Dynamic asymmetries of cardiac output transients in response to muscular exercise in man.

Yoshida, Takayoshi; Whipp, Brian J.

doi:10.1113/jphysiol.1994.sp020365

Cited by 66 publications

(79 citation statements)

References 27 publications

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“…Some authors, however, soon identified two components of the V O 2 kinetics: 1) a rapid, almost immediate phase (phase I) (5,54,55), which they attributed to an immediate increase in cardiac output (Q ) at exercise start; and 2) a subsequent slower phase (phase II), to which they restricted the influence of muscle metabolic adjustments. The strongest support to this view came from the demonstration that the kinetics of Q (12,13,16,60) and arterial O 2 flow (Q a O 2 ) (27) are very rapid.…”

mentioning

confidence: 85%

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

Lador¹,

Tam²,

Kenfack³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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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 Ϯ 3.4 yr, 82.1 Ϯ 13.7 kg, maximal aerobic power 330 Ϯ 67 W), we determined beat-by-beat cardiac output (Q ), oxygen delivery (Q a O 2 ), and breathby-breath lung oxygen uptake (V O2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O 2 ϭ 0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Q st, by model flow) and heart rate (fH, electrocardiography), and Q a O 2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state f H and Q were higher, and Qst and V O2 were unchanged. Q a O 2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A 1) for V O2 was unchanged. For fH, Q and Q a O 2 , A1 was lower. Phase I time constant (1) for Q a O 2 and V O2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Q st 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 A 1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Q st. Thus the dual origin of the phase I of Q and Q a O 2 , neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed. cardiovascular response ALTHOUGH OUR KNOWLEDGE of the central (neural) control of the cardiovascular system at the exercise steady state is quite well established (19,42,57), how the circulatory readjustments upon exercise onset occur and match the increase in pulmonary oxygen uptake (V O 2 ) is less understood, as are the mechanisms underlying this matching. The kinetics of V O 2 at exercise onset were seen for a long time as reflecting essentially the metabolic adaptations in the working muscles (15,31,33). Some authors, however, soon identified two components of the V O 2 kinetics: 1) a rapid, almost immediate phase (phase I) (5, 54, 55), which they attributed to an immediate increase in cardiac output (Q ) at exercise start; and 2) a subsequent slower phase (phase II), to which they restricted the influence of muscle metabolic adjustments. The strongest support to this view came from the demonstration that the kinetics of Q (12, 13, 16, 60) and arterial O 2 flow (Q a O 2 ) (27) are very rapid.The concept of a close correspondence between V O 2 and muscle O 2 consumption was further undermined by the recent demonstration that, upon the onset of light exercise, the V O 2 kinetics are faster than the kinetics of muscle O 2 consumption estimated from the monoexponential decrease in phosphocreatine concentration (7,14,43). This would imply dissociation of the kinetics of V O 2 and muscle O 2 consumption, which should respond to different control mechanisms.Our postulate is that the V O 2 kinetics are dictated by ...

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confidence: 85%

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

Lador¹,

Tam²,

Kenfack³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This view restricts the correspondence between lung O 2 uptake and muscle O 2 consumption to the monoexponential phase II. Perhaps the strongest piece of evidence in support of the phase I concept is the finding that the kinetics of cardiac output (Q ) upon light exercise onset is much faster than that of V O 2 (12,14,21,34,38,59,60). In fact, assuming invariant O 2 concentration in mixed venous blood in the first seconds of exercise, this finding would imply, according to the Fick principle, a corresponding rapid increase in V O 2 .…”

mentioning

confidence: 94%

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

Lador¹,

Kenfack²,

Moia³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Simultaneous determination of the kinetics of cardiac output, systemic O 2 delivery, and lung O2 uptake at exercise onset in men. Am J Physiol Regul Integr Comp Physiol 290: R1071-R1079, 2006. First published October 20, 2005 doi:10.1152/ajpregu.00366.2005.-We tested whether the kinetics of systemic O 2 delivery (Q aO2) at exercise start was faster than that of lung O 2 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 aO 2, 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 Ϯ 3.2 years, maximal aerobic power 333 Ϯ 61 W). V O2 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 steadystate method. This, along with the time course of hemoglobin concentration and arterial O 2 saturation (infrared oximetry) allowed computation of BBB Q aO 2. The Q , Q aO2 and V O2 kinetics were analyzed with single and double exponential models. f H, Qst, Q , and V O2 increased upon exercise onset to reach a new steady state. The kinetics of Q aO 2 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 O 2 consumption. The two components of Q and Q aO2 kinetics may reflect vagal withdrawal and sympathetic activation. cardiovascular response AT THE ONSET OF SQUARE-WAVE light aerobic exercise, O 2 consumption increases to attain a steady level, proportional to the exerted mechanical power. Its increase rises at a finite rate in response to the step increase in power, so that an O 2 deficit is incurred in the first minutes of exercise. The O 2 deficit reflects the decrease in high-energy phosphate concentration that is necessary to accelerate aerobic metabolic pathways (5,19,35,37). Analogous to the charge of a single capacitance, the increase in O 2 consumption was described by monoexponential equations (5,15,19). The monoexponential decrease in phosphocreatine concentration upon square-wave exercise onset (6, 46) is perhaps the strongest evidence provided so far in favor of this single capacitance model for O 2 consumption. Assuming close correspondence between O 2 consumption by the working muscles and O 2 uptake at the lungs (V O 2 ), the V O 2 was investigated to gain information on O 2 consumption (15, 16).This correspondence, however, was questioned. In fact, the kinetics of O 2 consumption requires that it be sustained by adequate O 2 transfer from ambient air to mitochondria. Thus, concomitant with the increase in O 2 consumption, th...

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“…O 2 at the onset of exercise. [27,33,34] In addition, during the stimulation at 70% of V . O 2max the O 2 partial pressure (PaO 2 ) in isolated dog muscle is always above 2mm Hg, the critical level for maintaining aerobic ATP turnover.…”

Section: O 2 Utilisationmentioning

confidence: 99%

Oxygen Uptake Kinetics During Exercise

1999

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Dynamic asymmetries of cardiac output transients in response to muscular exercise in man.

Cited by 66 publications

References 27 publications

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

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

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

Oxygen Uptake Kinetics During Exercise

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Dynamic asymmetries of cardiac output transients in response to muscular exercise in man.

Cited by 66 publications

References 27 publications

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

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

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

Oxygen Uptake Kinetics During Exercise

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

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

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