Constancy of stroke volume in ventricular responses to exertion

1959 ◽  
Vol 196 (4) ◽  
pp. 745-750 ◽  
Author(s):  
Robert F. Rushmer

Diastolic and systolic dimensions of the left ventricle and the free wall of the right ventricle in intact dogs are affected little by spontaneous exercise. The concept that stroke volume and heart rate in normal man increase by about the same relative amounts was derived from estimations of cardiac output, particularly in athletes, based upon indirect measurements using foreign gases or CO2. Data for man obtained with the modern cardiac catheterization or indicator dilution techniques confirm the impression derived from intact dogs that increased stroke volume is neither an essential nor a characteristic feature of the normal cardiac response to exercise. Stroke volume undoubtedly increases whenever cardiac output is increased with little change in heart rate (e.g. in athletes or in patients with chronic volume loads on the heart). Tachycardia produced experimentally with an artificial pacemaker in a resting dog causes a marked reduction in diastolic and systolic dimensions and in the stroke change of dimensions. The factors generally postulated to increase stroke volume during normal exercise may prevent the reduction in stroke volume accompanying tachycardia.

2010 ◽  
Vol 25 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Donald U Robertson ◽  
Lynda Federoff ◽  
Keith E Eisensmith

Heart rate, heart rate variability, stroke volume, and cardiac output were measured while six college students and six professionals played trumpet. One-minute rest periods were followed by 1 minute of playing exercises designed to assess the effects of pitch and articulation. Heart rate and heart rate variability increased during playing, but stroke volume decreased. Changes in heart rate between resting and playing were greater for students, although beat-to-beat variability was larger for professionals in the upper register. These results suggest that expertise is characterized by greater physiological efficiency.


1979 ◽  
Vol 237 (3) ◽  
pp. R197-R202
Author(s):  
G. E. Barnes ◽  
B. C. Chevis ◽  
H. J. Granger

Interactions between heart rate (HR) and the Frank-Starling mechanism in augmenting cardiac output (CO) during acute volume loading were studied in dogs under varying conditions. In normal conscious dogs with low HRs of 70--90 beats/min, end-diastolic diameter (EDD) was maximal and CO was increased reflexly by cardioacceleration. By contrast, anesthetized open-chest dogs with high HRs ranging from 140 to 160 beats/min, responded with bradycardia and CO was adjusted solely by increasing stroke volume (SV). In anesthetized open-chest dogs with low HRs, EDD was less than maximal and increases in both HR and SV contributed to augment CO. These data show that both the cardioacceleration reflex and the Frank-Starling mechanism are important determinants of the cardiac response to elevated preload. Although the relative contribution of each control mechanism varies with initial conditions, their interplay extends the range of cardioregulation beyond that attainable by either loop operating alone.


1962 ◽  
Vol 202 (6) ◽  
pp. 1171-1174 ◽  
Author(s):  
Theodore Cooper ◽  
Teresa Pinakatt ◽  
Max Jellinek ◽  
Alfred W. Richardson

Hyperthermia of 40.5 C was induced in anesthetized white rats by microwave exposure (2,450-Mc continuous wave, .08 w/cm2). Thermal response was accompanied by increased cardiac output, stroke volume, cardiac work, and heart rate. Blood pressure and total peripheral resistance decreased. Administration of reserpine as a single dose of 2.5 mg/kg body wt. 1 day before the experiment depleted the myocardial norepinephrine, but did not eliminate the accelerated heart rate and increase of cardiac output during hyperthermia. Hyperthermia after reserpine did not alter significantly the stroke volume and blood pressure, and the peripheral resistance decreased. These data suggest that the circulatory adaptation to microwave hyperthermia is mediated not only through the sympathetic nervous system, but by other mechanisms such as direct cardiac response to the increased tissue temperature.


