Dynamics and dimensions of cardiac output changes in humans at the onset and at the end of moderate rhythmic exercise.

Eriksen, Morten; Waaler, B. A.; Walløe, Lars; Wesche, Jarlis

doi:10.1113/jphysiol.1990.sp018147

Cited by 80 publications

(56 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The large increase in SV during squat would suggest that central blood volume translocation was already manifest during squatting. Others have demonstrated that SV is actually also maximized in the supine position due to central blood volume translocation, as evidenced by virtually no increase in SV with the onset of supine exercise (15). Despite this evidence, we cannot conclusively exclude the possibility that there could be some elevation in SV when standing up from supine, which might make the central hemodynamic environment evoked by rising from supine slightly different than rising from squat.…”

Section: Cardiopulmonary Baroreflex Does Not Explain Ioh On Rising Frmentioning

confidence: 52%

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

Tschakovsky

Matusiak

Vipond

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Tschakovsky ME, Matusiak K, Vipond C, McVicar L. Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat. Am J Physiol Heart Circ Physiol 301: H2102-H2112, 2011. First published August 19, 2011 doi:10.1152/ajpheart.00571.2011.-The cause(s) of initial orthostatic hypotension (transient fall in blood pressure within 15 s upon active rising) have not been established. We tested the hypothesis that this hypotension is due to local vascular phenomena in contracting leg muscles from the brief effort of standing up. Seventeen young healthy subjects (2 male and 15 female, 22.5 Ϯ 1.0 years) performed an active rise from resting squat after a 10-s squat, a 1-min squat, or a 5-min squat. Beat-by-beat arterial blood pressure, cardiac output, heart rate, and stroke volume (Finometer finger photoplethysmography) and right common femoral artery blood flow (Doppler and Echo ultrasound) were recorded. Data are means Ϯ SE. Quiet standing before squat represented baseline. Peak increases in lower limb and total vascular conductance (ml·min Ϫ1 ·mmHg Ϫ1 ) upon standing were not different within squat conditions (10-s squat, 50.0 Ϯ 12.4 vs. 44.3 Ϯ 5.0; 1-min squat, 54.7 Ϯ 9.2 vs. 50.5 Ϯ 4.5; 5-min squat, 67.4 Ϯ 13.7 vs. 58.8 Ϯ 3.9; all P Ͼ 0.574). Mean arterial blood pressure (in mmHg) fell to a nadir well below standing baseline in all conditions despite increases in cardiac output. The hypotension predicted by the increase in leg vascular conductance accounted for this hypotension [observed vs. predicted (in mmHg): 10-s squat, Ϫ17.1 Ϯ 2.1 vs. Ϫ18.3 Ϯ 5.5; 1-min squat, Ϫ22.0 Ϯ 3.8 vs. Ϫ25.3 Ϯ 4.9; 5-min squat, Ϫ28.3 Ϯ 4.0 vs. Ϫ29.2 Ϯ 6.7]. We conclude that rapid contraction induced dilation in leg muscles with the effort of standing, along with a minor potential contribution of elevated lower limb arterio-venous pressure gradient, outstrips compensatory cardiac output responses and is the cause of initial orthostatic hypotension upon standing from squat. blood pressure; syncope; muscle blood flow; muscle contraction; sympathetic withdrawal; cardiopulmonary baroreflex

show abstract

Section: Cardiopulmonary Baroreflex Does Not Explain Ioh On Rising Frmentioning

confidence: 52%

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

Tschakovsky

Matusiak

Vipond

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…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

View full text Add to dashboard Cite

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 ...

show abstract

“…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

View full text Add to dashboard Cite

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...

show abstract

Dynamics and dimensions of cardiac output changes in humans at the onset and at the end of moderate rhythmic exercise.

Cited by 80 publications

References 26 publications

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

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

Contact Info

Product

Resources

About

Dynamics and dimensions of cardiac output changes in humans at the onset and at the end of moderate rhythmic exercise.

Cited by 80 publications

References 26 publications

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

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

Contact Info

Product

Resources

About

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