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Left ventricular function in response to the transition from aerobic to anaerobic metabolism

POKAN, ROCHUS; HOFMANN, PETER; VON DUVILLARD, SERGE P.; BEAUFORT, FRIEDRICH; SCHUMACHER, MARTIN; FRUHWALD, FRITZ M.; ZWEIKER, ROBERT; EBER, BERND; GASSER, ROBERT; BRANDT, DIETER; SMEKAL, GERHARD; KLEIN, WERNER; SCHMID, PETER

Medicine & Science in Sports & Exercise: August 1997 - Volume 29 - Issue 8 - p 1040-1047
Basic Sciences: Original Investigations
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The purpose of this investigation was to study myocardial function at rest, during three phases of energy supply, and during recovery. Radionuclide angiography was performed during the aerobic phase (phase I, rest-first lactate increase), the aerobic-anaerobic transition phase (phase II, first lactate increase-second lactate increase), the anaerobic phase (phase III, second lactate increase-maximal work performance (Pmax)), and during recovery. Thirty-eight male patients (59 ± 7 d after myocardial infarction) were compared with 19 healthy control subjects and 21 sports students of comparable age. Left ventricular ejection fraction (LVEF) increased from rest to phase I and from phase I to phase II in sports students and control subjects. During phase III, LVEF did not change significantly in sports students, but it decreased significantly in control subjects. This is in contrast to the patients, who showed an increase of LVEF from resting values (47 ± 3%) to phase I (50 ± 1%), no change during phase II(51 ± 2%), and a decrease to resting values (45 ± 2) during phase III. All subjects showed an increase in stroke volume (SV) during phase I and II, reaching a maximum at phase II. This was evidenced by an improvement of the systolic function with a constant left ventricular end-diastolic volume(EDV) in control subjects and sports students. In contrast, an improved SV in patients was achieved through an increase in EDV and a less distinct increase in the left ventricular end-systolic volume (ESV). Maximal LVEF values were measured during the first 90 s of recovery in all subjects. Values during recovery are not representative of load dependent myocardial function. This increase in LVEF does not cause an increase in cardiac output but is a consequence of changes in the EDV and ESV, which decrease again immediately after the end of exercise performance.

Departments of Internal Medicine, Sports Sciences, and Radiology, University of Graz, AUSTRIA; Department of Sportphysiology, University of Vienna, Vienna, AUSTRIA; Center for Cardiac Rehabilitation, St. Radegund; Center for Cardiac Rehabilitation, Bad Schallerbach, AUSTRIA; and Human Performance Laboratory, Department of HPER, University of North Dakota, Grand Forks, ND

Submitted for publication October 1996.

Accepted for publication March 1997.

The authors wish to thank Mag. Ulrike Katary for her assistance in writing the manuscript.

Address for correspondence: Serge P. von Duvillard, Ph.D., Director-Human Performance Laboratory, Department of HPER, University of North Dakota, P.O. Box 8235, Grand Forks, ND 58202-8235. E-mail:vonduvil@badlands.nodak.edu

Radionuclide angiography is used extensively as a noninvasive method to assess ventricular function at rest and during exercise. In normal subjects, left ventricular ejection fraction (LVEF) increases during incremental cycle ergometer exercise. In contrast, LVEF fails to increase at peak exercise in patients with coronary artery disease(4,22). In patients with normal or mild-to-moderately depressed LVEF at rest, the magnitude and frequency of changes during exercise are significantly greater (32). Exercise testing, particularly in association with radionuclide imaging, has been extremely helpful in risk stratification after myocardial infarction(39). Grodzinski et al. (15) reported that LVEF at rest in relation to LVEF during exercise (ΔLVEF = LVEF(rest) - LVEF(exercise)) was the best prognostic factor following myocardial infarction. In most studies, ΔLVEF is related only to one measure of LVEF at submaximal or maximal work loads(4,8,14,15,18,22,31,32,35), although ΔLVEF is also dependent on exercise protocol(11) and on the degree of exhaustion(5,6). Rest and peak exercise LVEF are derived, but they may not adequately assess left ventricular function because exercise is a complex intervention of changing preload, afterload, heart rate, and contractile state (21,27). Hofmann et al.(17) showed that a change in the increased LVEF during incremental cycle ergometer exercise was significantly related to the second increase of blood lactate concentration (LA) in healthy subjects, which was also shown by Boucher et al. (5,6) for ventilatory threshold. Similar results have been presented by Koike et al.(20) in patients with chronic heart disease (ischemic heart disease with and without previous myocardial infarction, valvular-, hypertensive heart disease, and dilated cardiomyopathy).

