alterations circulatory response to exercise following...

Alterations in the Circulatory Responseto Exercise Following a Meal

and Their Relationshipto Postprandial Angina Pectoris

By ROBERT E. GOLDSTEIN, M.D., DAvm R. REwOOD, M.B., M.R.C.P.,DOUGLAS R. ROSING, M.D., G. DAVID BEISER, M.D.,

AND STEPHEN E. EPSTEIN, M.D.

SUMMARYIn order to study the mechanisms responsible for the more rapid precipitation of

angina in the postprandial state, we evaluated the circulatory response to uprightbicycle exercise in 12 patients with angina before and after a meal. Eleven of 12subjects developed angina sooner after eating (average 1.3 min, P < 0.001). Com-parison of circulatory responses revealed that a given amount of postprandial exerciseresulted in faster heart rate (12 beats/min, P < 0.001) and greater blood pressure(6 mm Hg, P < 0.05). The product of blood pressure and heart rate (an index ofmyocardial oxygen demand) at onset of angina during postprandial exercise was thesame as corresponding preprandial values. Our results suggest that the accelerated de-velopment of angina during exercise after meals is primarily due to a more rapid rise inheart rate and blood pressure, factors tending to augment myocardial oxygen require-ments, rather than the result of a deleterious effect of digestion and absorption on

myocardial oxygen delivery.

Additional Indexing Words:Myocardial oxygen requirements

S INCE THE writings of Heberden,' physi-cians have recognized that patients with

angina pectoris experienced a decrease inexercise capacity following the ingestion of ameal. The exercise studies of Wayne andGraybiel2 documented this phenomenon.Moreover, evidence that ischemic electrocar-diographic abnormalities may be precipitatedor exaggerated after a meal3-5 suggested thatthe postprandial state predisposes to myocar-dial ischemia.

From the Cardiology Branch, National Heart andLung Institute, Bethesda, Maryland 20014.

Address for reprints: Dr. Goldstein, CardiologyBranch, National Heart and Lung Institute, Bldg. 10,Room 7B-15, Bethesda, Maryland 20014.

Received November 12, 1970; revision accepted forpublication March 24, 1971.

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Despite the fact that the reduction inpostprandial exercise capacity in angina pa-tients has long been recognized, the physiolog-ic basis for this phenomenon has remaineduncertain. Studies in normal subjects,68 inpatients,9 and in animals0'11 have led someinvestigators to postulate a postprandial im-pairment of myocardial oxygen delivery andothers to suggest a postprandial augmentationof myocardial oxygen requirements (MV02).Results obtained in animals or in subjects notexperiencing angina, however, do not neces-sarily reflect similar changes occurring duringexercise in patients with angina. More impor-tantly, such studies do not permit an assess-ment of the role that altered coronary flow'1or possibly diminished oxygen transport8s9may play in the genesis of postprandial

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POSTPRANDIAL EXERCISE AND ANGINA PECTORIS

angina. Our study was designed to explore thephysiologic basis of the more rapid precipita-tion of angina after meals by measuringchanges in an index of MVO2 prior to andprecisely at the onset of angina. Since anginaoccurs when MVO2 exceeds the capacity ofthe coronary vessels to deliver oxygen, adecrease in an index of MVO2 at anginawould be consistent with a postprandialreduction in myocardial oxygen delivery.Alternatively, lack of change of MVO2 indexat angina after meals would tend to excludethis possibility, and would suggest instead thatdeterioration in postprandial exercise capacityis related to an increase in exercise-inducedmyocardial oxygen demands.

Unfortunately, techniques currently used tomeasure coronary flow preclude rapid repeti-tive measurements of MVO2 in patientsexercising in the upright position. Studies ofthe relationship of MVO2 to hemodynamicvariables,'2-14 however, have led to the use ofthe product of blood pressure, heart rate, andejection time as an index of MVO2.15' 16Detailed evaluation has demonstrated thatthis index is invariant at onset of angina withchanges in exercise load'5 or with theperformance of multiple serial exercise trials.'6This index has also been successfully appliedin analysis of the physiologic basis of a varietyof circumstances tending to precipitate angi-na'7-21 and in clarification of the action ofseveral types of therapeutic interventions.21-26The present study represents an extension ofthis same methodology as well as the use of auniquely sensitive exercise testing protocol'6to analyze another heretofore unexplainedaspect of angina, namely its more rapidprecipitation after meals.

