Regulation of cardiac output during upright exercise in patients with aortic regurgitation

The change in cardiac output during upright exercise in patients with aortic regurgitation (AR) is not well known. We measured left ventricular (LV) ejection fraction (EF) and volume, regurgitant fraction (RF), total cardiac output and forward cardiac output at rest, and peak upright exercise by means of radionuclide angiography in ten normal subjects and 15 patients with AR. In the normal subjects, there was no significant change in the end-diastolic volume but there was a significant decrease in the end-systolic volume (p = 0.0001) and a significant increase in EF (p = 0.0001). The increase in cardiac output during exercise was due to increases in both stroke volume and heart rate. In patients with AR, there was a significant decrease during exercise in RF (53 +/- 15% at rest, and 45 +/- 15% during exercise; p = 0.03), and in end-diastolic and end-systolic volume (p = 0.02, and p = 0.003, respectively). The EF increased during exercise (p = 0.003). The total stroke volume did not change (68 +/- 19 ml/m2 at rest, and 67 +/- 14 ml/m2 during exercise; p, NS). Thus, in patients with AR, individual changes in EF, RF, and volume are quite variable, but as a group a decrease in RF and an increase in heart rate contribute to the increase in forward flow. The total stroke volume may not increase during exercise, despite an increase in EF and a decrease in end-systolic volume because of a concomitant decrease in end-diastolic volume.     

Left ventricular response to submaximal exercise in endurance-trained athletes and sedentary adults.

This investigation examines the hypothesis that athletes increase stroke volume with submaximal exercise through an augmentation of left ventricular (LV) end-diastolic volume and a reduction of LV end-systolic volume, whereas sedentary adults only increase stroke volume modestly, because LV end-diastolic volume does not increase. Upright bicycle exercise was performed by 17 endurance-trained male athletes and 15 sedentary men. M-mode echocardiograms were obtained during submaximal exercise at predetermined heart rates. Athletes, at a heart rate of 130 beats/min, increased their stroke volume 67% from 72 +/- 18 ml to 120 +/- 26 ml (p less than 0.001). This resulted from an increase of LV end-diastolic volume from 119 +/- 23 to 152 +/- 28 ml (p less than 0.001) and a reduction in LV end-systolic volume from 46 +/- 14 to 31 +/- 9 ml (p less than 0.001). Sedentary men at the same heart rate increased stroke volume 22% from 63 +/- 15 to 77 +/- 21 ml (p less than 0.05). LV end-diastolic volume did not change (96 +/- 20 vs 97 +/- 28 ml) (p = not significant), but LV end-systolic volume decreased (33 +/- 11 vs 20 +/- 9 ml) (p less than 0.001). In conclusion, athletes increased cardiac output through a more prominent augmentation of stroke volume than sedentary subjects at submaximal exercise. This was accomplished through an augmentation of LV end-diastolic volume. This may have a conserving effect on myocardial oxygen consumption at these levels of exercise.     

Effect of isotonic exercise training on left ventricular volume during upright exercise

To determine the changes in left ventricular volume and their time course during exercise we studied 30 runners. Left ventricular end-diastolic and end-systolic volumes were measured from biapical two-dimensional echocardiograms recorded during graded upright bicycle exercise. The validity of this echocardiographic technique was assessed by comparing measurements at rest and exercise with results obtained by gated equilibrium radionuclide angiography in 10 patients with coronary artery disease. Although the absolute volume measurements were lower by echocardiography, ejection fraction was not significantly different and the directional changes in volume during exercise were comparable. In the runners, resting left ventricular end-diastolic volume measurements by echocardiography correlated with their maximum bicycle exercise endurance times (r = .80). Left ventricular end-diastolic volume, stroke volume, and ejection fraction increased during exercise with the most marked changes occurring in the first half of exercise. Systolic blood pressure/end-systolic volume (SBP/ESV) also increased during exercise, but the largest change occurred during the second half of exercise. Left ventricular volumes were larger in the 12 competitive marathon runners (maximum exercise duration greater than or equal to 27 min) as compared with the 18 noncompetitive runners (exercise duration less than or equal to 23 min): resting end-diastolic volume 130 +/- 29 (SD) ml vs 87 +/- 20 ml (p less than .001), respectively. During exercise the competitive runners exhibited a larger increase in end-diastolic volume and the noncompetitive athletes showed a greater increase in SBP/ESV. Therefore, highly trained competitive marathon runners make greater use of the less energy-consuming Frank-Starling mechanism to accomplish high levels of isotonic exercise performance as compared with less well-trained runners.     

