effects of isometric exercise on cardiac...

Effects of Isometric Exerciseon Cardiac Performance

The Grip Test

By CHARMLs Kivowirz, M.D., WILLIAM W. PARMLEY, M.D.,

ROBERTO DONOSO, M.D., HARoLD MARCUs, M.D., WrIAM GANz, M.D.,AND H. J. C. SwAN, M.D., PH.D.

SUMMARYTwenty-two patients with heart disease performed a standard isometric exercise,

sustained handgrip, during the course of diagnostic cardiac catheterization. Duringhandgrip an increase in mean arterial pressure (average 87 to 104 mm Hg) was notedin all patients. Coronary sinus blood flow and myocardial 02 consumption increased(average 45%) in all patients so monitored. Systemic vascular resistance increased in 19patients, in contrast to the response reported in normal volunteers. The relation betweenleft ventricular stroke-work index and LVEDP (left ventricular function curve) duringthe control state and during the fourth minute of sustained handgrip provided a simpleestimate of left ventricular reserve and correlated well with the New York HeartAssociation functional classification of the patient studied. Patients with good reserve

had a rise in stroke-work with little or no change in LVEDP. Patients with poor reserve

had a fall in stroke-work together with a substantial rise in LVEDP. It is concluded thatthe stress imposed by sustained handgrip provides a simple test for the evaluation of leftventricular reserve.

Additional Indexing Words:Left ventricular function Myocardial 02Force-velocity relations

A LTHOUGH cardiovascular function inmany patients with clinical heart disease

is apparently within the normal range, theapplication of a standardized stress will oftenreveal abnormalities. Stress tests that increaseoverall body metabolism, such as the Masters

From the Department of Cardiology, Cedars-SinaiMedical Center and the Department of Medicine,University of California at Los Angeles, California.

Supported in part by National Institutes of HealthGrants HE-05725 (training grant), HE-13297 (com-parative myocardial/force velocity relations), and U. S.Public Health Service 5-SOl-RR-05468 and the West-ern Cardiac Foundation.

Address for reprints: Charles Kivowitz, M.D.,Department of Cardiology, Cedars-Sinai MedicalCenter, 4833 Fountain Avenue, Los Angeles, Califor-nia 90029.

Received April 23, 1971; revision accepted forpublication July 27, 1971.

consumption Angiotensin infusion test

two-step test, or use of a treadmill or bicycleergometer, involve exercise of multiple groupsof large muscles, and have been of value inassessing cardiac performance and the natureand significance of chest pain.

In 1967, Donald et al.' demonstrated thatsustained isometric contraction, involving theextensor groups of the lower extremities atthe knee (leg pressure) or the flexor groups ofthe forearm at the elbow (sustained hand-grip) resulted in a marked increase in systolic,mean, and diastolic blood pressure. In thesenormal volunteers, this increase in arterialpressure was due primarily to an increase incardiac output associated with an increase inheart rate, with little change in stroke volumeor systemic vascular resistance. The increasein arterial pressure was surmised to maintain

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ISOMETRIC EXERCISE

blood flow through the muscles subject tostatic contraction.Because of the simplicity of handgrip as an

isometric exercise, the present study was

undertaken to evaluate its effect on thecardiovascular performance of patients withdifferent types and severity of heart disease.

MethodsTwenty-two patients were studied during

diagnostic right and left heart catheterization,which included left ventriculography and coro-

nary arteriography. There were 13 patients withcoronary artery disease, five with rheumatic heartdisease (three with significant mitral stenosis),and one patient each with essential hypertension,paroxysmal atrial fibrillation, Wolff-Parkinson-White syndrome, and aortic insufficiency due to a

congenitally bicuspid valve (table 1). Noselection criteria were applied to such patientsother than their physical ability to perform a griptest. Three other patients who were asked toperform this maneuver could not do so satisfactori-lv because of disability or poor cooperation and

were excluded from the study. Premedicationiprior to the study consisted of secobarbital 100mng.Each patient was asked to squeeze a handgrip