1965 ◽  
Vol 20 (3) ◽  
pp. 437-442 ◽  
Author(s):  
Harold Smulyan ◽  
Richard P. Cuddy ◽  
William A. Vincent ◽  
Udomporn Kashemsant ◽  
Robert H. Eich

The transient changes in cardiac output at the onset of mild exercise were measured in dogs trained to walk on a treadmill. Cardiac output was obtained using a krypton 85 infusion method, which permitted frequent determinations of flow. The first go sec of exercise were marked by a prompt rise and overshoot of heart rate and cardiac output, whereas increases in stroke volume occurred later after the onset of exercise, and to a lesser extent than heart rate. At rest, the right atrium was electrically driven at rates slightly faster than heart rates attained spontaneously with exercise and the studies repeated. Changes in cardiac output with exercise were similar to those in unpaced animals, but when the heart rate was fixed stroke volume increased immediately. These studies show a consistent rise in heart rate and cardiac output in the initial reaction to exercise, but when the prompt rise in heart rate was prevented by pacing from the right atrium, increases in stroke volume provided a comparable response in cardiac output. krypton 85; cardiac output; stroke volume; pacing of heart; oxygen consumption Submitted on September 23, 1964


1963 ◽  
Vol 205 (2) ◽  
pp. 393-400 ◽  
Author(s):  
David E. Donald ◽  
John T. Shepherd

Dogs with chronic cardiac denervation by the technic of regional neural ablation showed an unchanged capacity for work as measured by oxygen consumption. The relation of cardiac output to oxygen consumption during exercise remained unchanged from preoperational values. When the dogs started to run, the heart rate rose slowly over 1.5 min to reach a steady value proportional to the work performed. When exercise was stopped, the heart rate declined slowly. With mild exercise, the increase in cardiac output was mainly through stroke volume; with more severe exercise, increase in stroke volume and heart rate contributed equally, in contrast to the normal dog where the increase in rate predominates. Neither the pattern of the change in heart rate nor the plateau values were altered by adrenalectomy. The change in rate was not attributable to change in intravascular temperature. In an equivalent dose of base, norepinephrine caused tachycardia but little or no change in cardiac output, whereas epinephrine resulted in an increase in cardiac output with but a modest increase in heart rate.


1986 ◽  
Vol 251 (6) ◽  
pp. H1292-H1297 ◽  
Author(s):  
J. T. Shapiro ◽  
V. M. DeLeonardis ◽  
P. Needleman ◽  
T. H. Hintze

Little attention has been directed toward the action of atrial peptides on integrated cardiovascular function. In conscious dogs intravenous injection of atriopeptin 24 (10 micrograms/kg) reduced mean arterial pressure (11 +/- 3.2%), mean left atrial pressure (32 +/- 8.6%), left ventricular (LV) end-diastolic pressure (24 +/- 4.3%), and increased heart rate (25 +/- 6.2%). LV dP/dt and stroke volume increased 17 +/- 4.0 and 12 +/- 3.3%, respectively. Cardiac output increased 39 +/- 6.3%. These effects were only acute, lasting less than 10 min. The tachycardia and increase in LV dP/dt were abolished by combined beta-adrenergic and muscarinic cholinergic blocking agents. During an infusion of atriopeptin 24 (10 micrograms X kg-1 X min-1) blood flow, as measured with radioactive microspheres, increased to both the left (101 +/- 35%) and right kidney (122 +/- 37%) and to the spleen (140 +/- 50%). However, blood flow to the stomach, large and small intestine, pancreas, liver, and skeletal muscle did not change, indicating the selectivity of the atriopeptin. Blood flow in the right ventricle, septum, and in all layers of the left ventricle increased slightly, resulting in no change in the endocardial-to-epicardial blood flow ratio most likely due to the changes in myocardial function, i.e., heart rate and stroke volume. Thus, in conscious dogs, atriopeptins increase myocardial performance most likely indirectly secondary to baroreflex unloading after the direct hypotensive effects of atriopeptin 24. This serves to increase cardiac output at a time when renal and splenic blood flows are increased.


1989 ◽  
Vol 66 (2) ◽  
pp. 949-954 ◽  
Author(s):  
A. M. Rivera ◽  
A. E. Pels ◽  
S. P. Sady ◽  
M. A. Sady ◽  
E. M. Cullinane ◽  
...  

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.


