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

2006 ◽  
Vol 290 (4) ◽  
pp. R1071-R1079 ◽  
Author(s):  
Frédéric Lador ◽  
Marcel Azabji Kenfack ◽  
Christian Moia ◽  
Michela Cautero ◽  
Denis R. Morel ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Phase I ◽  
Time Course ◽  
Hemoglobin Concentration ◽  
Two Phase ◽  
Rapid Phase ◽  
Steady State Method ◽  
Exercise Onset ◽  
Kinetics Of

We tested whether the kinetics of systemic O2 delivery (Q̇aO2) at exercise start was faster than that of lung O2 uptake (V̇o2), being dictated by that of cardiac output (Q̇), and whether changes in Q̇ would explain the postulated rapid phase of the V̇o2 increase. Simultaneous determinations of beat-by-beat (BBB) Q̇ and Q̇aO2, and breath-by-breath V̇o2 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). V̇o2 was determined using Grønlund's algorithm. Q̇ was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate ( fh, electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB Q̇aO2. The Q̇, Q̇aO2 and V̇o2 kinetics were analyzed with single and double exponential models. fh, Qst, Q̇, and V̇o2 increased upon exercise onset to reach a new steady state. The kinetics of Q̇aO2 had the same time constants as that of Q̇. The latter was twofold faster than that of V̇o2. The V̇o2 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 Q̇ changes fully explained the phase I of V̇o2 increase. We suggest that in unsteady states, lung V̇o2 is dissociated from muscle O2 consumption. The two components of Q̇ and Q̇aO2 kinetics may reflect vagal withdrawal and sympathetic activation.

scholarly journals Kinetics of Cardiac Output at the Onset of Exercise in Precapillary Pulmonary Hypertension

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Frédéric Lador ◽  
Aurélien Bringard ◽  
Samir Bengueddache ◽  
Guido Ferretti ◽  
Karim Bendjelid ◽  
...  
Keyword(s):  
Heart Rate ◽  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Steady State ◽  
Cycle Ergometer ◽  
Healthy Controls ◽  
Sudden Drop ◽  
Exercise Onset ◽  
Kinetics Of

Purpose.Cardiac output (CO) is a cornerstone parameter in precapillary pulmonary hypertension (PH). The Modelflow (MF) method offers a reliable noninvasive determination of its beat-by-beat changes. So MF allows exploration of CO adjustment with the best temporal resolution.Methods.Fifteen subjects (5 PH patients, 10 healthy controls) performed a submaximal supine exercise on a cycle ergometer after 5 min of rest. CO was continuously determined by MF (COMF). Kinetics of heart rate (HR), stroke volume (SV), and CO were determined with 3 monoexponential models.Results.In PH patients, we observed a sudden and transitory drop of SV upon exercise onset. This implied a transitory drop of CO whose adjustment to a new steady state depended on HR increase. The kinetics of HR and CO for PH patients was slower than that of controls for all models and for SV in model 1. SV kinetics was faster for PH patients in models 2 and 3.Conclusion.This is the first description of beat-by-beat cardiovascular adjustments upon exercise onset in PH. The kinetics of HR and CO appeared slower than those of healthy controls and there was a transitory drop of CO upon exercise onset in PH due to a sudden drop of SV.

The steady-State corrosion kinetics of two-phase binary alloys forming the most-stable oxide

1996 ◽  
Vol 46 (5-6) ◽  
pp. 383-398 ◽  
Author(s):  
F. Gesmundo ◽  
P. Castello ◽  
F. Viani
Keyword(s):  
Steady State ◽  
Binary Alloys ◽  
Two Phase ◽  
Stable Oxide ◽  
Corrosion Kinetics ◽  
Kinetics Of

scholarly journals Phase I dynamics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men in acute normobaric hypoxia

2008 ◽  
Vol 295 (2) ◽  
pp. R624-R632 ◽  
Author(s):  
Frédéric Lador ◽  
Enrico Tam ◽  
Marcel Azabji Kenfack ◽  
Michela Cautero ◽  
Christian Moia ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Phase I ◽  
Acute Hypoxia ◽  
Vagal Activity ◽  
Rapid Phase ◽  
Lower Phase ◽  
Model Flow ◽  
O2 Delivery ◽  
Dual Origin ◽  
Vagal Withdrawal

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 (Q̇), oxygen delivery (Q̇aO2), and breath-by-breath lung oxygen uptake (V̇o2) 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 Q̇ from stroke volume (Qst, by model flow) and heart rate ( fH, electrocardiography), and Q̇aO2 from Q̇ and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q̇ were higher, and Qst and V̇o2 were unchanged. Q̇aO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for V̇o2 was unchanged. For fH, Q̇ and Q̇aO2, A1 was lower. Phase I time constant (τ1) for Q̇aO2 and V̇o2 was unchanged. The same was the case for Q̇ 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 Q̇ and Q̇aO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.