MethodsStudies were conducted in 12 patients ranging

in age from 31 to 61 years (median, 51). Eachgave a history typical of exertional angina, andeach had greater than 70% occlusion of one ormore coronary arteries on cineangiography. Amore complete clinical description is furnished intable 1. None manifested clinical evidence ofovert congestive heart failure or hypertension.Four patients were receiving digitalis at the timeof study. Four patients had hyperbetalipoprotein-Circulation, Volume XLIV, July 1971

emia, but none had diabetes or abnormnaltriglyceride levels. Propranolol and long-actingnitrates were discontinued several days prior tostudy. Patients refrained from cigarette smokingon the day of study.

Three or more hours after a light breakfastpatients exercised on a constant-load uprightbicycle ergometer (Godart) until the onset ofangina. Work load was increased 20 w every 3min; work load at outset was chosen individually(on the basis of prior exercise performance) sothat each patient developed angina after 3 to 6min of exercise in the fasting state. Bloodpressure, measured directly in either the brachialartery or in the thoracic aorta, and theelectrocardiogram (lead CM-5) were recordedcontinuously throughout the study. Measurementsof ejection time were made only in thoseindividuals who had aortic catheterization. Infour individuals cardiac output was measured bydye-dilution technique several times during thecourse of exercise. After two initial periods ofexercise, patients ate a noon meal of approximate-ly 1000 calories containing about 20% protein, 40%carbohydrate, and 40% fat. Caffeine-containingbeverages were excluded. Patients were instructedto eat at their own pace. They required 15 to 30min to consume the meal. A variable number ofexercise trials were performed in the postprandialstate, beginning immediately upon finishing themeal. A minimum of 15 min elapsed between anytwo successive exercise trials.

Results obtained in this laboratory whenrepeated exercise trials were performed in theabsence of any intervention have been publishedpreviously.'6 Participants in the control serieswere clinically very similar to those in the presentstudy (seven patients actually participated inboth studies). Patients were thoroughly familiar-ized with bicycle exercise in the laboratory, as inthe present study, and with each exerciseaccording to the protocol just described. Each ofnine patients experienced the onset of anginaafter nearly the same duration of exercise evenwhen performing as many as five bouts of exercisewithin a 2-hr period-the longest individualdeviation in the duration of exercise to angina(subsequently called "exercise capacity") was 70sec. On the average, exercise capacity was greaterby 21 sec when the second exercise trial wascompared with the first. No further change inexercise capacity was demonstrable with subse-quent exercise trials. The product of bloodpressure, heart rate, and ejection time at the onsetof angina remained virtually unchanged for agiven patient throughout the course of the serialexercise trials. The constancy of this index ofMVO2 at onset of angina was equally true foreach individual regardless of the absolute value of

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Table 1Clinical Data of Patients

Duration of symptoms Previous myocardialPatient Age Sex (yr) infarction ECG

A.M. )9 AI 7 Yes Old diaph. MIG.W. 52 m 3 No LVHP.D. 46 m 7 Yes Ischemic S-T chanige

O.H. 61 m 12 Yes Old ant. MI

F.C. 53 m 18 Yes Old diaph. MIL.G. 30 M 212 Yes Old diaph. MI; old ant. MID.L. 35 m 3 Yes Old diaph. MI

E.O. 40 m 2 Yes Old ant. and diaph. MI

P.B. 49 M 1 Yes NormalA.D. 3a M 9 Yes Old diaph. MIS.W. 35 M 7 Yes Old dipah. MIJ.W. 40 M 7 Yes Old ant. MI

Abbreviations: MI = myocardial infarction; CSNS = electrical stimulation of carotid sinus nerves; LCF = left cir-cumflex coronary artery; RCA = right coronary artery; TNG = nitroglycerin; TVD = triple vessel disease: ant. = an-terior; diaph. = diaphragmatic.

