.23 to + 9.89 litre · 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 (Q’ corrected)values. Q’ corrected valueswerecomparedwiththecorresponding Q’ C2H2values, 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 · min-1 and 3.48 litre · min-1 respectively, and 95 % limits of agreement ranged from - 6.58 to + 7.05 litre · 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
Factors determining the time course of V'O2 max decay during bedrest: implications for V'O2 max limitation.
No full textThe aim of this study was to characterizethe time course of maximal oxygen consumption (V'O2 max) changes during bedrests longer than 30 days,on the hypothesis that the decrease in V'O2 max tends toasymptote. On a total of 26 subjects who participatedin one of three bedrest campaigns without countermeasures,lasting 14, 42 and 90 days, respectively,_VO2 max maximal cardiac output (Qmax) and maximalsystemic O2 delivery (QaO2max) were measured. Afte rall periods of HDT, V'O2 max; Q'max and Q'aO2max weresignificantly lower than before. The 'V O2 max decreasedless than 'Qmax after the two shortest bedrests, but itsper cent decay was about 10% larger than that of _Qmaxafter 90-day bedrest. The 'V O2 max decrease after90-day bedrest was larger than after 42- and 14-daybedrests, where it was similar. The 'Qmax and 'QaO2maxdeclines after 90-day bedrest was equal to those after14- and 42-day bedrest. The average daily rates of the_VO2 max; Q'max and Q'aO2max decay during bedrest wereless if the bedrest duration were longer, with theexception of that of V'O2 max in the longest bedrest. Theasymptotic V'O2 max decay demonstrates the possibilitythat humans could keep working effectively even afteran extremely long time in microgravity. Two componentsin the 'VO2 max decrease were identified, which wepostulate were related to cardiovascular deconditioningand to impairment of peripheral gas exchanges dueto a possible muscle function deterioration
Prolonged head down bed rest-induced inactivity impairs tonic autonomic regulation while sparing oscillatory cardiovascular rhythms in healthy humans.
No full textBackground.
Physical inactivity represents a major risk for cardiovascular disorders, such as hypertension, myocardial infarction or sudden death; however, underlying mechanisms are not clearly elucidated. Clinical and epidemiological investigations suggest, beyond molecular changes, the possibility of an induced impairment in autonomic cardiovascular regulation. However, this
hypothesis has not been tested directly.
Methods.
Accordingly, we planned a study with noninvasive, minimally intrusive, techniques on healthy volunteers. Participants were maintained for 90 days strictly in bed, 24 h a day, in head-down (S6-) position (HDBR). Physical activity was thus virtually abolished for the entire period of HDBR. We examined efferent muscle sympathetic nerve activity, as a measure of vascular sympathetic control, baroreceptor reflex sensitivity, heart rate variability (assessing cardiovagal regulation), RR and systolic arterial pressure and low-frequency and high-frequency normalized components (as a window on central oscillatory regulation).
Measures.
were obtained at rest and during simple maneuvers (moderate handgrip, lower body negative pressure and active standing) to assess potential changes in autonomic cardiovascular responsiveness to standard stimuli and the related oscillatory profiles. Results HDBR transiently reduced muscle sympathetic
nerve activity,RR,heart ratevariabilityandbaroreceptor reflex
sensitivity late during HDBR or early during the recovery phase. Conversely, oscillatory profiles of RR and systolic arterial pressure variability were maintained throughout. Responsiveness to test stimuli was also largely maintained
Factors determining the time course of VO2 max decay during badrest: implications for VO2 max limitation.
No full text[no abstract available
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