dynamometer (Jamar Dynamometer) at themaximal force he could develop for an instant.This measurement was taken as an estimate of themaximum voluntary contraction (MVC) of hisforearm mucles. Each patient was then asked tosustain his grasp on the dynamometer at 25% ofhis MVC for a period of 5 minutes. A normalventilatory pattern was observed in each patientthroughout the test period. Direct intravascularmeasurements of left femoral arterial pressure, leftventricular pressure, and the electrocardiogramwvere recorded on an Electronics for Medicinerecorder, in the control period, and at 1-, 2-, and3-min intervals of the grip test. Cardiac outputswere determined in duplicate during the controlperiod and between the third and fourth minutesof the grip test.

Left femoral arterial pressure was measuredthrough a no. 18 thin-wall Cournand needleinserted percutaneously into the left femoralartery at the left inguinal ligament. A preshaped

able 1

Classification of Patients Studied by Handgrip

Failure class CoronarySex Patient Age Diagnosis (NYHA) Angina class Old MI DIG LV size disease

m MP 48 CAD I Severe + - 1+ 3F VL 33 CAD I Severe + + Normal 3m JI 40 Hypertension I - - Normal 0m JB 46 CAD I Severe + - Normal 3

restm HL 23 WPW I - - Normal 0m\I MR 63 CAD I Moderate + - 3-+ 2m LS 33 PAF I - + Normal 0mI LO .34 CAD I Moderate + + Normal 2MI AS 20 AS,AL I - + 1+ 0m Cm 40 CAD II Severe + + Normal 3F BS 32 PHD, MS II - + Normal 0M HE 61 CAD II 9+ + 3+ 3M FM 31 RHD, MI, AI, CAD II + + 3+ 3m MR 52 CAD II + - 1+ 3M JH 46 CAD II + + LV aneurysm 1m JS 48 CAD II + + LV aneurysm 2m MK 67 CAD,MJ IIM- + + 3+ 3F CS 37 RHD, MS III -- + Normal 0m BC 70 CAD III None + + LV aneurysm 3F OM 67 RHD,M S III - + 1+ 2F EL 49 RHD, MS, MI, AI III - + 2+ 0m mmI 42 CAD III Moderate + - LV aneurysm 3

Abbreviations: CAD = coronary artery disease; WPW = Wolff-Parkinson-White syndrome; PAF = paroxysmalatrial fibrillation; RHD = rheumatic heart disease; AS = aortic stenosis; AI = aortic insufficiency; MS = mitralstenosis; MI = mitral insufficiency.Circulation, Volume XLIV, December 1971

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no. 8 polyethylene ventricular catheter was insert-ed by percutaneous technique via the right fe-moral artery and passed retrograde into the cavityof the left ventricle. All pressures were measuredby equisensitive Statham P23DB strain gauges.Measurements of coronary sinus blood flow wereobtained according to the technique of Ganz andassociates2 in eight patients by means of a specialthermistor catheter inserted through the leftbrachial vein at the antecubital fossa andpositioned within the coronary sinus. Coronarysinus blood flow was measured by thermodilutiontechniques during the control period and duringthe fourth minute. Samples of arterial andcoronary sinus blood for P02 and lactate con-centration were obtained. Cardiac output wasmeasured by dye-dilution technique with injec-tion of indocyanine green into the pulmonaryartery or coronary sinus and sampling from theleft femoral artery. Determination of arterialsystolic, mean, and diastolic blood pressure, leftventricular peak systolic, and end-diastolic pres-sures (LVEDP) were made directly from theanalog tracing. Electronic differentiation of leftventricular pressure provided continuous dp/dtfrom which maximum dp/dt was measured. Thesystem used allowed accurate determination ofdp/dt to a value of 4,000 mm Hg/sec.Calculations of cardiac index, stroke index, leftventricular stroke-work index (LVSWI), systolicejection rate, and systemic vascular resistancewere made from standard formulae. Myocardialoxygen consumption index (cc/min) was calcu-lated as the product of coronary sinus blood flow(ml/min) and systemic artery-coronary sinusblood oxygen difference (ccO2/ml blood).