Peak exercise left ventricular performance in normal subjects and in athletes assessed by first-pass radionuclide angiography.

The role of Frank-Starling law of the heart in determining the increase in cardiac output during exercise in humans is still controversial (e.g., the mechanisms responsible for the enhancement of left ventricular [LV] filling during the shortened diastolic interval). Ten weight lifters, 12 swimmers and 12 sedentary subjects who underwent maximal upright bicycle exercise testing were studied. First-pass radionuclide angiography was performed both at rest and at peak exercise using a multicrystal gamma camera. Compared with resting values, heart rate and cardiac index at peak exercise increased by 101 +/- 16 beats/min (p less than 0.001) and 6.7 +/- 2.8 liters/min/m2 (p less than 0.001) in weight lifters, by 96 +/- 9 beats/min (p less than 0.001) and 9.5 +/- 2 liters/min/m2 (p less than 0.001) in swimmers, and by 103 +/- 9 beats/min (p less than 0.001) and 7.3 +/- 1.8 liters/min/m2 (p less than 0.001) in sedentary subjects. Stroke volume increased by 20.5 +/- 9.8 ml/m2 (p less than 0.001) in swimmers only. End-diastolic volume at peak exercise did not change in weight lifters and in swimmers; it decreased by 8.2 +/- 8.6 ml/m2 (p less than 0.01) in sedentary subjects. A significant correlation was found between the decrease in end-systolic volume and the increase in peak rapid filling rate at peak exercise in all 3 groups (r = 0.65, p less than 0.05 in weight lifters; r = 0.59, p less than 0.05 in swimmers; r = 0.67, p less than 0.05 in sedentary subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Regulation of stroke volume during submaximal and maximal upright exercise in normal man

To characterize the hemodynamic factors that regulate stroke volume during upright exercise in normal man, 24 asymptomatic male volunteers were evaluated by simultaneous right heart catheterization, radionuclide angiography, and expired gas analysis during staged upright bicycle exercise to exhaustion. From rest to peak exercise, oxygen consumption increased from 0.33 to 2.55 liters/min (7.7-fold), cardiac index increased from 3.0 to 9.7 liters/min per m2 (3.2-fold), and arteriovenous oxygen difference increased from 5.8 to 14.1 vol% (2.5-fold). The increase in cardiac index resulted from an increase in heart rate from 73 to 167 beats/min (2.5-fold), and an increase in left ventricular stroke volume index from 41 to 58 ml/m2 (1.4-fold). During low levels of exercise, there was a linear increase in cardiac index due to an increase in both heart rate and stroke volume index; stroke volume index increased as a result of an increase in left ventricular filling pressure and end-diastolic volume index and, to a much smaller extent, a decrease in end-systolic volume index. During high levels of exercise, further increases in cardiac index resulted entirely from an increase in heart rate, since stroke volume index increased no further. Left ventricular end-diastolic volume index decreased despite a linear increase in pulmonary artery wedge pressure; stroke volume index was maintained by a further decrease in end-systolic volume index. The degree to which stroke volume index increased during exercise in individuals correlated with the change in end-diastolic volume index (r = 0.66) but not with the change in end-systolic volume index (r = 0.07). Thus, the mechanism by which left ventricular stroke volume increases during upright exercise in man is dependent upon the changing relationship between heart rate, left ventricular filling, and left ventricular contractility. At low levels of exertion, an increase in left ventricular filling pressure and end-diastolic volume are important determinants of the stroke volume response through the Starling mechanism. At high levels of exertion, the exercise tachycardia is accompanied by a decrease in end-diastolic volume despite a progressive increase in filling pressure, so that stroke volume must be maintained by a decrease in end-systolic volume.     