*Stenosis and triple vessel disease refer to areas of niarrowing in excess of 73C .tPreprandial values.

the index. These findings agree closely withresults of similar exercise testing performed inanother laboratory.'5 They also furnish the controldata for the present study. On the basis of thesedata, changes in exercise capacity or in the indexof MVO2 during exercise after the meal (that is,during the third or subsequent exercise trial) willbe ascribed to some consequence of ingesting ameal rather than to the effects of performingserial exercise trials.

For each parameter, comparisons were madebetween postprandial performance and corre-sponding measurements made during the secondpreprandial exercise. Performance did not differconsistently between the first and second pre-prandial exercises. In evaluating postprandialchanges in the circulatory response to exercise,measurements made during exercise at the onsetof angina in the postprandial period werematched with corresponding measurements madeduring exercise after an equal amount ofpreprandial exercise (generally before the onsetof angina). The onset of angina was neverassociated with an abrupt change in any of theparameters measured-selection of data a fewseconds prior to the onset of angina rather than atthe actual point of onset would have had noinfluence on the values reported.

ResultsComparison of individual performances

before and immediately after a meal (fig. 1)revealed a highly significant decrease inpostprandial exercise capacity. Nine of the 12patients experienced angina at least 1 minsooner. The two patients who had virtually nodecrease in exercise capacity immediatelyafter eating both exhibited decrements exceed-ing 1 min on repeated testing 20 min later.Four of the 12 patients showed ischemicelectrocardiographic abnormalities in themonitored lead (1 min or more of flat S-Tdepression) when tested preprandially. Ineach instance the onset of ischemic changeswas hastened after eating, the correspondingchanges developing an average of 2.0 minsooner immediately after the meal. A similaracceleration of the onset of ischemic changesoccurred in the two patients receiving digitalisand in the two not receiving digitalis. Thetime course of exercise capacity was followedfor more than a half hour in six patients (fig.2). In each instance the decrease in postpran-dial exercise capacity persisted throughout thetesting period with only slight evidence ofrecovery. Three of the patients did not attainmaximum reduction in exercise capacity until

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Work load at anginatLV cine Coronary angiography* (watts) Therapy

Normal TVD 40 TNG; digitalisNormal TVD 40 Propranolol; digitalis; TNGParadoxical movement at apex; TVD 40 TNGakinesia of anterolateral wallPoorly contracting LV; TVD 60 Digitalis; diuretic; CSNSakinesia of apexNormal TVD 80 Digitalis; diuretic; CSNSPoorly contracting LV TVD 60 TNGDyskinesia of diaph. wall Total occlusion RCA; stenosis 80 TNG

obtuse marginalNormal Total occlusion RCA; 90 TNG

stenosis LCFNormal TVD; total occlusion LCF 70 TNGInferior akinesia TVD 60 Digitalis; TNGNormal TVD; total occlusion RCA 40 TNGLateral dyskinesia TVD 60 TNG

PREPRANDIAL

Figure 1

POSTPRAN D IAL

Comparison of exercise capacity before and immedi-ately after a meal. Individual preprandial perfor-mances (left) are connected by lines to correspondingpostprandial performances (right). The average decre-ment, 1.3 min, is denoted by the two circled bars.Dashed lines indicate 3-min intervals when work loadwas increased.


the second postprandial trial 20 min after themeal.

In order to evaluate the possible reasons forthis postprandial deterioration of exercisecapacity and the associated acceleration ofonset of ischemic electrocardiographic abnor-malities, we examined the circulatory responseto exercise immediately before and immedi-ately after eating (table 2). In each patient

tttiEi0066

0-

0 2 3TIME AFTER MEAL (hr.)

Figure 2Time course of exercise capacity for six individualsexercised serially for more than a half hour after themeal. Individual preprandial exercise capacity, to theleft of the stippling, is connected to values of ex-ercise capacity for the same patient determined serial-ly after the meal. Time scale in the postprandialperiod is shown at the bottom. Dashed lines denotetime when work load was increased.