There appear to be three phases during the progressive transition from low intensity exercise to maximal intensity exercise. Phase I primarily involves aerobic metabolism; phase II is signaled by the aerobic-anaerobic transition; and the onset of phase III is characterized by a sharp rise in LA, which appears to correspond to the onset of anaerobiosis (36). Morton et al. (25) suggest that two transitions or turn points in LA exist, which divide the time domain for LA in ramp exercise into three regions. These two transitions may correspond to the two ventilation thresholds. Figure 1 is an example of typical changes occurring in LA during progressive exercise. The two lactate turn points subdivide the three phases.

The aim of the present study was to investigate the behavior of myocardial function during the transition from aerobic to anaerobic metabolism up to maximal performance and during recovery in patients (after myocardial infarction), healthy control subjects of comparable age, and sports students.

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METHODS

Subjects. Out of 91 investigated subjects 13 were excluded from the analysis because of the poor quality of heart images from radionuclide angiography. Informed consent was provided by all participants.

A group of 38 male cardiac patients (age, 56 ± 2 yr; height, 172± 3 cm; body mass, 84 ± 4 kg) was compared with 19 healthy control subjects (age 55 ± 3 yr; height, 175 ± 3 cm; body mass, 78 ± 1 kg) and 21 sports students (age, 23 ± 1 yr; height, 180± 2 cm; body mass, 73 ± 1 kg). Only patients with ischemic heart disease with previous first myocardial infarction (posterior wall infarction in all cases), without angina pectoris at rest were included in this study. Echocardiography (2-D-mode, color doppler) showed no patient with a valvular or a hypertensive heart disease, or a dilated cardiomyopathy. All patients had a sinus rhythm without a bundle-branch block. No sports student or control subject had a history of chest pain, systemic hypertension, or any other cardiac disorder. Sports students and control subjects were considered free of cardiac disease on the basis of medical history, physical examination, normal rest and stress electrocardiographic findings. They were non-smokers with an appropriate exercise tolerance and a normal resting left and right ventricular function as assessed by radionuclide angiography. No subjects received cardioactive medication at the time of the study; patients stopped taking medications 1 wk before the examination.

In patients the exercise test was performed 59 ± 7 d after the myocardial event. Each subject performed an incremental exercise test on a cycle ergometer in an upright position to the limit of tolerance. For patients and control subjects, the exercise intensity was increased in increments of 10 W from an initial level of 20 W. For sports students, the exercise intensity was increased in increments of 20 W from an initial level of 40 W. For all subjects, increments were added every 90 s until the intensity limit of each individual was reached. Heart rate (HR) was monitored continuously and recorded every 5 s with a “Sporttester PE4000” (Polar Electro, Kempele, Finland). Systolic blood pressure (SBP) was measured by auscultation at rest, at the end of each exercise stage, and during recovery. The double product was calculated (DP = HR × SBP). ECG was monitored continuously, and a 12-lead ECG (I, II, III, aVR, aVL, aVF, V1 - V6) was recorded at rest, during the last 10 s of each intensity interval, and at the end of the exercise test. A significant ST-segment change with exercise was defined as a deviation of the J-point > 0.1 mV, and a horizontal or downsloping ST segment with a duration of 0.08 s.

Capillary blood was taken from the hyperemic ear lobe(28) at rest, during the last 10 s of each load interval without discontinuation, at the end of each exercise test, and after 90, 180, and 270 s of the recovery time (90s, 180s, 270s) for LA measurement. Lactic acid concentration was measured by a fully enzymatic photometric method in whole blood by immediately deproteinization with perchloric acid (Test Combination Lactate for Sports Medicine, Boehringer Mannheim, Germany)(20).

