Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans

1997 ◽  
Vol 83 (3) ◽  
pp. 712-717 ◽  
Author(s):  
Antonio C. L. Nóbrega ◽  
Jon W. Williamson ◽  
Jorge A. Garcia ◽  
Jere H. Mitchell

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712–717, 1997.—Ten patients with preserved inotropic function having a dual-chamber (right atrium and right ventricle) pacemaker placed for complete heart block were studied. They performed static one-legged knee extension at 20% of their maximal voluntary contraction for 5 min during three conditions: 1) atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HR fixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and 3) HR fixed at peak exercise rate (DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode), mean arterial pressure (MAP) increased by 25 mmHg with no change in stroke volume (SV) or systemic vascular resistance. During DOO-Rest and DOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of a SV-dependent increase in cardiac output (+1.3 and +1.8 l/min, respectively). The increase in SV during DOO-Rest utilized a combination of increased contractility and the Frank-Starling mechanism (end-diastolic volume 118–136 ml). However, during DOO-Ex, a greater left ventricular contractility (end-systolic volume 55–38 ml) mediated the increase in SV.

1986 ◽  
Vol 251 (6) ◽  
pp. H1101-H1105 ◽  
Author(s):  
G. D. Plotnick ◽  
L. C. Becker ◽  
M. L. Fisher ◽  
G. Gerstenblith ◽  
D. G. Renlund ◽  
...  

To evaluate the extent to which the Frank-Starling mechanism is utilized during successive stages of vigorous upright exercise, absolute left ventricular end-diastolic volume and ejection fraction were determined by gated blood pool scintigraphy at rest and during multilevel maximal upright bicycle exercise in 30 normal males aged 26-50 yr, who were able to exercise to 125 W or greater. Left ventricular end-systolic volume, stroke volume, and cardiac output were calculated at rest and during each successive 3-min stage of exercise [25, 50, 75, 100, and 125–225 W (peak)]. During early exercise (25 W), end-diastolic and stroke volumes increased (+17 +/- 1 and +31 +/- 4%, respectively), with no change in end-systolic volume. With further exercise (50–75 W) end-diastolic volume remained unchanged as end-systolic volume decreased (-12 +/- 4 and -24 + 5%, respectively). At peak exercise end-diastolic volume decreased to resting level, stroke volume remained at a plateau, and end-systolic volume further decreased (-48 +/- 7%). Thus the Frank-Starling mechanism is used early in exercise, perhaps because of a delay in sympathetic mobilization, and does not appear to play a role in the later stages of vigorous exercise.


1978 ◽  
Vol 234 (5) ◽  
pp. H525-H532
Author(s):  
A. Ilebekk ◽  
J. Lekven ◽  
F. Kiil

During right atrial pacing in open-chest anesthetized dogs, the relationships between reduction in stroke volume and rise in heart rate were identical in control experiments, during intravenous infusion of isoproterenol, and after blockade of adrenergic beta-receptors by propranolol. To examine the mechanism of this constant relationship, left ventricular volume was estimated by continuous recordings of myocardial chord length (MCL) between ultrasonic elements inserted into the anterior ventricular wall. Diastolic filling curves were curtailed by raising heart rate and end-diastolic MCL was reduced. At constant heart rate, end-diastolic MCL was not altered by isoproterenol infusion, except for a slight rise at heart rates exceeding 220 beats/min. End-systolic MCL, however, was reduced, accounting for larger stroke volume during isoproterenol than during propranolol infusion. The reduction in end-systolic MCL was constant at all heart rates examined. Hence, chronotropic changes influence end-diastolic volume and inotropic changes influence end-systolic volume; their effects on stroke volume regulation are, therefore, virtually independent.


1993 ◽  
Vol 75 (6) ◽  
pp. 2703-2710 ◽  
Author(s):  
A. C. Lentini ◽  
R. S. McKelvie ◽  
N. McCartney ◽  
C. W. Tomlinson ◽  
J. D. MacDougall