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Table 2Hemodynamic Values During Pre- and Postprandial Exercise

Mean blood Ejection Mean blood pressureLoad Time Heart rate pressure time X heart rate

Patient (w atts) (min) (beats/min) (mm Hg) (sec) (X 10 3)

A.M.

G.W.

P D.

O.H.

F.C.

L.G.

D.L.

Immed. (R)PrePr (M)

(A)Immed. (R)PoPr (A)30 min (R )PoPr60 min (R)PoPr (A)Immed. (R)PrePr (M)

(A)Immed. (R)PoPr (A)20 min (R)PoPr60 min (R)PoPr (A)Immed. (R)PrePr (M)

(A)Immed. (R)PoPr (A)Immed. (R)PrePr (M)

(A)Immed. (R)PoPr (A)35 min (R)PoPr (A)Immed. (R)PrePr (M)


(A)Immed. (R)PoPr (A)20 min (R.)PoPr (A)90 min (R)PoPr (A)120 min (R)PoPr (A)180 min (R)PoPr (A)Immed. (R)PrePr (M)

(A)

020400

200

200

200

20400

200200

20020400

200

40600

400

400

80800

800

800

60600

600

600

600

600

600

6080

01.83.001.802.001.802.34.302.301.201.503.04.803.00

3.5

04.3.3.5

4.503.54.803.50

3.7

3.36.006.003.30

3. -

04.003.503.56.8

809087749173917690809811186110791088610381981047911086

10210687

1038710672

10.31086810868

11478

10110582

12282

11.380103821087410610096132

929093939194918888

106108123112124109128106125105112118101125108123512341131251101358211511375

11263112835

103512991112871068010075978010096106103

0.290.290.290.2830.290.2830.280.280.28.;0.270.260.280.270.280.260.290.260.28

0.260.250.2450.2150.250.230.26

0.210.230.210.230.210.230.230.2450.240.240.2530.260.26

7.368.108.097.038.287.038.286.697.928.48

10.5813.659.63

13.648.6113.829.12

12.888.5110.9812.277.98

13.759.2912.7513.2510.0112.889.57

14.315.90

12.0812.425.10

12.104.4212.776.63

10.6113.557.46

13.667.13

12.196.40

10.306.15

10.483.92

10.609.6010.1813.60

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Table 2 (continued)

Mean blood Ejection Mean blood pressureLoad Time Heart rate pressure time X heart rate

Patient (watts) (min) (beats/min) (mm Hg) (sec) (X 10 3)

E.O.

P.B.

A.D.

S.W.

J.M.

Immed. (R)PoPr (A)30 min (R)PoPr (A)Immed. (R)PrePr (M)


(A)Immed. (R)PoPr (A)20 min (R)PoPr (A)40 min (R)PoPr (A)Immed. (R)PrePr (M)

(A)Immed. (R)PoPr (A)30 min (R)PoPr (A)60 min (R)PoPr (A)Immed. (R)PrePr (M)

(A)Immed. (R)PoPr (A)20 min (R)PoPr (A)40 min (R)PoPr (A)75 min (R)PoPr (A)120 min (R)PoPr (A)Immed. (R)PrePr (M)

(A)Immed. (R)PoPr (A)20 min (R)PoPr (A)

0600

60070900

700700

50700

500500

50040600

400

400

400

40400

400

400

400400

400

4060060060

05.50

5.503.34.703.302.502.74.30

2.702.803.001.13.101.101.301.503.84.403.802.002.302.802.50

4.36.005.804.3

9211688122831151231031299712590103116107117941119511869929878

11178108751087087897910070928095779487879511313010911873125

949891

101838395831009595105110110110110951051001079510812310312710312963858297978510278907885779384959512013098120100115

0.230.260.260.220.240.200.230.260.260.260.270.260.220.270.220.28

8.6511.378.01

12.326.899.5511.698.55

12.909.2211.889.4511.3312.7611.7712.878.9311.669.50

12.636.569.9412.058.03

14.108.03

13.934.739.185.748.448.636.7210.205.468.286.248.085.938.747.318.279.0313.5616.9010.6814.167.30