According to Skinner and McLellan (36) and Morton et al. (25), LA performance curves were used to determine the three phases of energy supply. Two lactate turn points (LTP1 and LTP2) were defined. LTP1 was defined as the point where the LA level began to increase systematically above resting values, which is comparable to the “lactate threshold” and shows a logical relationship to the “anaerobic threshold” according to Naimark et al. (26), Ribeiro et al. (33), and Wassermann et al. (38). LTP2 was defined as the second abrupt increase of LA, the so-called “lactate turn point” according to Davis et al. (9). Both LTP1 and LTP2 were analyzed as previously described (29). LTP1 was determined exclusively between the first LA value and 75% of the maximal performance (Pmax); LTP2 was determined exclusively between predetermined LTP1 and the LA value at Pmax. A computer-aided iterative calculation of the point of intersection of two regression lines with minimal standard deviation of the two straight lines was used to determine each of both lactate turn points in the section between the LA value at the end of the first work load level and 75% of Pmax(LTP1), and between predetermined LTP1 and Pmax(LTP2) (see Fig. 1). The LA values were determined as a function of work performance (P), with scaling of performance values to a value of 100% for Pmax. The two lactate turn points separated three phases: phase I from rest to LTP1, phase II from LTP1 to LTP2, and phase III from LTP2 to Pmax.

For the evaluation of the myocardial function, the ventricular end-diastolic volume (EDV) and LVEF were determined for each intensity by means of radionuclide angiography (RNVA). The left ventricular end-systolic volume (ESV) and the cardiac output (CO) were calculated. After intravenous administration of erythrocytes marked in vitro with technetium 99[activity 25 mCi (9.25 × 108 Bq)] in patients and control subjects and 15 mCi (5.55 × 108 Bq) in sports students, the heart variations were recorded by a gamma-camera (Elscint Apex 209; Elscint, Israel) which was equipped with an all-purpose collimator and positioned to provide optimal separation of the right and left ventricle. All subjects were seated with their chest fixed in a slightly backward position so that any artifacts during exercise could be kept to a minimum. Subjects whose recording showed artifacts were excluded from the study. Acquisition time during rest was 240 s and 90 s during exercise and recovery. During the exercise, three acquisition cycles before LTP1, LTP2, and Pmax were obtained with a total acquisition time of 270 s during each phase. An electro-cardiography-triggered computer was used to acquire 24 images per cardiac cycle in a 64 × 64 matrix. For each study, approximately 150,000 counts/frame were acquired at rest, approximately 180,000 counts/frame during exercise, and approximately 60,000 counts/frame during each phase of recovery. For optimal evaluation of the RNVA data, the region of interest over the left ventricle was focused automatically; in cases where the ventricular borders could not be determined exactly by the automatic process, it was then focused manually. The evaluation followed the method described by Standke et al.(37) where LVEF was calculated from the relationship LVEF(%) = (EDC-ESC)/(EDC) × 100 where EDC and ESC are the background-corrected end-diastolic and end-systolic counts, respectively. End-systolic volumes were calculated from the LVEF and EDV. Cardiac output was calculated by multiplying stroke volume (from EDV - ESV) times heart rate. This method is not presently reliable enough to make quantitative measurements during exercise. However, if one makes some conservative assumtions about the relationship of rest, the three phases of energy supply, and during recovery, it is possible to estimate left ventricular (LV) volumes and CO from the observed HR, LVEF, and EDV (12).

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STATISTICS

The results are expressed as means ± SD. ANOVA with repeated measures was used to evaluate differences in the time course of EDV, ESV, SV, LVEF, CO, SBP, and DP. Differences between rest, phase I, II, III, and during recovery were obtained by a post-hoc analysis test (last significant differences test). To assess individual changes, the difference (Δ) between phase II and phase III was calculated for EDV, ESV, SV, and LVEF. Linear regression analysis was used to find a relationship between ΔEDV,ΔESV, ΔSV, ΔLVEF, and age, as well as between the performance at LTP2 and significant ischemic ST segment changes.

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RESULTS

Values of HR, LA, P, and%P at rest, LTP1, LTP2, Pmax, and after 90 s, 180 s, and 270 s of recovery are given inTable 1; values for SBP and DP are provided inTable 2. Values of EDV, ESV, and SV during rest, phase I, phase II, phase III, and during 90 s, 180 s, and 270 s of recovery are presented in Table 3; LVEF and CO are presented inTable 4. Results of repeated measures ANOVA for EDV, ESV, SV, LVEF, and CO are depicted in Table 5.