Stroke volume increases by similar mechanisms during upright exercise in normal men and women

To define the effects of gender on stroke volume control during upright exercise in normal subjects, we examined central hemodynamics in 34 men and 27 women during staged bicycle ergometry. Central hemodynamics were assessed by right-sided cardiac catheterization and simultaneous radionuclide angiography. Left ventricular end-diastolic and end-systolic volumes were calculated from the stroke volume (by direct Fick) and the corresponding left ventricular ejection fraction. Men were larger than women (1.85 ± 0.11 vs 1.65 ± 0.13 m², p < 0.001) but groups were matched for age (39 ± 12 vs 36 ± 9 years, P = 0.27). Oxygen consumption at peak exercise was higher in men than in women (2.51 ± 0.50 vs 1.74 ± 0.30 liters/min, p < 0.001) but was not different when adjusted for body weight (31.5 ± 8.1 vs 28.4 ± 6.4 ml/kg/min, P = 0.14), indicating similar levels of overall fitness in the 2 groups. At rest and during submaximal and maximal exercise, stroke volume and left ventricular end-diastolic and end-systolic volumes were higher in men than in women, but there were no intergroup differences in stroke volume index, left ventricular ejection fraction, and left ventricular end-diastolic or end-systolic volume indexes. Comparison of derived regression equations of cardiac index, stroke volume index and left ventricular end-diastolic and end-systolic volume indexes revealed no differences in the time course or magnitude of changes with respect to oxygen consumption, expressed as percentage of peak oxygen consumption, in the 2 groups. The major increase in left ventricular end-diastolic volume from upright rest in both men and women occurred during early exercise and accounted for most of the increase in stroke volume with relatively small increases in pulmonary wedge pressure. With moderate to intense exercise, stroke volume was maintained because of decreases in left ventricular end-systolic volume, as left ventricular end-diastolic volume did not change or decreased slightly from 50 to 100% of peak oxygen consumption in both men and women. Our data indicate that in normal subjects, gender, independent of body size and physical fitness, is not an important determinant of cardiac output or left ventricular volume response to upright exercise.     

Sex-related differences in the normal cardiac response to upright exercise

In previous studies from this laboratory, we found that approximately 30% of women with chest pain and normal coronary arteries demonstrated either a decrease in or a failure to increase radionuclide ejection fraction during exercise. To examine the hypothesis that this apparent abnormality in left ventricular function represents a physiologic difference between men and women, we prospectively studied central and peripheral cardiovascular responses to exercise in 31 age-matched healthy volunteers (16 women and 15 men). A combination of quantitative radionuclide angiography and expired-gas analysis was used to measure ejection fraction and relative changes in end-diastolic counts, stroke counts, count output, and arteriovenous oxygen difference during symptom-limited upright bicycle exercise. Normal male and female volunteers demonstrated comparable baseline left ventricular function and similar aerobic capacity, as determined by weight-adjusted peak oxygen consumption (22.1 +/- 5.1 and 22.6 +/- 4.3 ml/kg/min, respectively). However, their cardiac responses to exercise were significantly different. Ejection fraction increased from 0.62 +/- 0.09 at rest to 0.77 +/- 0.07 during exercise in men (p less than .001), but was unchanged from 0.63 +/- 0.09 at rest to 0.64 +/- 0.10 during exercise in women. The ejection fraction increased by 5 points or more in 14 of 15 men, but in only seven of the 16 women. End-diastolic counts increased by 30% in women (p less than .001), but was unchanged in men. Because decreases in ejection fraction were matched by increases in end-diastolic counts, relative increases in stroke counts and count output were the same for men and women. These data demonstrate a basic difference between men and women with respect to the mechanism by which they achieve a normal response of stroke volume to exercise; these differences must be taken into account when measurements of cardiac function during exercise stress are used for diagnostic purposes.     