Force-velocity relations were calculated fromthree successive contractions, utilizing simulta-neous left ventricular pressure and dp/ dt at 10-msec intervals during isovolumic systole, employ-

ing the formula: V(E dp/dt .3 P was developedIl KPpressure, appropriate to the three-componentMaxwell model of muscle.4 The series elastic con-stant K was assumed to be 32,5 and Vmax wasestimated by linear extrapolation to zero devel-

oped pressure. Because p/d goes to infinityKPat zero developed pressure, calculations of VCEwere made only at developed pressures of 5 mmHg and above. The error imposed in the calcula-tion of Vmax in the present study was estimatedaccording to the method of Falsetti et al.6The frequency response of the catheter-mani-

fold-transducer system employed was analyzed byapplication of a square wave pressure transient,equivalent to approximately 150 mm Hg, to thesystem with the catheter acting as a vent. The

output of this response was amplified, electronic-ally filtered above 10 Hz at 6 Db per octave,and recorded at 100 mm/ sec. The resonantfrequency of the system was determined from therecorded waveform and found to range from 8 to22 Hz. The fraction of critical damping rangedfrom 0.4 to 0.2, respectively. The error incalculated Vmax for such a system is approxi-mately +15%, which compares favorably with themagnitude of error previously reported by fluid-filled catheter systems.6

Results

Sequential measurements during the griptest are illustrated in a representative patientin figure 1. This 40-year-old man had coronaryartery disease with angina pectoris, an oldmyocardial infarction, and minimal symptomsof congestive heart failure. During the hand-grip his mean arterial pressure rose from 80 to126 mm Hg, together with an increase in heartrate, cardiac index, systemic vascular resis-tance, left ventricular end-diastolic pressure,and coronary sinus blood flow. After release ofthe handgrip, arterial pressure returned tocontrol values within 5 to 10 sec.A detailed tabulation of the results in all

patients studied are listed in table 2. With thehandgrip, heart rate increased from 73 + 3 to82 + 3 beats/min (P < 0.01) during the fourthminute of isometric handgrip. There wereaverage increases in systolic, mean, anddiastolic blood pressure of 22, 17, and 12 mmHg, respectively. In six patients the coronarysinus blood flow increased by an average of23% (16 to 39%). In two other patients (C.M.shown in figure 1 and M.P.) the increase was124 and 151%.

Since the A-Va., difference across the heartdid not change significantly, there was asimilar increase in myocardial oxygen con-sumption. There was myocardial extraction ofblood lactate both at rest and during handgripin five patients. None of the patients withcoronary artery disease developed anginapectoris during the grip test. One patientdeveloped a short period of bigeminy. Noother arrhythmias or complications wereobserved.Left ventricular function curves were calcu-

lated by relating LVSWI to LVEDP for theCifculation. Volume XLIV, December 1971

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INDIVIDUAL RESPONSE TO HAND GRIP

PATI ENTCM.

180

120

60

0ClSVRCSF

C-5r-

1 2' 3' P-,- r

yUy

y y I -L ySBPy 1 1

- j T A ±MBPA> -iA ADBP

*.0.0 .-@@@*@'- 0LVEDP

2.45147190

3.621570202

Figure 1

An individual response to sustained handgrip. Ab-breviations and units as in table 2.

control period and after 3 to 4 min of hand-grip. Figure 2 plots the average results inthree groups of patients, separated on thebasis of the New York Heart Associationfunctional classification. Patients with coro-nary artery disease were classified on the basisof their symptoms of congestive heart failureand not on the presence of angina. The pa-tients with mitral stenosis were excluded andwill be discussed later. The tail of the arrowdesignates average control results for eachgroup, whereas the arrowhead plots averageresults during handgrip. The nine patients inclass I increased LVSWI with a slight increasein LVEDP. Five patients with class II symp-toms had a higher initial LVEDP and in-creased LVSWI to about the same degree asclass I patients, but with a greater increase inLVEDP. The three patients with class IIIsymptoms had a slight decrease in LVSWI,which was associated with a large increase inLVEDP.The general correlation between symptom

class and hemodynamic response to handgripis evident. The individual response of eachpatient, however, was of greater interest. Forexample, figure 3 includes all nine patientsCirculation, Volume XLIV, December 1971