We examined cardiac volumes (using echocardiography), intra-arterial blood pressure (BP), and intrathoracic pressure (ITP) in healthy males performing leg press exercise to failure at 95% of their maximum dynamic strength. Compared with preexercise, during the lifting phase of exercise, end-diastolic volume (EDV; 147 +/- 8 to 103 +/- 7 ml) and end-systolic volume (ESV; 54 +/- 5 to 27 +/- 4 ml) decreased (P < 0.05); heart rate (82 +/- 6 to 143 +/- 5 beats/min), systolic BP (160 +/- 6 to 270 +/- 21 Torr), diastolic BP (91 +/- 2 to 183 +/- 18 Torr), ITP (0.8 +/- 0.8 to 57.8 +/- 24 Torr), and peak systolic BP/ESV (SBP/ESV; 3.0 +/- 0.3 to 11.0 +/- 1.5 Torr/ml) increased (P < 0.05); and stroke volume decreased (94 +/- 3 to 77 +/- 4 ml; P > 0.05). Full knee extension was associated with most values returning to preexercise levels except for ESV (38 +/- 7 ml), heart rate (130 +/- 9 beats/min), and ITP (-12.5 +/- 2.1 Torr). During the lowering phase, significant decreases in EDV to 105 +/- 14 ml and ESV to 27 +/- 7 ml were observed with increases in systolic BP to 207 +/- 23 Torr, diastolic BP to 116 +/- 8 Torr, and SBP/ESV to 10.0 +/- 2.5 Torr/ml. Stroke volume decreased to 78 +/- 9 ml (P > 0.05). Thus rapid changes in cardiac volumes, contractility, and pressure occur during weight lifting that are related to different phases of the lift.


2011 ◽  
Vol 301 (2) ◽  
pp. H478-H487 ◽  
Author(s):  
Eric J. Stöhr ◽  
José González-Alonso ◽  
Rob Shave

During incremental exercise, stroke volume (SV) plateaus at 40–50% of maximal exercise capacity. In healthy individuals, left ventricular (LV) twist and untwisting (“LV twist mechanics”) contribute to the generation of SV at rest, but whether the plateau in SV during incremental exercise is related to a blunting in LV twist mechanics remains unknown. To test this hypothesis, nine healthy young males performed continuous and discontinuous incremental supine cycling exercise up to 90% peak power in a randomized order. During both exercise protocols, end-diastolic volume (EDV), end-systolic volume (ESV), and SV reached a plateau at submaximal exercise intensities while heart rate increased continuously. Similar to LV volumes, two-dimensional speckle tracking-derived LV twist and untwisting velocity increased gradually from rest (all P < 0.001) and then leveled off at submaximal intensities. During continuous exercise, LV twist mechanics were linearly related to ESV, SV, heart rate, and cardiac output (all P < 0.01) while the relationship with EDV was exponential. In diastole, the increase in apical untwisting was significantly larger than that of basal untwisting ( P < 0.01), emphasizing the importance of dynamic apical function. In conclusion, during incremental exercise, the plateau in LV twist mechanics and their close relationship with SV and cardiac output indicate a mechanical limitation in maximizing LV output during high exercise intensities. However, LV twist mechanics do not appear to be the sole factor limiting LV output, since EDV reaches its maximum before the plateau in LV twist mechanics, suggesting additional limitations in diastolic filling to the heart.


1999 ◽  
Vol 84 (7) ◽  
pp. 2308-2313 ◽  
Author(s):  
George J. Kahaly ◽  
Stephan Wagner ◽  
Jana Nieswandt ◽  
Susanne Mohr-Kahaly ◽  
Thomas J. Ryan

Exertion symptoms occur frequently in subjects with hyperthyroidism. Using stress echocardiography, exercise capacity and global left ventricular function can be assessed noninvasively. To evaluate stress-induced changes in cardiovascular function, 42 patients with untreated thyrotoxicosis were examined using exercise echocardiography. Studies were performed during hyperthyroidism, after treatment with propranolol, and after restoration of euthyroidism. Twenty- two healthy subjects served as controls. Ergometry was performed with patients in a semisupine position using a continuous ramp protocol starting at 20 watts/min. In contrast to control and euthyroidism, the change in end-systolic volume index from rest to maximal exercise was lower in hyperthyroidism. At rest, the stroke volume index, ejection fraction, and cardiac index were significantly increased in hyperthyroidism, but exhibited a blunted response to exercise, which normalized after restoration of euthyroidism. Propranolol treatment also led to a significant increase of delta (Δ) stroke volume index. Maximal work load and Δ heart rate were markedly lower in hyper- vs. euthyroidism. Compared to the control value, systemic vascular resistance was lowered by 36% in hyperthyroidism at rest, but no further decline was noted at maximal exercise. The Δ stroke volume index, Δ ejection fraction, Δ heart rate, and maximal work load were significantly reduced in severe hyperthyroidism. Negative correlations between free T3 and diastolic blood pressure, maximal work load, Δ heart rate, and Δ ejection fraction were noted. Thus, in hyperthyroidism, stress echocardiography revealed impaired chronotropic, contractile, and vasodilatatory cardiovascular reserves, which were reversible when euthyroidism was restored.