14.38

Abbreviations: Immed. = immediate; PrePr = preprandial; PoPr = postprandial; (R)values at times matched to subsequent times of angina; (A) = values at onset of angina.

comparisons were made between measure-ments obtained after equal duration of exer-Circulation, Volume XLIV, July 1971

= values at rest; (M) =

cise. Heart rate during postprandial exercise(fig. 3, left) was higher in every patient when

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HEART RATE

PRE POSTPRANDIAL PRANDIAL

MEAN BLOOD PRESSURE

20H

110H

E

E

1O00

90H

PREPRANDIAL F

Figure 3

POSTPRANDIAL

EJECTION TIME


Comparison of heart rate, mean blood pressure, and (in those six individuals who hadaortic catheterization) ejection time during exercise before and immediately after a meal.Postprandial values, measured at onset of angina, are connected to preprandial values reachedafter an amount of exercise equal to that which precipitated angina in the postprandialperiod. Averages are denoted by circled bars.

compared with heart rate measured after an

equal amount of postprandial exercise. Theaverage difference, 11.6 beats/min, was highlysignificant. A less consistent (though stillstatistically significant) increase was observedin mean blood pressure during exercise (fig. 3,middle) when corresponding preprandial andpostprandial values were compared. Theaverage difference was 6 mm Hg. Systolicblood pressures in those individuals withaortic catheters also showed a significantincrease during postprandial exercise, averag-

ing 7 mm Hg. Ejection time during exercise(fig. 3, right), measured in the patients withaortic catheters, was not different followingthe meal.We determined cardiac output and calculat-

ed total peripheral resistance in four patientsto investigate the cause of the observed bloodpressure rise. Cardiac output was not incorpo-rated in the index of M'O2 because theinfluence of cardiac output per se on MVO2 is

relatively slight.13 When measured at equiva-lent times during exercise, cardiac output was

not significantly different in the postprandialperiod. Differences in output that did occur,however, were found to correlate positivelywith changes in blood pressure during exercise(r +0.77, P <0.05). Total peripheral resis-tance tended to fall when blood pressure rose

(r =-0.75, P < 0.05). Thus, when bloodpressure during exercise was higher followinga meal, the higher value appeared to resultfrom a greater increase in cardiac outputrather than from a postprandial augmentationin total peripheral resistance.Most patients had maximal decrease in

exercise capacity and maximal increases inheart rate and blood pressure during exerciseimmediately after eating. It is noteworthy,however, that those patients who had a

delayed onset of maximal deterioration ofpostprandial exercise capacity similarly had a

delayed appearance of maximal increase ofCirculation, Volume XLIV, July 1971

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Figure 4The product of mean blood pressure and heart rateafter equal duration of exercise (left) was significantlygreater immediately after the meal. Pressure-rateproduct at onset of angina (right) showed no con-sistent change. Mean differences are indicated by thecircled bars.

heart rate and blood pressure after a givenamount of exercise. Thus, changes in sympto-matic status were paralleled by characteristicalterations in the circulation response toexercise.

Since blood pressure and heart rate are bothcorrelated with myocardial metabolic require-

ments, the product of these two quantities hasfrequently been used as an index of myocar-dial oxygen demand.15 Adjustment for ejectiontime, which has improved the value of thisindex in certain situations,'5' 16 was eliminatedin this instance because ejection time duringexercise was found not to change after meals.The product of mean blood pressure and heartrate after equal amounts of exercise wassignificantly increased in the postprandialperiod (fig. 4, left). Pressure-rate product atonset of angina, however, was the same beforeand after the meal (fig. 4, right). Similarresults were obtained in the patients who hadaortic catheterization when systolic pressurewas substituted for mean pressure and whencorrection was made for ejection time. Thus,the postprandial state appeared to acceleratethe rise in pressure-rate product and, presum-ably, in myocardial oxygen demands thatoccurred during the course of exercise. Thecritical pressure-rate product associated withthe onset of ischemic pain, however, did notchange following the meal. Consequently, thiscritical level was reached more rapidly in the

HEART RATE

PRANDIALPOST

PRAN DIAL

MEAN BP EJECTION TIMEI I

0.3k-Ca1)Uf)

0.2[

J, NSx

olr 1N vPRE POST

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Comparison of heart rate, mean blood pressure, and (in those individuals who had aorticcatheterization) ejection time while patients were seated at rest before and immediately aftera meal. The mean diferences, indicated by the circled bars, are not statistically significant.