Attenuated responses of Doppler-derived hemodynamic parameters during supine bicycle exercise in heart transplant recipients

The aim of this study was to characterize Doppler-derived hemodynamic parameters in heart transplant recipients at rest and during symptom-limited supine bicycle exercise. Eighteen sedentary patients aged 54.0 +/- 2 years, 1.6 +/- 1.0 years following cardiac transplantation, and 18 sedentary healthy volunteers aged 51.8 +/- 4 years were investigated. Basic hemodynamic parameters and Doppler-derived parameters were recorded at rest and at peak dynamic exercise. Resting heart rate, blood pressure and rate-pressure product were higher in the transplanted patients (p < 0.001). However, in comparison with the resting state, the increase in these parameters at exercise was lower in heart transplant recipients. In the healthy, dynamic exercise induced an increase in peak flow velocity, mean acceleration, flow velocity integral, stroke volume, cardiac output and cardiac index (p < 0.001 for all) while systemic vascular resistance, ejection time and acceleration time decreased (p < 0.001 for all). The following parameters increased in the transplanted patients at dynamic exercise: peak flow velocity, cardiac output and cardiac index (p < 0.001), mean acceleration (p < 0.01) and flow velocity integral (p < 0.05). Ejection time decreased (p < 0.05) and acceleration time and systemic vascular resistance remained unchanged. In conclusion, at rest peak flow velocity, mean acceleration, flow velocity integral and stroke volume are lower in the transplanted than in the healthy controls, while cardiac output, cardiac index and systemic vascular resistance are equal. Our study demonstrates attenuated responses of basic hemodynamic parameters and Doppler-derived cardiovascular indices at symptom-limited supine bicycle exercise in heart transplant recipients compared to healthy volunteers.     

Cardiovascular adaptations to intense swim training in sedentary middle-aged men and women

Central and peripheral cardiovascular adaptations to 12 weeks of intense swim training were characterized in 12 previously sedentary middle-aged men and women. Peak oxygen uptake (VO2) during upright bicycle exercise improved from 29.2 +/- 5.6 to 34.7 +/- 6.7 ml/kg/min (mean +/- SD, p less than .01) because of similar increases in peak cardiac output (CO) and calculated arteriovenous oxygen difference (both p = .02). Peak supine VO2 was 10% higher after training (p less than .005) solely because of enhanced CO (p = .005). Peak heart rate decreased in both postures; therefore stroke volume at peak exercise was greater by 10% and 18% in the upright and supine postures, respectively (p = .05 and p = .005). There was an identical 18% rise (p = .01) in peak supine left ventricular end-diastolic volume index by radionuclide ventriculography but no change in left ventricular ejection fraction or end-systolic volume index (ESVI). Peak systolic blood pressure (SBP) was unchanged in the upright posture but was 8% higher (p = .002) during recumbency despite a similar total peripheral resistance and SBP/ESVI ratio. Maximal calf conductance (Gmax), assessed separately by venous occlusion plethysmography after local ischemic exercise to fatigue, was augmented 20% (p less than .02) by training, resulting in an 18% greater hyperemic blood flow (p = .05). Peak VO2, CO, and Gmax were unchanged in five nonexercising control subjects. We conclude that in middle-aged humans, intense swim training for 12 weeks produces adaptations that include a greater capacity for vasodilatation in skeletal muscle and an enhanced cardiac pump capacity.     

Effect of preload change on resting and exercise cardiac performance in hypertrophic cardiomyopathy

The purpose of this study was to investigate the hemodynamic responses, at rest and on exercise, of patients with hypertrophic cardiomyopathy to changes in circulating volume. After Swan-Ganz and radial arterial cannulation, 13 patients with hypertrophic cardiomyopathy performed maximal exercise tests after diuretic (frusemide 20 mg intravenously) and after fluid loading (0.9% saline at 10 ml/kg body weight intravenously) on different days. At rest, right atrial and pulmonary capillary wedge pressures increased with volume loading and decreased with a diuretic. There were no significant changes in the resting, supine cardiac or stroke indexes but in the upright position, the cardiac index and stroke index were higher after volume loading (2.5 +/- 0.7 vs 2.2 +/- 0.5 liters/min/m2, p less than 0.05; 33 +/- 11 vs 27 +/- 9 ml/m2, p less than 0.005, respectively). Although the right atrial, pulmonary arterial and pulmonary capillary wedge pressures were higher during exercise after volume loading, there were no significant differences in exercise heart rate, systemic blood pressure, cardiac index, stroke index, systemic vascular resistance index or overall exercise capacity compared to exercise after diuresis. The data show that the cardiac index and stroke index, at supine rest and during upright exercise, were not influenced by the preload changes induced in these patients with hypertrophic cardiomyopathy. The results suggest that these patients are operating on the plateau of left ventricular Frank-Starling function (filling pressure/output) curve.     

Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume

To determine the role of preload in maintaining the enhanced stroke volume of upright exercise-trained endurance athletes after deconditioning, six highly trained subjects undergoing upright and supine bicycle ergometry were characterized before and after 3, 8 and 12 weeks of inactivity that reduced oxygen uptake by 20%. During exercise, oxygen uptake, cardiac output by carbon dioxide rebreathing, cardiac dimensions by M-mode echocardiography, indirect arterial blood pressure and heart rate were studied simultaneously. Two months of inactivity resulted in a reduction in stroke volume, calculated as cardiac output/heart rate, during upright exercise (p less than 0.005) without a significant change during supine exercise. A concomitant decrease in the left ventricular end-diastolic dimension from the trained to the deconditioned state was observed in the upright posture (5.1 +/- 0.3 versus 4.6 +/- 0.3 cm; p = 0.02) but not with recumbency (5.4 +/- 0.2 versus 5.1 +/- 0.3 cm; p = NS). There was a strong correlation between left ventricular end-diastolic dimension and stroke volume (r greater than 0.80) in all subjects. No significant changes in percent fractional shortening or left ventricular end-systolic dimension occurred in either position after cessation of training. Estimated left ventricular mass was 20% lower after 3 and 8 weeks of inactivity than when the subjects were conditioned (p less than 0.05 for both). Thus, the endurance-trained state for upright exercise is associated with a greater stroke volume during upright exercise because of augmented preload. Despite many years of intense training, inactivity for only a few weeks results in loss of this adaptation in conjunction with regression of left ventricular hypertrophy.     

Dynamics of left ventricular diastolic filling during exercise: a Doppler echocardiographic study of boys 10 to 14 years old.

STUDY OBJECTIVE: Factors influencing diastolic filling of the left ventricle may serve as critical determinants of both maximal cardiac output and oxygen uptake. This study was conducted to assess diastolic filling dynamics of the left ventricle during progressive upright cycle exercise in children. METHODS: Twelve boys aged 10 to 14 years underwent cycle testing with determination of transmitral flow velocities and pressure gradients as well as cardiac stroke volume using Doppler echocardiography. RESULTS: Estimated diastolic filling period shortened from 0.479 +/- 0.043 s at rest to 0.138 +/- 0.015 s at peak exercise. The peak and mean transmitral pressure gradient rose fourfold from rest to peak exercise. Mitral flow volume per beat rose by only 40% and remained stable beyond mild-to-moderate intensity work. CONCLUSIONS: Increases in transmitral pressure gradient with exercise may serve principally to augment velocity of ventricular filling with the progressively shortening diastolic time period.     

Doppler echocardiographic measurement of flow velocity in the ascending aorta during supine and upright exercise.

Doppler echocardiography was used to measure stroke volume, peak flow velocity, and acceleration of flow in the ascending aorta in 10 healthy young volunteers during unlimited supine bicycle exercise and upright treadmill exercise. High quality studies were obtained in all subjects through the suprasternal notch acoustic window; there was no appreciable degradation in Doppler signal caused by interference by increased respiration or chest wall motion. Stroke volume index increased from 54 ml/m2 at rest to 63.5 ml/m2 at peak supine exercise and from 38 ml/m2 standing at rest to 63.3 ml/m2 during peak upright exercise. Mean peak flow velocity rose from 0.91 m/s at supine rest to 1.36 m/s during maximum supine exercise. In the upright position mean peak flow velocity increased from 0.75 m/s at rest to 1.39 m/s during maximum exercise. Mean peak velocities were lower in the upright position at rest but were not significantly different at peak exercise. Mean acceleration of flow in the ascending aorta increased from 12.02 m/s2 during supine rest to 21.6 m/s2 during supine exercise and from 10.8 m/s2 at rest on the treadmill to 21.9 m/s2 during peak upright exercise. This study shows that echocardiographic measurement of ascending aortic blood flow by the Doppler technique is feasible even during vigorous exercise; that stroke volume and peak flow velocity at rest are lower in the upright position than in the supine position but equalise at peak exercise; and that acceleration of flow in the ascending aorta is the same in both the supine and upright positions and increases equally at peak exercise in both positions.     