W 800

C)

2-J

= 6031'l- 400

V) 20

I

NYHA CLASS -*

TT

2 10 20 30LV END DIASTOLIC PRESSURE

Figure 2

Left ventricular functional relationships of patientswith coronary artery disease, segregated according toNew York Heart Association classification. Abbrevia-tions and units as in table 2.

with coronary artery disease who had acontrol LVEDP in the high-normal range (12to 17 mm Hg). There were four patients whohad a rise in LVSWI in response to thehandgrip, together with a fall in LVEDP.Similarly, two patients had a rise in LVSWI,together with a slight increase in LVEDP.Three patients, however, had a decline inLVSWI, together with large increases inLVEDP to near pulmonary-edema levels.

XLUJC)Z

'CX

03,

-JJ

...-0X

CD

8070605040302010

%t-1. LV RESERVE%A GOOD -V POOR-

ra - -.F

ALL PATIENTS WITH INITIAL LVEDP12-17 mmHg

10 20 30 40 50LV END DIASTOLIC PRESSURE

Figure 3Left ventricular functional relationship of individualpatients with coronary artery disease and initialLVEDP between 12 and 17 mm Hg. Abbreviationsand units as in table 2.

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Table 2Hemodynamic Measurements before and during the Fourth Minute of Sustained Handgrip

Patient HR Rhythm BP S/D BP LVED Max dp/dtMP

VL

Controlfourth min

JM

JB

HL

MR

LS

LO

AS

CM

BS

HE

FM

MR

JH

JS

MK

CS

BC

OM

EL

MM

Mean

Mean

Before

AfterSE

SEPaired-t

6173919184917592899860746684747371856880

72666067709284816675859576837579697361655872101114732.4822.6

P <.01

RSRRSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

RSR

AF

RSR

142/72170/79139/82150/83165/93182/97113/67140/79110/67127/80127/58193/81123/70165/9682/5287/55144/85168/96125/60184/89188/80180/7568/3588/47

128/55169/78137/75147/78110/60128/74107/63123/77159/70156/78110/53125/65110/50128/68117/50140/55165/87182/89116/61151/92127/665.9/3.0149/786.3/2.9P < 0.01

103127101110111

1258610484978111888

12263

6510513580

126115110466079106971007792789210311480857088708511312779

112873.7

1044.5

P <0.01

1628541616121767

223313128

1012111218

161922292846171630312331163889

121215147

102737161.5

212.5P < 0.01

6311445130914601070116013931250160921361554393013331951

1235

176026121230152515681344655683941115822852199637608915953133013351333148010801040880105612781464117014151237

85.41534156.3

P <0.05Units and abbreviations: HR = heart rate: beats/min; BP = blood pressure; S/D = sytolic/diastolic; BP= mear

blood pressure: mm Hg; LVED = left ventricular end-diastolic pressure: mm Hg; Max dp/dt = maximum dp/dt: mirHg/sec; Vmax = maximum velocity of contractile element shortening: muscle lengths/sec; CI = cardiac index: litersyminim2; LVSWI = left ventricular stroke-work index g-m/m2; SVR = systemic vascular resistance: dyne-sec-cm-5CSF = coronary sinus blood flow: m/min; A-VO0 = arterial coronary oxygen content diference; MV2= myocardiaoxygen consumption: ml/min; Art. lactate = arterial lactate concentration: mM/ml; CS lactate = coronary sinus lactateconcentration: mM/ml.