1963 ◽  
Vol 204 (3) ◽  
pp. 446-450 ◽  
Author(s):  
Franz J. Hallermann ◽  
G. C. Rastelli ◽  
H. J. C. Swan

In each of 12 mongrel dogs, data for end-diastolic volume, end-systolic volume, and stroke volume of the left ventricle were obtained by two independent methods: the indicator dilution method and a radiographic method. While the values for stroke volume showed good agreement between the two methods, a significant and directionally constant difference was found between values for end-diastolic volume and end-systolic volume calculated by the two different methods. This was observed in dogs with fast heart rates (exceeding 150 beats/min), as well as in dogs with heart rates of about 100 beats/min. The findings strongly suggest that a fundamental error is present in estimations of volume based on the washout of an indicator dye.


2018 ◽  
Vol 14 (1) ◽  
pp. 3-8
Author(s):  
Mohammad Ashraf Hossain ◽  
Khurshed Ahmed ◽  
Md Faisal Ibn Kabir ◽  
Md Fakhrul Islam Khaled ◽  
Rakibul H Rashed ◽  
...  

Background: Chronic heart failure (CHF) is the most common and prognostically unfavorable outcome of many diseases of the cardiovascular system. Recent data suggest that beta-blockers are beneficial in patients with CHF. Among β-blocker class of drugs, bisoprolol is a highly selective β1-adrenergic receptor blocker whereas Carvedilol is non-selective. Many large-scale trials have confirmed that both these β-blockers are superior to placebo and other β-blockers. This study was designed to compare the effects of carvedilol and bisoprolol in patients with chronic HF in a single center.Methods: It was a quasi experimental study. A total of 288 cases of heart failure were selected by purposive sampling, from January 2017 to June 2017. Each patient was allocated into either of the two groups, and was continued receiving treatment with either bisoprolol (Group-I) or carvedilol (Group-II). Each patient was evaluated clinically and echocardiographically at the beginning of treatment (baseline) and at the end of 3rd month. Echocardiography was performed to find out change in left ventricular systolic function.Result: After 3 months of treatment, ejection fraction was found higher in the bisoprolol group (42.6 ± 6.5 versus 38.3 ± 4.6%; P < 0.05). Ejection fraction (EF) changes were 8.4% in bisoprolol group and 4.1% in carvedilol group. A significant reduction in left ventricular end-systolic volume (21.9±2.5 in group I versus 14.9±5.7 in group II; P < 0.05) and left ventricular systolic diameter (3.2±0.1 in group I versus 2.3±0.5 in group II; P<0.05) occurred after 3 months of treatment. But no significant differences were observed in left ventricular end-diastolic volume (10.1±3.2 versus 6.1±6.4; P=0.101) and left ventricular diastolic diameter (1.7±0.8 versus 1.3±0.8; P=0.081) between groups. Three months after treatment, heart rate was reduced in the bisoprolol group from 87.7±9 to 74.5±8.1 and carvedilol group from 88.8±9.1 to 80.1±8.7. Differences in heart rate responses between 2 groups were not statistically significant (P=0.113). Assessment of blood pressure three months later of treatment shows, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were improved in both group but difference between two groups were statistically non significant (p>0.05).Conclusion: In this study, bisoprolol was superior to carvedilol in increasing left-ventricular ejection fraction, improving left ventricular end systolic volume and left ventricular end systolic diameter but no significant difference was observed in LV end diastolic volume, LV end diastolic diameter, heart rate and blood pressure.University Heart Journal Vol. 14, No. 1, Jan 2018; 3-8


1986 ◽  
Vol 250 (3) ◽  
pp. H464-H473
Author(s):  
J. D. Lee ◽  
T. Tajimi ◽  
J. Patritti ◽  
J. Ross