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postprandial period, and angina was experi-enced sooner.Although changes occurred in the circula-

tory response to exercise following a meal,blood pressure, heart rate, and ejection time atrest were not significantly altered in thepostprandial period (fig. 5).

DiscussionWithin 20 min following a meal, all 12

patients with angina experienced an appre-ciable decrease in exercise capacity, in agree-ment with previous clinical impressions1 andexercise testing.2 The earlier development ofischemic electrocardiographic abnormalitiesassociated with this decrease suggests that theacceleration in onset of pain reflects anunderlying acceleration in development ofmyocardial hypoxia.The changes in exercise capacity manifested

in the postprandial period were accompaniedby correlative alterations in the circulatoryresponse to exercise. The most consistentchange was a greater rise in heart rate when agiven amount of exercise was performed aftera meal, a finding in agreement with resultsobtained in normal individuals6' 7 and inpatients with coronary disease.2 3 Blood pres-sure rise after a given amount of exercise wasalso augmented in the postprandial period,although less consistently than heart rate. Asimilar increase in blood pressure response hasbeen observed in normal subjects exercisingin the upright position7 but not in normal sub-jects exercising supine.6 In our patients, aug-mented blood pressure rise during exercise,when present, was associated with a largercardiac output and a slightly diminished totalperipheral resistance. On the average, how-ever, cardiac output measured at equivalenttimes during postprandial exercise did not altersignificantly in the four patients in whom thisquantity was measured. Similarly, ejection timeduring exercise was unaltered in the postpran-dial period. Studies in normal subjects alsohave shown no statistically demonstrablechange in cardiac output6 or in ejectiontime6 when exercise performed less than 45min after a meal was compared with pre-

prandial exercise. Lack of consistent changesin cardiac output during postprandial exercisemight superficially appear inconsistent withthe fourfold postprandial increase in mesen-teric artery blood flow which Vatner and co-vorkers27 demonstrated using chronically im-planted flowmeters. However, these sameinvestigators also found that exercise markedlyattenuated this increase in mesenteric flow.Thus, in some individuals (especially thosewith impaired circulatory function), post-prandial exercise might result in a redistribu-tion of blood flow from viscera to exercisingmuscles rather than an increase in cardiacoutput above levels attained with preprandialexercise.Our findings indicate that diminished exer-

cise capacity and associated changes incirculatory response to exercise persist for atleast 1 hr. Prolonged alteration of circulatoryparameters during exercise has also beenobserved in normal subjects7 with significantchanges demonstrable up to 3 hr after a meal.

*/

X' GW 07-78-95 p10/3169ll

0 2 3DURATION OF EXERCISE (min.

Figure 6

Pre ProndiaiImmediatelyPost Prandiol20 minutesPost Prandial

4

1

Plot of pressure-rate product as a function of theduration of exercise. Angina is indicated by asterisks.With each period of exercise the patient stopped atvery nearly the same pressure-rate product. Duringeach postprandial exercise, however, pressure-rateproduct rose more rapidly so that the critical level wasattained sooner. The decrease in exercise capacity ob-served immediately after eating waas followed byfurther deterioration 20 min after eating. This wasaccompanied by a further acceleration in the rate ofrise of pressure-rate product. Correction of these datafor ejection time did 'not alter the relationship de-scribed.