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Vmax CI sI LVSWI SVR CSF A-V02 AMIVo2 Art. lactate CS lactate

1.6 3.553.52

1.8 2.7a3.48

2.3 3.563.83

2.0 2.492.86

2.1 4.354.30

1.63 2.192.90

1.6 2.412.832.713.184.073.08

1.8 2.453.624.022.45

1.8 2.002.08

1.6 4.044.06

2.7 3.603.10

1.6 3.433.37

1.0 3.693.73

1.45 2.22.3

3.0 3.803.37

1.8 2.482.13

1.5 1.711.60

1.7 1.71.8

1.56 3.23.130.230.2NS

59 8348303842423331494437393633364458603645563733315743313852454439282751433629282329253228412.2

381.9NS

73476471783948616341654658323989

10745821046316196034403639484038463360563734303352483033504.7

5154.5NS

1187147817921543121512701421132871883814061547149717651037912110211371471157013212070981

12,5179410581384135610131232903105219072161103212362538371621782821311733879a813781417126.1

1650141.6P <0.01

96 13.4 14.8 8.1 7.5241137163107123112183

170198

14.714.615.313.516.313.213.2

16.116.5

90 13.3.5202 14.3

146183

13.013.2

127 13.9135 15.0123 15

9.6 0.4179 1613.4 0.4P < 0.01 NS

35.22021516.520.114.724.2

27.332.7

13.928.8

116.

10.110.3

5.65.8

12.714.8

10.6

8.08.6

2.92.8

11.213.3

1924.2

17.6 5.5 5.122 7.0 7.418 8.4 6.91.3 1.4 1.4

27 9.9 8.51.8 1.6 1.8P < 0.01 P <0.0O P < 0.05

Figure 4 illustrates the average comparative and for the three patients with significantchanges in cardiac index, mean arterial mitral stenosis. In response to handgrip, thepressure, and systemic vascular resistance for patients with mitral stenosis developed onlypatients grouped according to symptom class, 10% increase in arterial pressure, as comparedCirculation, Volume XLIV, December 1971

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NEW YORK HEART ASSOCIATION CLASSIFICATIONAND MITRAL STENOSISI TT mitral stenosis

35

30

210

C-)

EU mean BP

-20 - cardiac indexsystemic vascularresistance

Figure 4

Changes in mean blood pressure, cardiac index, andsystemic vascular resistance of patients with coronaryartery disease segregated according to New YorkHeart Association classifications and with significantmitral stenosis.

with a 20 to 25% increase in the other threegroups. The increase in arterial pressure inmitral stenosis was produced by a largeincrease in systemic vascular resistance, sincethere was a moderate decline in cardiac index.In the patients with mitral stenosis, theaverage LVEDP (13 mm Hg) did not changewith handgrip. The obstruction at the mitralvalve probably prevented an increase incardiac output, so that arterial pressure was

increased predominantly by an increase insystemic vascular resistance. Thus, the hemo-dynamic response to the grip test may bedifferent in patients with obstructive valvularheart disease and must be interpreted accord-ingly.There was also a general correlation be-

tween the response to the handgrip andindices of contractile state (tables 3 and 4). Inthe five patients with a control maximumdp/dt greater than 1,400 mm Hg/sec, LVSWIincreased, together with a slight increase inaverage LVEDP (table 3). In the 11 patientswith a maximum dp/dt between 1,000 and1,400 mm Hg/sec, there was an increase inLVSWI from 46 to 52 g-m/m2, accompaniedby an increase in LVEDP from 12 to 17

Table 3

Relation of Maximum dp/dt to LV Reserve

Initial max dp/dt LVSWI LVEDP(mm Hg/sec) N (g-m/m2) (mm Hg)

> 1400 5 61 1577 17

1000- 1400 11 46 1252 17

600- 1000 6 48 2248 30

Patients are divided on the basis of their controlmaximum LV dp/dt. The average values of LVSWIand LVEDP are indicated for each group before andduring the fourth minute of handgrip.

mm Hg. In the six patients with a maximumdp/dt between 600 and 1,000 mm Hg/sec,LV stroke-work index was unchanged, where-as average LVEDP rose from 22 to 30 mmHg.