1998 ◽  
Vol 275 (1) ◽  
pp. H322-H329 ◽  
Author(s):  
Kelly P. McKeown ◽  
Artin A. Shoukas

We have developed a chronic technique to isolate the carotid sinus baroreceptor region in the conscious rat model. Our technique, when used in conjunction with other methods, allows for the study of the control of arterial pressure, heart rate, and cardiac output by the carotid sinus baroreceptor reflex in conscious, unrestrained rats. The performance of our technique was evaluated in two strains: normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Each rat was instrumented with an aortic flow probe and a catheter placed in the right femoral artery to monitor cardiac output and arterial pressure, respectively. The cervical sympathetic trunk and aortic depressor nerve were ligated and cut bilaterally, leaving vagus nerves intact. The right and left carotid sinuses were isolated using our new technique. We tested the open-loop function of the carotid sinus baroreceptor reflex system in the conscious rat after recovery from the isolation surgery. We found that changes in nonpulsatile carotid sinus pressure caused significant changes in arterial pressure, heart rate, and total peripheral resistance in both rat strains. However, the cardiac output responses differed dramatically between strains. Significant changes were seen in the cardiac output response of SHR, whereas no significant changes were observed in normotensive SD rats. We have found this technique to be a highly reliable tool for the study of the carotid sinus baroreceptor reflex system in the conscious rat.


1973 ◽  
Vol 51 (4) ◽  
pp. 249-259 ◽  
Author(s):  
G. P. Biro ◽  
J. D. Hatcher ◽  
D. B. Jennings

The participation of the aortic chemoreceptors in the reflex cardiac responses to acute hypoxia is suggested only by the indirect evidence of pharmacological stimulation of these receptors. In order to assess their role more directly, the response to a 15 min period of hypoxia was determined after surgical denervation of the aortic chemoreceptors (A.D.), and compared with the response of sham-operated (S.O.) dogs, anesthetized with morphine–pentobarbital. In the control period, while breathing room air, the cardiovascular and respiratory parameters measured in the A.D. animals were not different from those of the S.O. dogs. Hypoxia (partial pressure of oxygen approximately 30 mm Hg) in the S.O. dogs was associated with a statistically significant rise in the heart rate (+71 ± 7 min−1, mean ± S.E.M.) and of the cardiac output (+25 ± 10 ml kg−1 min−1). In the A.D. animals, the significantly smaller increment in heart rate (+29 ± 6 min−1) was associated with a fall of the cardiac output (−16 ± 12 ml kg−1 min−1). The hypoxia-induced changes in heart rate and cardiac output in the S.O. animals were different (p < 0.05) from those in the A.D. group. The minute volume of ventilation was significantly augmented in both groups, and to a comparable extent. These findings indicate that the aortic chemoreceptors play a significant role in the cardiac response to hypoxia, but they do not affect, to a significant extent, the respiratory response.


1993 ◽  
Vol 71 (2) ◽  
pp. 136-144 ◽  
Author(s):  
Scott G. Thomas ◽  
Donald H. Paterson ◽  
David A. Cunningham ◽  
Douglas G. McLellan ◽  
William J. Kostuk

Studies of the cardiovascular response to exercise in older subjects have presented conflicting data regarding left ventricular function, the cardiac output – oxygen consumption [Formula: see text] relationship, and the pattern of change in [Formula: see text], stroke volume (SV), and arteriovenous O2 difference. We have examined the cardiovascular response to submaximal and strenuous exercise in 96 men of mean age 63 years during an incremental treadmill test with [Formula: see text] determined by CO2 rebreathing, and in 12 subjects studied during incremental supine exercise with left ventricular volumes evaluated by radionuclide angiocardiography. During treadmill exercise the [Formula: see text] was approximately 10% lower than reported for younger samples, with a lower intercept of the [Formula: see text] relationship. During near-maximal exercise [Formula: see text] was approximately 15 L∙min−1, with SV of 95 mL plateauing or showing a small decline in heavy work. Peak arteriovenous O2 difference (150+ mL∙L−1) approached values of the young. During the supine exercise SV increased from rest to exercise, with a consistent increase in ejection fraction (rest, 66%, to peak exercise, 76%). In contrast to a prior report, the end-diastolic volume was constant, with the increase of SV attributable to a reduced end-systolic volume. Also, in contrast to a number of reports in older subjects, our findings show only small losses in cardiovascular response, and in left ventricular performance during light through strenuous exercise.Key words: ejection fraction, stroke volume, arteriovenous oxygen difference, [Formula: see text]peak, age.


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