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Such changes may reflect prolonged circula-tory demands by the splanchnic bed, whichhave been shown to last up to 6 hr after a

meal when assessed by flowmeters chronicallyimplanted about the mesenteric artery.27The absence of postprandial change in heart

rate, blood pressure, ejection time, and cardiacoutput at rest agrees with the findings of Jones

and coworkers,6 who also found no significantchanges at rest after a meal similar in size andcomposition to the meal given in this study.However, postprandial increases in heart rate,blood pressure, and cardiac output at resthave been observed by others.7 These discre-pant findings (despite general agreement ofresults during exercise) may well be related todifferences in meal size and composition as

well as the posture, 'emotional state, andcomfort of the experimental subject. Since thepurpose of this investigation was the study ofaccelerated precipitation of exertional anginain the postprandial period, a meal of ordinarycomposition was chosen which reproducedthis familiar clinical phenomenon in thelaboratory without necessarily requiring a

change in resting hemodynamics. A largermeal may well have changed resting values,but it may also have severely restrictedexercise capacity or produced postprandialangina decubitus in some patients, thusrendering an exercise study impossible.Because of an accelerated rise in heart rate

and blood pressure, the pressure-rate product,an index of myocardial oxygen demand, was

greater when any given amount of exercisewas performed in the postprandial period.The pressure-rate product at angina, however,was unchanged after the meal. This criticallevel, presumably corresponding to that levelof myocardial oxygen demand which justexceeds the oxygen transport capacity of thenarrowed coronary arteries, was thus reachedsooner in the postprandial period with a

resultant acceleration in onset of ischemicpain. An example of these findings is shown infigure 6.Two mechanisms could have caused the

postprandial impairment in exercise capacity:myocardial blood flow or myocardial oxygen

Circulation, Volume XLIV, Jisy 1971

transport could have been reduced, or myo-cardial oxygen demands could have increasedexcessively. If a decrease in myocardial bloodflow or oxygen transport played a major rolein the postprandial symptomatic deterioration,pressure-rate product at angina would havediminished. The fact that pressure-rate prod-uct at angina was unchanged in the post-prandial period suggests that meals probablydo not alter the maximum rate of oxygendelivery to critically ischemic regions ofmyocardium. Our data indicate, therefore,that postprandial augmentation of heart rateand blood pressure during exercise, alterationswhich each independently tend to increaseexercising myocardial oxygen requirements,reduce the time required for the demands ofunderperfused regions of myocardium toexceed their limited oxygen supply andthereby hasten the onset of ischemic pain.Our data suggest that the current practice

of treating postprandial anginal episodes withpropranolol and nitroglycerin is physiological-ly sound. Since the more rapid precipitation ofangina is mediated primarily, if not exclusive-ly, by an accelerated rise in heart rate andblood pressure during exercise, the adminis-tration of drugs that attenuate these changeswould logically be expected to reverse post-prandial deterioration in exercise capacity.

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2. WAYNE EJ, CRAYBIEL A: Observations on theeffects of food, gastric distension, externaltemperature, and repeated exercise on anginaof effort, with a note on angina since dolore.Clin Sci 1: 287, 1934

3. KLAKEG CH, PRUITT RD, BURCHELL HB: Astudy of electrocardiograms recorded duringexercise tests on subjects in the fasting stateand after the ingestion of a heavy meal. AmerHeart J 49: 614, 1955

4. SIMONSON E, MCKINLAY CA, HENSCHEL A:Effects of meals on the electrocardiogram ofcardiac patients. Proc Soc Exp Biol Med 63:542, 1946

5. BERMAN B, BRAUNSTErIN TR, MCGuIRE J: Theeffects of meals on the electrocardiogram andthe ballistocardiogram in patients with anginapectoris. Circulation 1: 1017, 1950

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6. JONES WB, THOMAS HD, REEvES TJ: Circulatoryand ventilatory responses to postprandialexercise. Amer Heart J 69: 668, 1965

7. DAGENAIS CR, ORuOL A, McGREcoR M:Hemodynamic effects of carbohydrate andprotein meals in man: Rest and exercise. J ApplPhysiol 21: 1157, 1966

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DAVID BEISER and STEPHEN E. EPSTEINROBERT E. GOLDSTEIN, DAVID R. REDWOOD, DOUGLAS R. ROSING, G.

Relationship to Postprandial Angina PectorisAlterations in the Circulatory Response to Exercise Following a Meal and Their

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