LVEF increased significantly from resting values up to phase I (P< 0.001), and from phase I to phase II (P < 0.001), in sports students (Fig. 2), and in control subjects(Fig. 3). Similar LVEF values were obtained at phase II and III in sports students. Control subjects showed a tendency to decrease in LVEF (Figs. 2 and 3) during phase III. In contrast, patients showed an increase only from resting values up to phase I(P < 0.01), no significant change during phase II, and a decrease to resting values during phase III (P < 00.1)(Fig. 4). The highest LVEF values recorded in all subjects occurred during the first 90 s of recovery. All subjects showed a significant increase of SV between rest and phase II (sports students and control subjects(P< 0.001)), which occurred through improvement in systolic function and expressed in a significant decrease of ESV between rest and phase II sports students (P< 0.001) and control subjects(P< 0.05). In contrast to sports students, control subjects showed in phase III an increase in ESV (P < 0.05). The EDV was more constant in sports students and control subjects with a limited but significant increase from rest to phase I (P < 0.05) and a tendency to increase up to phase III (Fig. 5). In contrast, the improvement of SV in patients between rest and phase II(P< 0.001) was achieved through an increase in EDV between rest and phase II (P< 0.001) and in comparison with that, a less distinct increase of the ESV between rest and phase II (P< 0.01)(Fig. 5). No significant change was found for SV during recovery in sports students. In control subjects and patients, SV significantly decreased (P < 0.01) during recovery because of a significant decrease of EDV (P < 0.001) and a less distinct decrease in ESV (P < 0.001).

For sports students and older healthy control subjects, there exists a positive correlation between age and individual change in myocardial function, expressed as ΔLVEF (r = 0.415; P < 0.01). Whereas, forΔESV a negative correlation was found (r = -0.309; P < 0.05). There was no significant correlation for ΔSV or ΔEDV.

Significant differences (P < 0.001) were found between rest and LTP1, LTP1, and LTP2, and between LTP2 and Pmax for the SBP and DP in all investigated groups(Table 2). Also, the increase in cardiac output was significantly different in all groups (P < 0.001) between rest and phase I, phase I and II, and a less distinct but significant increase between phase II and III (Table 4) in patients and sports students but not significantly increased in control subjects.

Percentages of Pmax at LTP1 and LTP2 were independent of groups in a comparable range between 44-50% (LTP1) and 72-75%(LTP2), despite a different time course of LA and different absolute values for LA.

A significant horizontal or downsloping ST-segment change with exercise was found in six patients. When P at significant ST-segment change was compared with P at LTP2 a significant correlation was found (r = 0.806, P< 0.05). A significant correlation between the decrease of LVEF from phase II to III and the depth of the ischemic ST-segment change could not be observed.

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DISCUSSION

Threshold determination (38) was an objective measure of exercise capacity and functional state in healthy subjects and cardiac patients independent of the subjects' motivation (23). The present study used an incremental exercise protocol with each increment lasting 90 s in duration with increasing increments of 10 and 20 W. This method was chosen to avoid inappropriate leaps from one step to the next. After many pre-tests, 90-s intervals per increment appeared to be the optimal period of time. According to the results of these pre-tests, the quality of the images was considered to be satisfactory during recovery. Periods of 90 s were used to determine the rapid changes of functional variables during the early phase of recovery. During exercise a total acquisition time of 270 s was obtained by using three load phases to reach reliable results. Additionally, the total testing time for the patients did not exceed reasonable limits(24).

When evaluating the time course of hemodynamic parameters during incremental cycle ergometer exercise, one must consider results of other studies (9,25,33) of the three phases of energy supply. In studies by Davis et al. (9) and Ribeiro et al. (33), two turn points were determined by the lactate performance curve to define these three phases. The definition for“lactate turn point” as a characterization of the lactate performance curve was chosen according to Davis et al. (9) and Morton et al. (25) to avoid mistakes when comparing threshold conceptions of others who may have used different stress protocols and threshold definitions. According to Morton et al.(25), two transitions divide the time domain into three regions for blood lactate concentration in ramp protocol exercise. These two transitions may correspond to the two ventilation thresholds(25). Cabrera and Chizeck (7) presented similar results using system identification analysis techniques. They reported that the identified parameter changes over time suggest that the exercise intensity range (from rest to maximal ˙VO2) is divided into three main intensity domains, each with distinct dynamics. Using this assumption, we found similar%Pmax values independent of groups, which is contrary to the findings of others. The reason may be that most investigators used different protocols and threshold concepts. On the other hand, Aunola and Rusko (3) demonstrated that the LTP concept was an objective measure of the MaxLAss and that both LTP's were highly reproducible independent of age (2). Studies involving patients could not be found.

