Left ventricular response in healthy young men during heavy-intensity weight-lifting exercise

1993 ◽  
Vol 75 (6) ◽  
pp. 2703-2710 ◽  
Author(s):  
A. C. Lentini ◽  
R. S. McKelvie ◽  
N. McCartney ◽  
C. W. Tomlinson ◽  
J. D. MacDougall
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Dynamic Strength ◽  
Intrathoracic Pressure ◽  
Knee Extension ◽  
Left Ventricular ◽  
Weight Lifting ◽  
Systolic Volume ◽  
Arterial Blood ◽  
Cardiac Volumes

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.

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
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Knee Extension ◽  
Left Ventricular ◽  
Voluntary Contraction ◽  
Peak Exercise ◽  
Ventricular Contractility ◽  
Static Exercise ◽  
Systolic Volume ◽  
End Diastolic Volume

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.

scholarly journals Stress Echocardiography in Hyperthyroidism

1999 ◽  
Vol 84 (7) ◽  
pp. 2308-2313 ◽  
Author(s):  
George J. Kahaly ◽  
Stephan Wagner ◽  
Jana Nieswandt ◽  
Susanne Mohr-Kahaly ◽  
Thomas J. Ryan
Keyword(s):  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Stress Echocardiography ◽  
Maximal Exercise ◽  
Stroke Volume Index ◽  
Work Load ◽  
Left Ventricular ◽  
Volume Index ◽  
Systolic Volume

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.

Cardiac performance: independence of adrenergic inotropic and chronotropic effects

1978 ◽  
Vol 234 (5) ◽  
pp. H525-H532
Author(s):  
A. Ilebekk ◽  
J. Lekven ◽  
F. Kiil
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Right Atrial ◽  
Diastolic Filling ◽  
Atrial Pacing ◽  
Heart Rates ◽  
Systolic Volume ◽  
End Diastolic Volume

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.

scholarly journals 2363

2017 ◽  
Vol 1 (S1) ◽  
pp. 36-36
Author(s):  
Leo Buckley ◽  
Justin Canada ◽  
Salvatore Carbone ◽  
Cory Trankle ◽  
Michele Mattia Viscusi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Volume Index ◽  
Stroke Work ◽  
Systolic Volume ◽  
Arterial Blood ◽  
End Systolic Volume

OBJECTIVES/SPECIFIC AIMS: Our goal was to compare the ventriculo-arterial coupling and left ventricular mechanical work of patients with systolic and diastolic heart failure (SHF and DHF). METHODS/STUDY POPULATION: Patients with New York Heart Association Functional Class II-III HF symptoms were included. SHF was defined as left ventricular (LV) ejection fraction<50% and DHF as >50%. Analysis of the fingertip arterial blood pressure tracing captured with a finger plethysmography cuff according to device-specific algorithms provided brachial artery blood pressure and stroke volume. LV end-systolic volume was measured separately via transthoracic echocardiography. Arterial elastance (Ea), a measure of pulsatile and nonpulsatile LV afterload, was calculated as LV end-systolic pressure (ESP)/end-diastolic volume. End-systolic elastance (Ees), a measure of load-independent LV contractility, was calculated as LV ESP/end-systolic volume. Ventriculo-arterial coupling (VAC) ratio was defined as Ea/Ees. Stroke work (SWI) was calculated as stroke volume index×LV end-systolic pressure×0.0136 and potential energy index (PEI) as 1/2×(LV end-systolic volume×LV end-systolic pressure×0.0136). Total work index (TWI) was the sum of SWI+PEI. RESULTS/ANTICIPATED RESULTS: Patients with SHF (n=52) and DHF (n=29) were evaluated. Median (IQR) age was 57 (51–64) years. There were 48 (58%) and 59 (71%) patients were male and African American, respectively. Cardiac index was 2.8 (2.2–3.2) L/minute and 3.0 (2.8–3.3) L/minute in SHF and DHF, respectively (p=0.12). Self-reported activity levels (Duke Activity Status Index, p=0.48) and heart failure symptoms (Minnesota Living with Heart Failure Questionnaire, p=0.55) were not different between SHF and DHF. Ea was significantly lower in DHF compared with SHF patients [1.3 (1.2–1.6) vs. 1.7 (1.4–2.0) mmHg; p<0.001] whereas Ees was higher in DHF vs. SHF [2.8 (2.1–3.1) vs. 0.9 (0.7-1.3) mmHg; p<0.001). VAC was 1.8 (1.3–2.8) in SHF Versus 0.5 (0.4–0.7) in DHF (p<0.001). Compared with SHF, DHF patients had higher SWI [71 (57–83) vs. 48 (39–68) gm×m; p<0.001) and lower PEI [19 (12–26) vs. 44 (36–57) gm×m; p<0.001]. TWI did not differ between SHF and DHF (p=0.14). Work efficiency was higher in DHF than SHF [0.80 (0.74–0.84) vs. 0.53 (0.46–0.64); p<0.001]. DISCUSSION/SIGNIFICANCE OF IMPACT: The results underscore the differences in pathophysiology between SHF and DHF patients with similar symptom burden and exercise capacity. These results highlight the difference in myocardial energy utilization between SHF and DHF.

