Mechanisms of Cardiac Control in Exercise

Rushmer, Robert F.; Smith, Orville A.; Franklin, Dean

doi:10.1161/01.res.7.4.602

Cited by 177 publications

(43 citation statements)

References 61 publications

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“…These observations provide an interesting contrast with studies which have shown that SV does not fall with the tachycardia of exercise, even at rates faster than those in our study (6)(7)(8). The exercise response of stroke volume to tachycardia differs from the results of electrical pacing, although the EDV becomes smaller in both situations.…”

Section: )contrasting

confidence: 99%

The Influence of Heart Rate on Left Ventricular Volume in Dogs*

Bristow¹,

Ferguson²,

Mintz³

et al. 1963

J. Clin. Invest.

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The effects of changes in heart rate must be understood before ventricular performance can be evaluated in studies of the response to drugs, injury, or abnormal circulatory states. This report describes the effects of sudden changes in heart rate on the stroke, end-systolic, and enddiastolic volume of the canine left ventricle. The ventricular volumes were measured by thermodilution, an indicator dilution method in which injected cold blood serves as the indicator (1). METHODSThere were 160 experimental periods in 11 mongrel dogs that were anesthetized with a chloralose-urethane mixture. Aortic thermodilution curves were obtained after rapid injection of cooled autologous blood into the left ventricle. A 4F catheter with an ultrasmall bead thermistor secured to its end 1 was used to record blood temperature. It was introduced into a carotid artery and advanced so that its tip was just above the aortic valve. The time constant of this assembly was 0.12 second when tested in slowly flowing water. A 7F catheter with multiple side holes and a closed end was manipulated into the left ventricle from a femoral artery for injection purposes and to record left ventricular pressure with a strain gauge. A bead thermistor was secured within its lumen near the tip to monitor the temperature of the injected blood immediately before it entered the left ventricle. This assembly had a time constant of 0.05 second in flowing water. Inj ections were made with a metal syringe driven by compressed air that introduced a known amount, usually 3 to 5 ml, of cooled, heparinized, autologous blood into the left ventricle in less than 0.5 second. The mean temperature of the inj ected blood was determined by planimetry of the recorded temperature curve during injection. Stroke volume (SV), end-systolic volume (ESV), and end-diastolic volume (ED V) were calculated from the resultant aortic thermodilution curve sensed by the aortic thermistor catheter. The formulas used to calculate these volumes were:where Vi = volume of injected cooled blood in ml, Tb = left ventricular blood temperature before injection, T1 = mean temperature of injected blood, just before it entered the left ventricle, and 2;(ATb) = the sum of the differences between base-line aortic temperature and that resulting in the aorta from each systole, as measured at end-diastole;2) ES V/ED V = AT,+, ATn' where AT,, and AT,,+, are differences between base-line aortic temperature and that at beats n and n + 1, respectively, measured at end-diastole from the exponential step-function of the aortic thermodilution curve;3) SV ED V(ml) = ES V; EDV ESV(ml) = EDV -SV; 4) and 5) Cardiac output (L/min) = (heart rate) (S V)The details of this method have been published previously (1) -One to five determinations of left ventricular volumes, left ventricular pressure, and heart rate were made during each control and experimental period. Various heart rates faster than control were produced with a 6F electrode catheter passed up a femoral vein and placed fluoroscopically against the right...

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Section: )contrasting

confidence: 99%

The Influence of Heart Rate on Left Ventricular Volume in Dogs*

Bristow¹,

Ferguson²,

Mintz³

et al. 1963

J. Clin. Invest.

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“…The finding that the end-diastolic size of the heart usually does not increase and, in fact, most commonly declines (9,(27)(28)(29)(30)(31), has been used to support the view that the Frank-Starling mechanism does not play a role in the cardiac response to exercise (32). It is clear from the present study that induced tachycardia in the absence of exercise reduces ventricular dimensions to a greater extent than do similar changes in heart rate during exercise.…”

Section: Discussionsupporting

confidence: 70%

Effects of exercise on myocardial force-velocity relations in intact unanesthetized man: relative roles of changes in heart rate, sympathetic activity, and ventricular dimensions.

Sonnenblick¹,

Braunwald²,

Williams³

et al. 1965

J. Clin. Invest.

213

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It is generally agreed that an increase in cardiac output is one of the primary circulatory adjustments that occurs during exercise. However, the nature of the alterations in the activity of the myocardium that permit this augmentation of output and the relative importance in the response to exercise of the various factors known to affect the performance of the heart and its contractile state has not been defined. It has been shown that the contractile state of cardiac muscle may be characterized by the force-velocity relation (1-3). The applicability of this concept to isolated human heart muscle has recently been demonstrated (4), and a technique has been described by which the force-velocity relation of the myocardium of intact human subjects can be evaluated (5), thus allowing determination of the effect of a variety of interventions on the contractile state of the heart. The purpose of the present investigation was to apply this technique in studying the effects of exercise on the force-velocity relations of the human heart, to define the relative roles of the changes in heart rate and of sympathetic activity that occur during exercise on the force-velocity relation, and to delineate the role of changes in ventricular end-diastolic size in the response of the heart to exercise. MethodsTwelve studies were carried out in eleven patients ranging in age from 24 to 55 years (average = 44 years). All had undergone cardiac operations consisting of the closure of an atrial septal defect in six patients, closure of a ventricular septal defect in two, aortic valve re-* Submitted for publication April 22, 1965; accepted September 16, 1965. t Address requests for reprints to Dr. Edmund H. Sonnenblick, Cardiology Branch, National Heart Institute, Bethesda, Md. 20014. placement with a Starr-Edwards prosthesis in one, and mitral valvulotomy in two patients. At the time of cardiac operation small silver-tantalum markers were sutured to the right ventricle in seven patients, the left ventricle in two patients, and to the surface of both ventricles in two patients, as described in detail previously (6). Hemodynamic studies carried out 1 to 14 months postoperatively are summarized in Table I. The resting cardiac output was normal in all patients (> 2.50 L per minute per m2), as was the right atrial pressure, although the right ventricular end-diastolic pressure was slightly elevated in one patient (C.D.). The right ventricular systolic pressure was also slightly elevated in four patients (C.D., I.D., M.W., and S.C.).The techniques for determining ventricular end-diastolic dimensions and the force-velocity relation have been described in detail elsewhere (5). At the time of postoperative catheterization, cineradiograms were exposed at 30 frames per second while intraventricular pressures were recorded simultaneously at a paper speed of 100 mm per second. A mechanical marker, activated by the R wave of the electrocardiogram and recorded on the cineradiogram, permitted precise temporal correlation of ventricular dimension...

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“…This is well documented by the studies of Beattie et al (1930), Manning & Peiss (1958, 1960 and Rushmer et al (1959).…”

Section: Resultssupporting

confidence: 63%