Anticonvulsants modify inactivation but not activation processes of sodium channels in Myxicola axons

1987 ◽  
Vol 65 (6) ◽  
pp. 1220-1225 ◽  
Author(s):  
C. L. Schauf
Keyword(s):  
Steady State ◽  
Time Course ◽  
Internal Surface ◽  
Slow Inactivation ◽  
Fast Inactivation ◽  
Inactivation Curve ◽  
Kinetics Of ◽  
Enzyme Application ◽  
Voltage Axis ◽  
Pronase Treatment

The effects of pronase and the anticonvulsant drugs diphenylhydantoin, bepridil, and sodium valproate on fast and slow Na+ inactivation were examined in cut-open Myxicola giant axons with loose patch-clamp electrodes applied to the internal surface. Pronase completely eliminated fast Na+ inactivation without affecting the kinetics of Na+ activation or the maximum Na+ conductance. The time and voltage dependences of slow inactivation following pronase treatment were identical to those measured before enzyme application in the same axons. All three anticonvulsants slowed the time course of recovery from fast Na+ inactivation in untreated axons, and shifted the steady-state fast inactivation curve in the hyperpolarizing direction along the voltage axis. Anticonvulsants enhanced steady-state slow inactivation and retarded recovery from slow inactivation in both untreated and pronase-treated axons. Although some quantitative differences were seen, the order of potency of the anticonvulsants on slow Na+ inactivation was the same as that for recovery from fast inactivation.

Time course and kinetics of proximal tubular processing of insulin

1992 ◽  
Vol 262 (5) ◽  
pp. F813-F822 ◽  
Author(s):  
S. Nielsen
Keyword(s):  
Steady State ◽  
Time Course ◽  
Accumulation Rate ◽  
Compartmental Analysis ◽  
Proximal Tubules ◽  
Hydrolysis Rate ◽  
Time Courses ◽  
High Concentrations ◽  
Kinetics Of

The present study was undertaken to determine the time courses and kinetics of the subcellular processing of 125I-insulin in isolated and in vitro perfused proximal tubules. Morphometric analysis demonstrated well-preserved ultrastructure after 90 min of perfusion. After luminal perfusion for 90 min the absorption was constant with time and reached steady state within 5 min (177 +/- 7 fg.min-1.mm-1). Also the hydrolysis rate and tubular accumulation rate were constant and averaged 84 +/- 8 and 93 +/- 10 fg.min-1.mm-1, respectively. Free 125I appeared already within 5 min of perfusion and reached steady state within 10 min. From proximal tubules perfused with 125I-insulin for 30 min and chased for 60 min, a compartmental analysis revealed two compartments; half time (t1/2) for delivery of insulin to the lysosomes was determined to be 8.5 min, and t1/2 for lysosomal degradation was 72 min. The results demonstrated that internalization by endocytic invaginations, incorporation in endocytic vacuoles, fusion with lysosomes, and hydrolysis were rapid processes and reached maximum rates within few minutes. A significant transtubular transport of insulin to the peritubular compartment was determined to be a constant rate of 11.2 +/- 0.7 fg.min-1.mm-1. Perfusion of tubules with insulin at high concentrations in the perfusate revealed that the transport was dependent on the absorbed amount and not on the perfused load, compatible with transport through the cells and not via a paracellular mechanism. The intactness of the tight junctions was supported by the following: 1) [14C]inulin leak did not increase with time and 2) enzyme-free intercellular spaces were evident after perfusion for only 5 min with microperoxidase (mol wt of 1,700). The transported 125I-insulin was trichloroacetic acid precipitable and immunoprecipitable.