Left ventricular dimensions during hemorrhagic shock measured by biplane cinefluorography

1992 ◽  
Vol 263 (5) ◽  
pp. H1554-H1559
Author(s):  
J. W. Horton ◽  
J. H. Mitchell
Keyword(s):  
Stroke Volume ◽  
Hemorrhagic Shock ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Total Blood ◽  
Systolic Volume ◽  
Dimensional Changes ◽  
Arterial Blood ◽  
Left Ventricular Dimensions ◽  
Ventricular Dimensions

The effects of hemorrhagic shock on left ventricular dimensions and volume were studied in 15 splenectomized dogs. A 42 +/- 1% decrease in total blood volume caused arterial blood pressure to fall 60% (from 120 +/- 5 to 48 +/- 3 mmHg); the first derivative of left ventricular pressure at a developed pressure of 40 mmHg fell 54% (from 1,930 +/- 94 to 905 +/- 93 mmHg/s, P < 0.05). Cardiac output fell 76% due to a 73% decrease in stroke volume; heart rate was unchanged at the end of hemorrhage but increased 50% during 3 h of sustained shock (from 110 +/- 6 to 166 +/- 8 beats/min, P < 0.05). During hemorrhage the septal-lateral and the anterior-posterior end-diastolic dimensions fell to a greater extent (7.8 mm, -21% and 7.0 mm, -18%, respectively) than the apex-base dimension (2.3 mm, -3.3%, P < 0.05). As a result of these dimensional changes, left ventricular end-diastolic volume fell 39% (from 48 +/- 2 to 28 +/- 1 cm3, P < 0.01). End-systolic dimensions fell in the same proportion during hemorrhage, resulting in a 30% decrease in end-systolic volume (from 30 +/- 2 to 21 +/- 1 cm3, P < 0.05). After 120 min of sustained shock, all end-diastolic dimensions remained unchanged, but end-systolic dimensions and volume increased significantly from values measured at end hemorrhage (P < 0.05), causing ejection fraction and stroke volume to fall to a greater extent. This study confirms a pronounced reduction in the minor axes of the left ventricle during hemorrhagic shock with subsequent reduction in ventricular function.

Left ventricular mechanical limitations to stroke volume in healthy humans during incremental exercise

2011 ◽  
Vol 301 (2) ◽  
pp. H478-H487 ◽  
Author(s):  
Eric J. Stöhr ◽  
José González-Alonso ◽  
Rob Shave
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Incremental Exercise ◽  
Diastolic Filling ◽  
Systolic Volume ◽  
Young Males ◽  
Healthy Humans ◽  
End Diastolic Volume

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.

First clinical trial with etomoxir in patients with chronic congestive heart failure

2000 ◽  
Vol 99 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Stephan SCHMIDT-SCHWEDA ◽  
Christian HOLUBARSCH
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Sarcoplasmic Reticulum ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