In our study, two turn points could be identified in the LA performance curve by a linear regression turn point analysis in all subjects, leading us to the conclusion that all tested subjects, including patients, reached the anaerobic area independent of the individual LA values. The determination of both LTP1 and LTP2 provided more information on the metabolic state of the organism than the single threshold obtained by ventilatory determination (20). The determination of these two turn points allowed a definition of three different metabolic areas according to Skinner and McLellan (36): I) aerobic conditions without an increase in LA between rest and LTP1; II) aerobic conditions between LTP1 and LTP2 with an increase of LA representing the onset of blood lactate and increasing anaerobic energy production; and III) accumulating LA above LTP2, which was also demonstrated by Helal et al.(16) for healthy subjects.

Our investigation revealed two important findings: The first was that in contrast to healthy older subjects and young subjects who showed an increase in LVEF values up to phase II (Figs. 2 and 3), cardiac patients (Fig. 4) showed an increase only from rest to phase I in without a further increase during phase II.

The second is that independent of group, a marked change in LVEF between phase II and III was observed. This is similar to the findings of Foster et al. (12) and Koike et al. (20), although we used mean values of the three load increments only. Koike et al.(20) reported that the ventilatory anaerobic threshold, determined by V-slope method, occurred at a work rate at which left ventricular function decreased during exercise in patients with chronic heart disease. Additionally, they found an increase in LVEF between rest and 45.2± 10.7% ˙VO2max (similar to our findings), which shows values of 44-50% Pmax for P at LTP1. LVEF values were found at ventilatory anaerobic threshold of 65.4 ± 9.1% ˙VO2max, and a decrease of LVEF between ventilatory anaerobic threshold and peak exercise was also present (20). The LVEF values at rest and during exercise were similar to the values found in our study. The results by Koike et al. (20) are in agreement with our findings, but without a precise distinction between the first two phases from aerobic to anaerobic transition according to Skinner and McLellan(36). Foster et al. (12) described a similar pattern of the LVEF behavior in 35-yr-old untrained subjects despite different aquisition time of RNVA. The LVEF increased significantly from rest to exercise at the ventilatory threshold. There was no further change in LVEF at maximal exercise which is in agreement with our findings for sports students and for the older control subjects.

Conclusions about hemodynamic effects can only be made if the heart volumes are taken into consideration. The ESV of the sports students examined in our study decreased during the aerobic-anaerobic transition and remained constant during phase III (Fig. 5). These results are similar to the results of Imbriaco et al. (19), who investigated 7 male and 3 female, healthy subjects (age range 23-60 yr, mean age 42 ± 11), In contrast to the findings of Imbriaco (19), the healthy older subjects, however, showed a limited increase in EDV(Fig. 5). Contrary to the group of sports students(Fig. 1), the older control group had a tendency to decline in LVEF (Fig. 3) during phase III, resulting in a larger caculated ESV in these older subjects. These findings compare with those of Boucher et al. (6), who found similar changes in heart volumes above the anaerobic threshold determined by gas exchange criteria at the point of nonlinear increase in the ventilatory equivalent for oxygen, which has been previously associated with elevations in simultaneously obtained arterial lactate samples (40). In contrast to our results, the differences in rest or exercise LVEF-values found by Boucher et al. (6) were not related to age. This may be because Boucher et al. examined 10 men in the age range of 34-53 yr (mean 48 ± 5). On the one hand, the number of subjects tested in this study might have been too low; on the other hand, the difference in age might have been too small to find a correlation between the heart volumes under stress-conditions and age, as we did in our study.

In contrast to our control subjects and sports students(30), cardiac patients showed an increase in ESV and EDV at low work loads, whereby the increase in SV up to phase II was achieved by a greater increase in EDV (Fig. 5). The impossibility of LVEF to increase between phase I and II is the consequence of LVEF as a function of the dimension of the left ventricle [LVEF = (EDV - ESV)/EDV·100]. The decrease in LVEF and the beginning decrease in SV during phase III are caused by a greater increase in ESV compared to the increase in EDV. Also, in patients, a general dilatation of the left ventricle was evident during the exercise test. Contrary to cardiac patients, in control subjects only a moderate dilatation of the left ventricle during phase III(Fig. 5) was found. Anholm et al. (1) examined a group of subjects of various fitness levels and found that the cardiovascular adaptation to habitual physical activity are grossly reflected by differences in LVEF. However, the magnitude of these differences suggest that dimensional rather than functional adaptation are of potentially greater significance. In opposition to their findings, we detected a dimensional as well as a functional adaptation of the heart to physical activity, depending on the age and also on the physical condition of the myocardium. However, our findings showed that all three groups of subjects are limited in their SV above LTP2. The slightly increased cardiac output above LTP2 could only be determined by an increase in heart rate.