β-Blockade and oxygen delivery to muscle during exercise

1991 ◽  
Vol 69 (2) ◽  
pp. 285-289 ◽  
Author(s):  
Richard L. Hughson ◽  
John M. Kowalchuk
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Muscle Mass ◽  
Time Course ◽  
The Body ◽  
Peripheral Blood Flow ◽  
Cycle Exercise ◽  
Kinetics Of ◽  
Oral Propranolol ◽  
Total Muscle

The most commonly observed effect of β-blockade on cardiovascular function has been a reduction in heart rate both at rest and during exercise. The body attempts to compensate by increasing stroke volume and (or) increasing the extraction of O2 from the blood to maintain O2 delivery to the muscle. This paper examines the roles of muscle mass involved in the exercise as well as the time course of change in cardiac output and peripheral blood flow in an attempt to understand whether O2 supply is limited by β-blockade. Experiments are reported in which the kinetics of cardiac output response at the onset of submaximal cycle exercise were slowed in subjects taking oral propranolol. Taken in consideration with other data from our laboratory and with data in the literature, it was concluded that β-blockade does impair O2 transport. The degree of impairment is dependent on the total muscle mass involved and the metabolic demand.Key words: blood flow, cardiac output, fatigue, propranolol, oxygen uptake.

V˙o 2 kinetics of mild exercise are altered by RER

1999 ◽  
Vol 87 (6) ◽  
pp. 2097-2106 ◽  
Author(s):  
Paul A. Molé ◽  
James J. Hoffmann
Keyword(s):  
Steady State ◽  
Time Course ◽  
Respiratory Exchange Ratio ◽  
Short Term ◽  
Men And Women ◽  
Adult Men ◽  
Wide Range ◽  
Leg Cycling ◽  
Biexponential Model ◽  
Kinetics Of

We propose that variations in fat and carbohydrate (CHO) oxidation by working muscle alter O2 uptake (V˙o 2) kinetics. This hypothesis provides two predictions: 1) the kinetics should comprise two exponential components, one fast and the other slow, and 2) their contribution should change with variations in fat and CHO oxidation, as predicted by steady-state respiratory exchange ratio (RER). The purpose of this study was to test these predictions by evaluating theV˙o 2 kinetic model:V˙o 2( t) = αR + αF{1 − exp[( t − TD)/−τF]} + αC{1 − exp[( t − TD)/−τC]} for short-term, mild leg cycling in 38 women and 44 men, whereV˙o 2( t) describes the time course, αR is resting V˙o 2, t is time after onset of exercise, TD is time delay, αF and τF are asymptote and time constant, respectively, for the fast (fat) oxidative term, and αC and τC are the corresponding parameters for the slow (CHO) oxidative term. We found that 1) this biexponential model accurately described the V˙o 2kinetics over a wide range of RERs, 2) the contribution of the fast (αF, fat) component was inversely related to RER, whereas the slow (αC, CHO) component was positively related to RER, and 3) this assignment of the fast and slow terms accurately predicted steady-state respiratory quotient and CO2 output. Therefore, the kinetic model can quantify the dynamics of fat and CHO oxidation over the first 5–10 min of mild exercise in young adult men and women.

scholarly journals A steady-state mechanism can account for the properties of inositol 2,4,5-trisphosphate-stimulated Ca2+ release from permeabilized L1210 cells

1993 ◽  
Vol 289 (3) ◽  
pp. 861-866 ◽  
Author(s):  
J W Loomis-Husselbee ◽  
A P Dawson
Keyword(s):  
Steady State ◽  
Small Proportion ◽  
Time Course ◽  
Initial Rate ◽  
Atpase Inhibitor ◽  
Efflux Rate ◽  
Rapid Phase ◽  
L1210 Cells ◽  
Low Concentrations ◽  
Stimulation Of

We have investigated the effects of sub-maximal Ins(2,4,5)P3 concentrations on the Ca2+ permeability of the residual undischarged Ca2+ stores in electroporated or digitonin-permeabilized L1210 cells by measuring Ca(2+)-efflux rate after addition of the ATPase inhibitor thapsigargin. Low concentrations of Ins(2,4,5)P3, causing rapid discharge of a small proportion of the releasable Ca2+, result in a substantial stimulation of Ca2+ efflux after thapsigargin addition. This indicates firstly that in the absence of thapsigargin there must have been a substantial, counterbalancing, increase in rate of Ca2+ pumping, and secondly that the increased Ca2+ permeability is more consistent with a steady state than with a quantal model of Ca2+ release. Similar increases in passive Ca2+ permeability are produced by addition of concentrations of ionomycin which produce equivalent changes in Ca2+ loading to those produced by Ins(2,4,5)P3, although the time course and initial rate of Ca2+ release are very much slower. In the presence of a Ca(2+)-buffering system, the time course of Ca2+ release by Ins(2,4,5)P3 becomes superimposable on that of ionomycin, indicating that the initial rapid phase of Ins(2,4,5)P3-stimulated Ca2+ is at least partially due to positive feedback from extravesicular Ca2+.

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