In the failing human myocardium, both impaired calcium homoeostasis and alterations in the levels of contractile proteins have been observed, which may be responsible for reduced contractility as well as diastolic dysfunction. In addition, levels of a key protein in calcium cycling, i.e. the sarcoplasmic reticulum Ca2+-ATPase, and of the α-myosin heavy chain have been shown to be enhanced by treatment with etomoxir, a carnitine palmitoyltransferase inhibitor, in normal and pressure-overloaded rat myocardium. We therefore studied, for the first time, the influence of long-term oral application of etomoxir on cardiac function in patients with chronic heart failure. A dose of 80 mg of etomoxir was given once daily to 10 patients suffering from heart failure (NYHA functional class II–III; mean age 55±4 years; one patient with ischaemic heart disease and nine patients with dilated idiopathic cardiomyopathy; all male), in addition to standard therapy. The left ventricular ejection fraction was measured echocardiographically before and after a 3-month period of treatment. Central haemodynamics at rest and exercise (supine position bicycle) were defined by means of a pulmonary artery catheter and thermodilution. All 10 patients improved clinically; no patient had to stop taking the study medication because of side effects; and no patient died during the 3-month period. Maximum cardiac output during exercise increased from 9.72±1.25 l/min before to 13.44±1.50 l/min after treatment (P < 0.01); this increase was mainly due to an increased stroke volume [84±7 ml before and 109±9 ml after treatment (P < 0.01)]. Resting heart rate was slightly reduced (not statistically significant). During exercise, for any given heart rate, stroke volume was significantly enhanced (P < 0.05). The left ventricular ejection fraction increased significantly from 21.5±2.6% to 27.0±2.3% (P < 0.01). In acute studies, etomoxir showed neither a positive inotropic effect nor vasodilatory properties. Thus, although the results of this small pilot study are not placebo-controlled, all patients seem to have benefitted from etomoxir treatment. Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca2+-ATPase and the α-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction.

Interaction of interval-force relationship with aortic pressure and stroke volume

1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Right Heart Bypass ◽  
Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

Use of the Frank-Starling mechanism during submaximal versus maximal upright exercise

1986 ◽  
Vol 251 (6) ◽  
pp. H1101-H1105 ◽  
Author(s):  
G. D. Plotnick ◽  
L. C. Becker ◽  
M. L. Fisher ◽  
G. Gerstenblith ◽  
D. G. Renlund ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Blood Pool ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Vigorous Exercise ◽  
Systolic Volume ◽  
Early Exercise ◽  
End Diastolic Volume ◽  
Blood Pool Scintigraphy ◽  
End Systolic Volume

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.

Breathing through an inspiratory threshold device improves stroke volume during central hypovolemia in humans

2008 ◽  
Vol 104 (5) ◽  
pp. 1402-1409 ◽  
Author(s):  
Kathy L. Ryan ◽  
William H. Cooke ◽  
Caroline A. Rickards ◽  
Keith G. Lurie ◽  
Victor A. Convertino
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Lower Body Negative Pressure ◽  
Systolic Arterial Pressure ◽  
Intrathoracic Pressure ◽  
Subsequent Increase ◽  
Arterial Blood ◽  
Threshold Device ◽  
Inspiratory Resistance

Inspiratory resistance induced by breathing through an impedance threshold device (ITD) reduces intrathoracic pressure and increases stroke volume (SV) in supine normovolemic humans. We hypothesized that breathing through an ITD would also be associated with a protection of SV and a subsequent increase in the tolerance to progressive central hypovolemia. Eight volunteers (5 men, 3 women) were instrumented to record ECG and beat-by-beat arterial pressure and SV (Finometer). Tolerance to progressive lower body negative pressure (LBNP) was assessed while subjects breathed against either 0 (sham ITD) or −7 cmH2O inspiratory resistance (active ITD); experiments were performed on separate days. Because the active ITD increased LBNP tolerance time from 2,014 ± 106 to 2,259 ± 138 s ( P = 0.006), data were analyzed (time and frequency domains) under both conditions at the time at which cardiovascular collapse occurred during the sham experiment to determine the mechanisms underlying this protective effect. At this time point, arterial blood pressure, SV, and cardiac output were higher ( P ≤ 0.005) when breathing on the active ITD rather than the sham ITD, whereas indirect indicators of autonomic activity (low- and high-frequency oscillations of the R-to-R interval) were not altered. ITD breathing did not alter the transfer function between systolic arterial pressure and R-to-R interval, indicating that integrated baroreflex sensitivity was similar between the two conditions. These data show that breathing against inspiratory resistance increases tolerance to progressive central hypovolemia by better maintaining SV, cardiac output, and arterial blood pressures via primarily mechanical rather than neural mechanisms.

Sign in / Sign up

Export Citation Format

Share Document