Preload reserve and mechanisms of afterload mismatch were examined in 10 normal conscious dogs. The left ventricular (LV) pressure, wall thickness, and external major and minor axis diameters (sonomicrometry) were measured during sinus rhythm, and beat-averaged pressure-volume loops were generated. With maximum angiotensin II infusion, LV end-diastolic volume (EDV) increased by 13 +/- 2% (SEM), LV peak pressure (LVSP) increased by 44 +/- 6%, and stroke volume decreased by 12 +/- 3% (P less than 0.01), demonstrating an apparent descending limb of LV performance. With volume load alone, EDV increased by 9 +/- 2% from control (P less than 0.01), and stroke volume increased by 13 +/- 2%; mean wall stress during ejection was not increased, and heart rate and end-systolic pressure-volume relations showed no changes. To test whether the descending limb of function was due to maximum use of preload reserve or to inadequate venous return, angiotensin infusion was repeated during volume load. The descending limb relating LVEDV to stroke volume was always shifted upward and to the right after volume load, and the stroke volume at a comparable wall stress was 12 +/- 3% higher than during control angiotensin infusion (P less than 0.01). During pressure loading plus volume loading, the maximum EDV increase was 16 +/- 2%, and assuming unchanged afterload and end-systolic volume, an average maximum stroke volume reserve of 31 +/- 4% is calculated. 1) We conclude that sizable preload and stroke volume reserves exist in the normal resting dog; and 2) we describe a mechanism for the descending limb of LV performance curves produced by pressure loading in the intact circulation, which is related to inadequate venous return.


2019 ◽  
Author(s):  
Emanuele F. Osimo ◽  
Stefan P. Brugger ◽  
Antonio de Marvao ◽  
Toby Pillinger ◽  
Thomas Whitehurst ◽  
...  

AbstractBackgroundHeart disease is the leading cause of death in schizophrenia.AimsWe investigated cardiac structure and function in patients with schizophrenia using cardiac magnetic resonance imaging (CMR) after excluding medical and metabolic comorbidity.Methods80 participants underwent CMR to determine biventricular volumes and function and measures of blood pressure, physical activity, and glycated haemoglobin levels. Patients and controls were matched for age, sex, ethnicity, and body surface area.ResultsPatients with schizophrenia had significantly smaller indexed left ventricular (LV) end-diastolic volume, end-systolic volume, stroke volume, right ventricular (RV) end-diastolic volume, end-systolic volume, and stroke volume but unaltered ejection fractions relative to controls. LV concentricity and septal thickness were significantly larger in schizophrenia. The findings were largely unchanged after adjusting for smoking or exercise levels and were independent of medication dose and duration.ConclusionsPatients with schizophrenia show evidence of prognostically-adverse cardiac remodelling compared to matched controls, independent of conventional risk factors.


1995 ◽  
Vol 268 (4) ◽  
pp. H1490-H1498 ◽  
Author(s):  
R. S. Szwarc ◽  
D. Laurent ◽  
P. R. Allegrini ◽  
H. A. Ball

The conductance catheter gain factor, alpha, is usually determined by an independent measure of stroke volume and, as such, is assumed to be constant. However, nonlinearity of the conductance-volume relation has been proposed on theoretical grounds. The present study was designed to establish the extent of nonlinearity, or variability of alpha, within the cardiac cycle using magnetic resonance imaging (MRI) as the reference method. Pentobarbital-anesthetized minipigs (n = 10, 10–13 kg) were instrumented with left ventricular (LV) conductance and Millar catheters. Conductance catheter signals were recorded, and volumes were corrected for parallel conductance using a saline-dilution technique. Animals were then placed in a 4.7-T magnet, and first time derivative of LV pressure-gated transverse MRI images (5-mm slices) acquired during isovolumic contraction (end diastole) and relaxation (end systole). LV cavity volumes were then determined using a third-order polynomial model. The gain alpha was computed three ways: by dividing conductance stroke volume by MRI stroke volume (alpha SV), by dividing conductance end-diastolic volume by MRI end-diastolic volume (alpha ED), and by dividing conductance end-systolic volume by MRI end-systolic volume (alpha ES). alpha SV was 0.62 +/- 0.15, with alpha ED (0.71 +/- 0.17) significantly lower than alpha ES (0.81 +/- 0.21; P < 0.001). Using alpha SV to adjust conductance gain (i.e., assuming constant gain) resulted in a significantly larger end-diastolic volume (25.8 +/- 4.6 ml) and smaller ejection fraction (46.8 +/- 7.2%) than those obtained with MRI (23.0 +/- 4.1 ml and 53.1 +/- 7.3%, respectively; P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)


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