Doppler echocardiographic measurement of flow velocity in the ascending aorta during supine and upright exercise

Doppler echocardiography was used to measure stroke volume, peak flow velocity, and acceleration of flow in the ascending aorta in 10 healthy young volunteers during unlimited supine bicycle exercise and upright treadmill exercise. High quality studies were obtained in all subjects through the suprasternal notch acoustic window; there was no appreciable degradation in Doppler signal caused by interference by increased respiration or chest wall motion. Stroke volume index increased from 54 ml/m2 at rest to 63.5 ml/m2 at peak supine exercise and from 38 ml/m2 standing at rest to 63.3 ml/m2 during peak upright exercise. Mean peak flow velocity rose from 0.91 m/s at supine rest to 1.36 m/s during maximum supine exercise. In the upright position mean peak flow velocity increased from 0.75 m/s at rest to 1.39 m/s during maximum exercise. Mean peak velocities were lower in the upright position at rest but were not significantly different at peak exercise. Mean acceleration of flow in the ascending aorta increased from 12.02 m/s2 during supine rest to 21.6 m/s2 during supine exercise and from 10.8 m/s2 at rest on the treadmill to 21.9 m/s2 during peak upright exercise. This study shows that echocardiographic measurement of ascending aortic blood flow by the Doppler technique is feasible even during vigorous exercise; that stroke volume and peak flow velocity at rest are lower in the upright position than in the supine position but equalise at peak exercise; and that acceleration of flow in the ascending aorta is the same in both the supine and upright positions and increases equally at peak exercise in both positions.     

Position as a variable for cardiovascular responses during exercise

Twenty-one normal young male subjects underwent resting and exercise (bicycle) radionuclide angiography in the full supine and 70 degrees upright tilt positions in order to examine the effects of position on left ventricular size and performance, hemodynamics, and exercise duration. All subjects also underwent full (90 degrees) upright bicycle ergometry with respiratory gas analysis to establish the level of maximal exercise capacity for each. Body position significantly (p less than 0.05) affected resting and exercise cardiovascular parameters. End-diastolic and endsystolic left ventricular volumes and stroke volume were larger in the supine position, both at rest and during exercise. The cardiac output at rest and during exercise were comparable for the two positions; an increase in resting and exercise heart rate in the 70 degrees tilt position compensated for the reduced stroke volume of this posture. At maximal exercise, the 70 degrees upright position was associated with a greater response in left ventricular ejection fraction, otherwise this parameter was not position related. Exercise capacity, in terms of duration and workload, was significantly higher in the supine (1870 +/- 390 s) and full upright (1830 +/- 250 s) positions than in the 70 degrees tilt position (1730 +/- 260 s). Changes in body position significantly alter parameters of ventricular, cardiovascular, and exercise performance.     