Similar results were evident in the correla-tion between Vmax and the response tohandgrip (table 4). For example, the fourpatients with a control Vmax greater than 2.0muscle lengths/sec had an increase in LVSWIwith no change in average LVEDP. The 11patients with a Vma, between 1.5 and 2.0muscle length/sec had an average increase inLVSWI from 46 to 54 g-m/m2, but this wasaccompanied by a rise in LVEDP from 17 to25 mm Hg. The four patients with a V.,xbelow 1.5 muscle lengths/sec had no changein LVSWI, but increased LVEDP from anaverage of 18 to 24 mm Hg.

Table 4

Relation of V,, to LV Reserve

Initial Vmax LVSWI LVEDP(muscle lengths/see) N (g-m/m') (mm Hg)

>2.0 4 58 1263 12

1.5 - 2.0 11 46 1754 25

<1.5 4 40 1840 24

Patients are divided on the basis of their controlVmax. The average values of LVSWI and LVEDP areindicated for each group before and during the fourthminute of handgrip.

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DiscussionThis study indicates that the isometric

exercise associated with sustained handgripprovides a substantial stress to the leftventricle. The hemodynamic changes noted inthe present study, however, were slightlydifferent from the previous investigations innormal volunteers.' Though arterial pressureelevations were similar in the normal volun-teers and in our patients, the systemic vascularresistance was unchanged in the normalvolunteers,1 but it increased substantially inmost of our patients. Although the commonresult of both groups was an elevation ofarterial pressure, the normal volunteers raisedtheir blood pressure solely by increasingcardiac output, whereas our patients withcoronary artery disease without failure andwith mild heart failure (class I and II)showed a rise in both cardiac output andsystemic vascular resistance (fig. 2). In thepatients with more severe heart failure (classIII) cardiac index declined, but arterialpressure was elevated by a marked increase insystemic vascular resistance. Similarly, thethree patients with mitral stenosis also had amoderate decline in cardiac index, but wereable to elevate their arterial pressure becauseof a substantial increase in systemic vascularresistance. In patients with significant mitralregurgitation, it would be expected that anincrease in aortic pressure might worsen thedegree of regurgitation and tend to reduce theforward stroke volume.The exact mechanism of the cardiovascular

response to isometric exercise is not clear. Areflex increase in cardiac output is apparentlythe first mechanism used to increase arterialpressure. In those patients with a reduction inventricular reserve, however, a further in-crease in vascular tone is also required to raisearterial pressure. Further, clarification of thisprocess awaits study by blocking the responseto isometric exercise with pharmacologicagents.The relation between left ventricular per-

formance (stroke volume or stroke-work) andpreload (LVEDP) describes the left ventricu-lar function curve. Patients with normalCirculation, Volume XLIV, December 1971

function generally have an increase in ventric-ular performance with an increase in preload,but patients with heart disease have little orno change in ventricular performance with anincrease in preload.7 The results of the presentstudy conform to this general pattern. Theresponse to handgrip, however, appears to bemore than just an increase in preload inresponse to the increase in arterial pressure.Thus, the increase in stroke-work or strokevolume associated with a decrease in LVEDPin some patients suggests an increase in con-tractile state, presumably mediated throughthe cardiac sympathetic nerves. Furthermore,the increase in heart rate that occurred despitean increase in arterial pressure suggests thatan increase in sympathetic tone predominatedover the baroreceptor-induced increase invagal tone, which usually decreases heart rate.The use of angiotensin to increase vascular

resistance reported by Ross et a18 yields asimilar estimate of ventricular reserve. Theyalso noted that those patients with the bestventricular reserve increased LVSWI withlittle or no change in LVEDP in response toan increased afterload. Conversely, thosepatients with poor left ventricular reserve hada decline in LVSWI and an increase inLVEDP. Although the results are similar, thesimplicity of the handgrip stress test appearsto favor its use as an LV function test whencompared to the constant intravenous infusionof angiotensin or other drugs. Since the effectsof handgrip disappear within a few secondsafter release, untoward and potentially dan-gerous responses such as angina and arrhy-thmia can be relieved almost immediately. Aswith any stress test, however, equipment forimmediate resuscitative measures must bepresent since the substantial stress of the griptest can conceivably be associated with a life-threatening event. In those patients who areunable to perform the handgrip test eitherbecause of disability or inability to cooperate,a standard pharmacologic test, such as infusionof angiotensin, may be useful.The handgrip test has recently been used as

a tool in the clinical evaluation9' 10 of heartsounds and heart murmuis. During handgrip,

