Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery and lung O2 uptake at exercise onset in men.

We 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

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

Prolonged head down bed rest-induced inactivity impairs tonic autonomic regulation while sparing oscillatory cardiovascular rhythms in healthy humans.

Background. 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

Cardiac output by model flow method from intra-arterial and finger tip pulse pressure profiles

Modelflow®, when applied to non-invasive fingertip pulse pressure recordings, is a poor predictor of cardiac output (Q’ litre· min-1). The use of constants established from the aortic elastic characteristics, which differ from those of finger arteries, may introduce signal distortions, leading to errors in computing Q’. We therefore hypothesized that peripheral recording of pulse pressure profiles undermines the measurement of Q’ withModelflow®, so we compared Modelflow® beat-by-beat Q’ values obtained simultaneously non-invasively from the finger and invasively from the radial artery at rest and during exercise. Seven subjects (age, 24.0 + - 2.9 years; weight, 81.2 + - 12.6 kg) rested, then exercised at 50 and 100 W, carrying a catheter with a pressure head in the left radial artery and the photoplethysmographic cuff of a finger pressure device on the third and fourth fingers of the contralateral hand. Pulse pressure from both devices was recorded simultaneously and stored on a PC for subsequent Q’ computation. The mean values of systolic, diastolic and mean arterial pressure at rest and exercise steady state were significantly (P < 0.05) lower from the finger than the intra-arterial catheter. The corresponding mean steady-state Q’ obtained from the finger (Q’porta) was significantly (P < 0.05) higher than that computed from the intra-arterial recordings (Q’pia). The line relating beat-by-beat Q’porta and Q’pia was y = 1.55x - 3.02 (r2 = 0.640). The bias was 1.44 litre · min-1 and the precision was 2.84 litre · min-1.The slope of this line was significantly higher than 1, implying a systematic overestimate of Q’ by Q’porta with respect to Q’pia. Consistent with the tested hypothesis, these results demonstrate that pulse pressure profiles from the finger provide inaccurate absolute Q’ values with respect to the radial artery, and therefore cannot be used without correction with a calibration factor calculated previously by measuring Q’ with an independent method

Factors determining the time course of V'O2 max decay during bedrest: implications for V'O2 max limitation.

The 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

Simultaneous determination of kinetics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men.

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 +/- 3.2 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

Effects of prolonged bed rest on the cardiopulmonary response to postural changes in humans

none8In order to gain a better understanding of the cardio-pulmonary impairment induced by prolonged bed rest, we measured steady-state oxygen uptake (V’O2) and carbon dioxide output (V’CO2), by Grønlund’s algorithm on a breath-by-breath basis, cardiac output (Q’), by open circuit acetylene washout, heart rate (HR), by electrocardiography, and mean arterial pressure (MAP), by fingertip plethysmography, on 18 male subjects (33.1 years ± 0.9; 71.1 kg ± 1.1; 1.75 m ± 0.01) before (BB) and after (AB) 90 days of head down tilt bed rest, in the following conditions : upright and supine posture, both at rest and at the 50 W exercise. The stroke volume (SV) was calculated as the ratio of Q’ to HR. The total peripheral resistance (TPR) was calculated as the ratio of MAP to Q’. V’O2 was lower (p&lt;0.01) supine than upright (0.43 l/min vs 0.52 l/min at rest; 1.06 l/min vs 1.27 l/min at 50W) in BB. In AB, V’O2 was 0.81 l/min at rest and 1.61 l/min at 50W upright, whereas supine it was 0.74 l/min at rest and 1.54 l/min at 50W. All the values in AB were significantly higher than the corresponding values in BB. V’CO2 followed the same patterns as V’O2, so that the gas exchange ratio was the same in all conditions. In BB, Q’ was the same supine and upright. In AB, Q’ was significantly higher supine than upright at rest (6.11 l/min vs 5.40 l/min). All Q’ values observed in AB were significantly higher than the corresponding values in BB (rest: 5.40 vs 4.50 upright; 6.11 vs 5.05 supine. 50 W exercise 8.26 vs 6.99 upright and 9.18 vs 7.38 supine). SV was higher supine than upright (71.2 ml vs 51.2 ml BB, 78.6 vs 55.4 ml AB at rest; 76.9 ml vs 67.2 ml BB, 87.5 ml 70.8 ml AB at 50W). HR was lower supine (70.3 bpm at rest, 95.2 at 50W) than upright (87.8 bpm at rest, 104.7 at 50 W) in BB, and was (77.3 bpm at rest, 103.9 at 50W) and (97.7 bpm at rest, 116.8 at 50 W) in AB. SV was the same in AB as in BB, whereas HR was higher in AB than in BB. MAP was lower supine than upright in AB (94.3 mmHg vs 105.4 mmHg at rest; 101.6 mmHg vs 115.4 mmHg at 50W). In supine posture, MAP was lower in AB than in BB, both at rest and at exercise. TPR was lower supine than upright in AB (17.8 mmHg*min/l vs 21.6 mmHg*min/l at rest; 12.8 mmHg*min/l vs 16 mmHg*min/l at 50W). In supine posture, TPR was lower in AB than in BB, both at rest and at exercise. These results suggest that the cardio-pulmonary system adjusts to reduced blood volume and increased venous compliance essentially by increasing HR, perhaps modulated by increase in sympathetic output tone. The HR increase is larger than the drop in SV, so that Q' is increased in AB. This is coherent with the higher V’O2 levels in AB than in BB at the same power. The V’O2 increase could be mainly due to an impairment of the motor control system after 90 days of bed rest.Autore/i del volume: HOPPELER H., REALLY T., TSOLAKIDIS E., GFELLER L., KLOSSNER S.mixedE. Tam; N. Fagoni; M. A. Kenfack; M. Cautero; F. Lador ; C. Moia; C. Capelli; G. FerrettiE. Tam; N. Fagoni; M. A. Kenfack; M. Cautero; F. Lador ; C. Moia; C. Capelli; G. Ferrett