Cardiovascular response to dynamic exercise in patients with chronic symptomatic mild-to-moderate and severe aortic regurgitation

Fifteen patients with symptomatic mild-to-moderate and severe chronic aortic regurgitation (AR) performed supine bicycle exercise while measurements of rest and exercise hemodynamics and left ventricular function were obtained. A continuous Doppler method was used to determine the change in distribution of total left ventricular stroke volume between forward stroke volume and regurgitant volume (RgV) with exercise. The pulmonary arterial wedge pressure (PAWP) was lower in the mild-to-moderate AR group than in the severe AR group at rest (8 +/- 1.2 vs 19 +/- 3.6 mm Hg, p = 0.01) and during exercise (15 +/- 3.9 vs 30 +/- 4.3 mm Hg, p = .02). In all patients there were increases in heart rate (78 +/- 4 to 96 +/- 5 beats/min, p less than .001), forward stroke volume (41 +/- 2 to 46 +/- 2 ml/m2), and the cardiac index (3.1 +/- 0.2 to 4.4 +/- 0.3 liters/min-m2, p less than .001), despite a fall in total left ventricular stroke volume index from 84 +/- 5 to 76 +/- 5 ml/m2 (p = .03). The systemic vascular resistance (SVR) decreased with exercise from 1277 +/- 72 to 1031 +/- 64 dynes-sec/cm5 (p less than .001), and the RgV and regurgitant fraction (RgF) both decreased with exercise from 43 +/- 5 ml/m2 to 30 +/- 4 ml/m2 (p = .002) and 0.50 +/- 0.03 to 0.37 +/- 0.03 (p less than .001), respectively. Left ventricular ejection fraction increased on exercise from 0.51 +/- 0.03 to 0.55 +/- 0.03 (p = .02) for the group, but it either decreased or failed to increase by at least 0.05 in seven of 13 patients. The change in ejection fraction on exercise was directly related to the change in SVR (r = .80, p less than .001). We conclude that: in patients with mild-to-moderate AR, the PAWP is generally normal at rest and exercise, in most of those with severe AR, the PAWP is elevated at rest and increases significantly with exercise, which is the likely mechanism for dyspnea on exertion in these patients, the cardiac index in both groups is normal at rest and increases on exercise, the increase in cardiac output results from both an increased heart rate and forward stroke volume, the increase in forward stroke volume results from reductions of RgV and RgF, the RgV and RgF are decreased due to a decreased SVR, and the ejection fraction response to exercise is variable and correlates best with changes in SVR with exercise.     

Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac dilatation and increased stroke volume compensate for a diminished heart rate

To assess the effect of age on cardiac volumes and function in the absence of overt or occult coronary disease, we performed serial gated blood pool scans at rest and during progressive upright bicycle exercise to exhaustion in 61 participants in the Baltimore Longitudinal Study of Aging. The subjects ranged in age from 25 to 79 years and were free of cardiac disease according to their histories and results of physical, resting and stress electrocardiographic, and stress thallium scintigraphic examinations. Absolute left ventricular volumes were obtained at each workload. There were no age-related changes in cardiac output, end-diastolic or end-systolic volumes, or ejection fraction at rest. During vigorous exercise (125 W), cardiac output was not related to age (cardiac output [1/min] = 16.02 + 0.03 [age]; r = .12, p = .46). However, there was an age-related increase in end-diastolic volume (end-diastolic volume [ml] = 86.30 + 1.48 [age]; r = .47, p = .003) and stroke volume (stroke volume [ml] = 85.52 + 0.80 [age]; r = .37, p = .02), and an age-related decrease in heart rate (heart rate [beats/min] = 184.66 - 0.70 [age]; r = -.50, p = .002). The dependence of the age-related increase in stroke volume on diastolic filling was emphasized by the fact that at this high workload end-systolic volume was higher (end-systolic volume [ml] = 3.09 + 0.65 [age]; r = .45, p = .003) and ejection fraction lower (ejection fraction = 88.48 - 0.18 [age]; r = -.33, p = .04) with increasing age. These findings indicate that although aging does not limit cardiac output per se in healthy community-dwelling subjects, the hemodynamic profile accompanying exercise is altered by age and can be explained by an age-related diminution in the cardiovascular response to beta-adrenergic stimulation.     