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auscultation may reveal third and fourth heartsounds which were absent at rest. Thelarge increase in left ventricular end-diastolicpressure seen in some patients means thattheir ventricles are poorly compliant in thatrange. Therefore, blood entering the ventriclewith the opening of the mitral valve or withatrial systole can produce a third and/orfourth heart sound.The marked increase in coronary blood flow

and myocardial oxygen consumption pro-duced by handgrip indicates the magnitude ofthe stress imposed upon the heart by isometricexercise. Since there was no lactate productionor episode of angina pectoris seen during thegrip test in these patients, the secondarycoronary vasodilatation was presumably ade-quate to meet the increased oxygen needs.However, in patients with severe coronarydisease, it is conceivable that the grip testcould precipitate an episode of sustained chestpain or an ischemia-induced arrhythmia.Furthermore, the results of the present studyunderscore the potential danger of isometricexercise in any patient with serious heartdisease. Predominantly isometric exercise,such as shoveling snow or lifting heavyobjects, long associated with cardiac catastro-phe, can easily produce episodes of conges-tive heart failure or pulmonary edema insusceptible patients and should be avoided.

References1. DONALD KW, LIND AR, FLUE D, MCNICOL

GW, HUMPHREYS PW, TAYLOR SH, STANTON

HP: Cardiovascular responses to sustainedstatic contraction. Circ Res 21: 1, 1967

2. GANZ W, TAMURA K, MARCUS HS, DONoso R,YOSHIDA S, SWAN HJC: Measurement of coro-nary sinus blood flow by continuous thermo-dilution in man. Circulation 44: 181, 1971

3. URSCHEL CW, VOKONAS PS, HENDERSON AH,LIEDTKE AJ, HoRwIrz LD, SONNENBLICK EH:A comparison of indices of contractility derivedfrom isovolumic force-velocity relation. (Ab-str) Circulation 42 (suppl III): III-115, 1970

4. PARMLEY WW, SONNENBLICK EH: Reevaluationof Vmax as an index of contractile state: Ananalysis of different muscle models. (Abstr)Circulation 42 (suppl III): III-115, 1970

5. YEATMAN LA JR, PARMLEY WW, SONNENBLICKEH: Effects of temperature on series elasticityand contractile element motion in heart muscle.Amer J Physiol 217: 1030, 1969

6. FALSErrI HL, MATES RE, GREEN DG, BUNNELLIL: Vmax as an index of contractile state inman. Circulation 43: 467, 1971

7. Ross J JR, BRAUNWALD E: Studies on Starling'slaw of the Heart. IX. Effects of impedingvenous return on performance of normal andfailing left ventricle. Circulation 30: 719,1964

8. Ross J JR, BRAUNWALD E: The study of leftventricular function in man by increasingresistance to ventricular ejection with angioten-sin. Circulation 29: 739, 1964

9. STONECIPHER HK, SIEGEL W, GILBERT CA,NUTrER DO, SCHLANr RC, HURST JW:Response of heart murmurs to isometrichandgrip exercise. (Abstr) Circulation 42(suppl III): Ill-30,. 1970

10. MATTHEWS OA, BLOMQVIST CG, COHEN LS,MULLINS CB: Left ventricular function duringisometric exercise (handgrip): Significance ofan atrial gallop (S4). (Abstr) Circulation 42(suppl III): III-31, 1970

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HAROLD MARCUS, WILLIAM GANZ and H. J. C. SWANCHARLES KIVOWITZ, WILLIAM W. PARMLEY, ROBERTO DONOSO,

Effects of Isometric Exercise on Cardiac Performance: The Grip Test

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1971 American Heart Association, Inc. All rights reserved.

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