The second important finding was that the maximal load dependent values of LVEF were found during phase II for all subjects. The absolute highest LVEF values were measured during the first 90 s of recovery in all subjects. All individuals, especially the cardiac patients, showed an increase in LVEF immediately after the end of their performance tests. Similar results have been presented by Rowland and von Duvillard (34) in a recovery echocardiographic study in men and boys and by Foster et al.(13) in an incremental as well as steady state exercise RNVA study in patients with CHD with and without ischemia. The increase in LVEF and decrease in EDV and calculated ESV immediatly post exercise, may be a reflection of the very rapid changes in preload and afterload on the left ventricle. This phenomenon must not be interpreted as an improvement of the cardiac output, as there was no considerable change in SV(Fig. 5). Whereas the left ventricle is quickly reduced to its normal size after the end of the exercise test, LVEF (which indicates the percentage of SV at EDV) increases according to the reduction of the left ventricle along with unchanged (sports students) or decreased SV (control subjects, patients). Thus this increase in LVEF after the end of the exercise test is caused by a decrease in the dilatation of the left ventricle, but definitely not by an increase in SV or CO. This dilatation of the left ventricle appears during the exercise test and is most distinct in cardiac patients. In agreement with previously described results(10,11), these data indicate that the hemodynamic state inferred from radionuclide angiography studies during the immediate post-exercise period, used to achieve technically better images, may not be representative of the hemodynamic state actually occurring during Pmax. If only post-exercise imaging is used, many patients with significant coronary artery disease will be erroneously classified as normal.

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CONCLUSION

For an evaluation of the exercise dependent myocardial function, it is necessary to include the measurements of heart volumes apart from considering LVEF.

It is recommended that at least one measurement should be taken each at rest during phase I (up to 50% Pmax), phase II (up to 75% Pmax), and during phase III.

Measurements taken during the post-exercise period are not representative of the conditions during exercise.

Figure 1-Principle of the determination of the two lactate turn points. The two lactate turn points separated three phases of energy supply. LTP1 = first lactate turn point; LTP2 = second lactate turn point; Pmax = maximal work performance, phase I = from rest to LTP1, phase II = from LTP1 to LTP2 and phase III = from LTP2 to Pmax.

Figure 1-Principle of the determination of the two lactate turn points. The two lactate turn points separated three phases of energy supply. LTP1 = first lactate turn point; LTP2 = second lactate turn point; Pmax = maximal work performance, phase I = from rest to LTP1, phase II = from LTP1 to LTP2 and phase III = from LTP2 to Pmax.

Figure 2-Left ventricular ejection fraction (LVEF) during cycle ergometer exercise in healthy sports students at rest, during the three phases of energy supply (phase I, phase II, phase III), and during 90 s, 180 s, and 270 s of recovery. *Pb < 0.05, **P < 0.01, ***P< 0.001, significant differences.

Figure 2-Left ventricular ejection fraction (LVEF) during cycle ergometer exercise in healthy sports students at rest, during the three phases of energy supply (phase I, phase II, phase III), and during 90 s, 180 s, and 270 s of recovery. *Pb < 0.05, **P < 0.01, ***P< 0.001, significant differences.

Figure 3-Left ventricular ejection fraction (LVEF) during cycle ergometer exercise in healthy control subjects at rest, during the three phases of energy supply. See

Figure 3-Left ventricular ejection fraction (LVEF) during cycle ergometer exercise in healthy control subjects at rest, during the three phases of energy supply. See

Figure 4-Left ventricular ejection fraction (LVEF) during cycle ergometer exercise in patients after myocardial infarction at rest, during the three phases of energy supply. See

Figure 4-Left ventricular ejection fraction (LVEF) during cycle ergometer exercise in patients after myocardial infarction at rest, during the three phases of energy supply. See

Figure 5-End-diastolic volume (EDV), end-systolic volume (ESV), and stroke volume (SV) during cycle ergometer exercise in healthy older control subjects at rest, during the three phases of energy supply. See

Figure 5-End-diastolic volume (EDV), end-systolic volume (ESV), and stroke volume (SV) during cycle ergometer exercise in healthy older control subjects at rest, during the three phases of energy supply. See

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Keywords:

ERGOMETRY; ISCHEMIC HEART DISEASE; RADIONUCLIDE ANGIOGRAPHY; INDIVIDUAL PHYSICAL STRAIN

©1997The American College of Sports Medicine