Postural exercise abnormalities in symptomatic patients with mitral valve prolapse

The hemodynamics of the supine and upright exercise response in 16 symptomatic women with mitral valve prolapse (Group I) was compared with that in 8 asymptomatic normal control women (Group II). All subjects had supine and upright echocardiography and phonocardiography at rest and none demonstrated mitral regurgitation. All participants then underwent same day graded bicycle exercise, with simultaneous radionuclide angiography in both the upright and the supine posture. Catecholamines were measured, and a variety of volumetric and hemodynamic data were obtained. Group I (patients with mitral valve prolapse) demonstrated a reduced exercise tolerance, especially during upright exercise, as measured by both total exercise duration and maximal work load achieved. Mean total catecholamine measurements were similar between the two study groups at comparable mean heart rate, mean blood pressure and mean rate-pressure (double) product. No difference was observed in the ratio of right to left ventricular stroke counts at rest or during exercise regardless of posture, suggesting that exercise-induced mitral regurgitation did not occur. A difference was noted, however, in left ventricular end-diastolic volume index. At rest, Group I patients exhibited a 42% decrease in this index when sitting upright, and this difference from supine values persisted at submaximal (300 kpm/min) and peak work loads (34 and 29% difference, respectively). This contrasted with the control subjects whose upright end-diastolic volumes at rest, at 300 kpm/min and at peak exercise were reduced 21, 10 and 3%, respectively, compared with supine values. Cardiac index measurements reflected the reduced left ventricular end-diastolic volume observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Beat-to-beat evaluation of cardiac function during recovery from upright bicycle exercise in patients with coronary artery disease

The purpose of this study was to evaluate the time course of cardiac function during recovery from upright bicycle exercise in patients with coronary artery disease. Twelve patients with coronary artery disease performed a symptom-limited exercise test on a cycle ergometer. Left ventricular function was continuously monitored during exercise and recovery with a computerized cadmium telluride detector following the intravenous injection of technetium-labeled red blood cells. Although the end-diastolic volume (153.4 +/- 76.1 ml) and end-systolic volume (100.5 +/- 67.3 ml) at the end of exercise were significantly higher than the respective resting values, stroke volume (52.8 +/- 16.1 ml) and ejection fraction (38.0 +/- 12.2%) were not different from the respective resting values. The recovery of cardiac output was relatively slow compared with that of heart rate, because stroke volume rose sharply early in recovery. The rise in stroke volume was chiefly a result of a significant decrease in end-systolic volume between 1 and 4 minutes of recovery. These changes may result from an immediate afterload reduction coupled with a relatively slow decrease in sympathetic stimulation. The time course of cardiac function during recovery from exercise in cardiac patients is substantially different from that of normal subjects and may be a sensitive way to evaluate the peripheral vascular function and deteriorated cardiac function in cardiac patients.     

Effectiveness of preload reserve as a determinant of clinical status in patients with left ventricular systolic dysfunction. The SOLVD Investigators.

The hemodynamic determinants of clinical status in patients with left ventricular (LV) systolic dysfunction have not been established. In the present study, preload reserve--LV distension during exercise--was related to clinical status, and the effect of acute angiotensin-converting enzyme inhibition was examined in 97 patients with ejection fraction less than or equal to 0.35 enrolled in the trial, Studies of Left Ventricular Dysfunction (SOLVD). Sixty-one asymptomatic patients (group I) were compared with 36 patients with symptomatic heart failure (group II). Radionuclide LV volumes were measured at rest and during maximal cycle exercise. Group II patients had higher resting heart rates, end-diastolic and end-systolic volumes, and lower ejection fractions (all p less than 0.005). During exercise, only patients in group I had increased stroke volume (from 35 +/- 8 to 39 +/- 11 ml/m2 [mean +/- SD; p less than 0.0005]) due to an increase in end-diastolic volume (from 119 +/- 29 to 126 +/- 29 ml/m2 [p less than 0.0005]), contributing to a greater increase in LV minute output (p less than 0.0001, group I vs group II). After administration of intravenous enalapril (1.25 mg), LV end-diastolic volume response to exercise was augmented in group II (rest, 140 +/- 42; exercise, 148 +/- 43 ml/m2; p less than 0.0005) and LV output response increased slightly (p less than 0.05). Thus, in patients with asymptomatic systolic dysfunction, recruitment of preload during exercise is responsible for maintaining a stroke volume contribution to the cardiac output response.(ABSTRACT TRUNCATED AT 250 WORDS)