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Gradual Changes of ECG Waveform During and After Exercise in Normal Subjects By M. L. SIMOONS, M.D., AND P. G. HUGENHOLTZ, M.D. SUMMARY The directions and magnitudes of time-normalized P, QRS, and ST vectors, and other ECG parameters analyzed during and after multistage exercise in 56 ostensibly healthy men aged 23 to 62. By selective averaging with a digital computer system a single representative beat was obtained from each stage. Measurements were taken from this beat. During exercise, the interval between the spatial maximum of the P wave and the onset of the QRS complex decreased while the magnitude of the P wave increased. The direction of the P vectors did not change. This pattern corresponds to the electrocardiographic manifestations of predominant right atrial overload. No significant changes in the QRS duration were observed. Also the magnitude and spatial orientation of the maximum QRS vectors remained constant. The interval between the QRS onset and the maximum spatial magnitude of the T wave shortened. The terminal QRS vectors and the ST vectors gradually shifted toward the right, and superiorly. The T magnitude lessened during exercise. In the first minute of the recovery period the P and T magnitudes markedly increased. Afterward all measurements gradually returned to the resting level. Mechanisms which may explain the observed ECG changes during and after exercise are discussed, including changes in the blood conductivity and intracardiac blood volume. Age did not contribute to the variance of the ECG measurements, but a significant reduction of this variance could be obtained in some ST-segment measurements by relating them to heart rate with linear regression equations (P i 0.05). Therefore it is expected that the sensitivity of the exercise ECG for detection of ischemic heart disease would be increased when heart rate dependent normal limits for ST-segment measurements are used. Different criteria should be employed for the interpretation of the ECG during and after exercise. were Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 CHANGES IN THE ELECTROCARDIOGRAM (ECG) during exercise in normal subjects were described by Simonson in 1953.' He observed decreased R wave amplitude and right axis deviation as well as junctional depression of the ST segment and decreased T wave amplitude. Sjostrand2 showed that the depression of the QRS-ST junction during exercise in normal subjects is related to heart rate. Later, Irisawa3 demonstrated a marked increase of the P wave amplitude during exercise. These findings have been confirmed in recent years by quantitative ECG analysis with modern computer techniques. 4-12 Blomqvist4 " and Bruce et al.5' 6 demonstrated that such ECG changes occur gradually when a multistage exercise test is performed. In the recovery period, these changes reverse, although the relation between ST-segment amplitude and heart rate in the recovery period seems to follow a different pattern than during exercise.' ` When a corrected orthogonal lead system is employed, the changes in the magnitude and in the direction of the heart vector can be separated. Results from one such study" indicate that after exercise changes only in the magnitudes of QRS and T occur, while the directions of these vectors remain constant. On the other hand, Rautaharju et al.12 found changes in both magnitudes and directions of Chebychev waveform vectors of the P wave and the ST-T segment during submaximal exercise. Although changes in various ECG measurements during or after exercise are indicated by these reports,' 12 none of the authors presents a complete description of the entire ECG at all levels during a multistage exercise test and after exercise in normal subjects. In addition little information is available on the mechanisms which cause these ECG changes. The present study has been designed to provide a quantitative description of the entire ECG from rest until maximal exercise and in the recovery period. Both ECG measurements at time-normalized intervals of the P, QRS, and ST segments4 8, 12 and at fixed intervals after the end of the QRS complex5 6, 10 as well as time integrals of the negative parts of the ST segments were analyzed.9 These results show gradual changes in the P, QRS, and T wave which can be related to heart rate. However, the relation between many ECG measurements and heart rate in the recovery period differed significantly from the same relation during exercise. On the basis of these observations it is postulated From the Department of Physiology, University of Utrecht and the Thoraxcenter of the Medical Faculty and University Hospital, Erasmus University. Rotterdam, The Netherlands. Address for reprints: Maarten L. Simoons, M.D., Thoraxcentrum, Erasmus Universiteit, postbus 1738, Rotterdam, The Netherlands. Received September 3, 1974; revision accepted for publication May 6, 1975. 570 Circulation, Volume 52, October 1975 ECG CHANGES DURING & AFTER EXERCISE that correction of ECG measurements for heart rate determined from the same record will considerably increase the diagnostic power of exercise ECGs, while further analysis of changes in vector magnitudes may be of use in the assessment of the hemodynamic function of the heart as a pump. Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 Materials and Methods Orthogonal electrocardiograms at rest, during exercise, and recovery were analyzed in 56 ostensibly healthy men. Thirty-five of these were studied at the Occupational Health Center of Rotterdam Harbour.'3 The other 21 recordings were obtained in cooperation with the KRIS.* All subjects were selected for the present study because they had no history of cardiovascular disease, no chest pain, blood pressure lower than 160/95, fasting serum cholesterol below 6.7 mM/L, blood sugar below 10 mM/L one hour after ingestion of 75 grams glucose, and a normal ECG at rest. The age distribution is shown in table 1. Exercise was performed on a calibrated bicycle ergometer. The workload was increased in a stepwise manner with 10 W/min (KRIS) or 30 W/3 min, starting at 15 W (Harbour). The subjects were encouraged to exercise to their maximum. The tests at the Harbour Occupational Health Service were terminated in 20 subjects when the exercise stage of 165 W was completed. The ECG was recorded on analog tape. t A modified Frank lead system was used. Chest electrodes were placed at the level of the 5th intercostal space in the upright position. The H electrode was placed in the neck, the F electrode at the sacrum. The ECGs were processed off-line with a PDP-8E4 computer system. Twenty second periods were sampled at a rate of 500/sec at rest in a sitting position, every second or third minute during exercise, and the first, third, sixth, and ninth minute of the recovery period. A total of 642 ECGs was processed. A single representative beat with a low noise level was obtained from each record by averaging of all detected beats, except those with an aberrant waveform. The onset and end of the different waves were identified by a program developed especially for waveform analysis in serial ECGs.'4 The waveform analysis was checked visually in all ECGs. In 69 records (11%) P wave detection proved to be incorrect. On the other hand, QRS errors were not found. The maximum of the T wave was detected erroneously in only one record. The incorrect records were not used for further analysis. The mean amplitude 20 to 10 msec before the onset of the QRS complex was used as a zero reference level for all measurements. The following types of measurements were taken: (table 2): 1) Intervals from the maximum spatial magnitude of the P wave until the onset of the QRS complex (PPK-Q); from the onset to the end of the QRS complex; and from the onset of the QRS complex to the maximum spatial magnitude of the T wave (Q-TPK). The conventionally measured P-Q and Q-T intervals were not chosen because, in most records, at heart rates over 120 beats per minute, the P wave is superimposed on the preceding T wave. In those records the true onset 'Kaunas Rotterdam Intervention Study; Health Organization. fTotemite Inc., USA. tDigital Equipment Corporation, USA. Circulation, Volume 52, October 1975 a project of the World 571 Table 1 Age Distribution of Study Population Age 21-25 26-30 31-35 36-40 41-45 46-50 51-55 56-60 61-65 3 3 13 4 N 2 8 14 3 6 of the P wave and end of the T wave could not be detected. 2) Amplitudes at eight time normalized intervals of the PPK-Q segment, the QRS complex, and the S-TPK segment.4' 8 3) Amplitudes at fixed intervals after the end of the QRS complex.5 6 4) The area of the negative part of the ST segment in orthogonal leads X and Y.9 These measurements were plotted against heart rate, and linear regression analysis was performed for rest and exercise records, and for the recovery records. The relative influences of heart rate and age were analyzed with linear multiple regression analysis. Paired and unpaired Student's t-tests were used to compare the differences of various parameters at selected heart rate intervals. Results In figure 1 the PPK-Q, QRS, and Q-TPK intervals have been plotted against heart rate. The means of the time-normalized ECGs at rest and during exercise at a heart rate of 160-180 beats per minute are presented in figure 2. P Wave Changes The PPK-Q interval shortened from 108 ± 16 msec (mean and standard deviation) at a heart rate of 70 beats/min at rest to 72 ± 10 msec during exercise at a heart rate of 170 beats per minute (fig. 1). In the recovery period the PPK-Q interval lengthened again, with a similar linear relation toward heart rate. The spatial orientation of the P vectors was not altered significantly (fig. 2). The spatial magnitude of the P wave increased from 0.122 + 0.035 mV at a heart rate of 70 to 0.221 + 0.046 mV at 170 beats per minute. In figure 3 the maximum P vectors have been plotted against heart rate. These plots show that the amplitude changes occurred gradually when the heart rate increased. In the first minute of the recovery period a further augmentation of the P wave was observed in all three leads although the heart rate decreased. Therefore the spatial magnitude of the P wave in the recovery period was higher than during exercise at corresponding heart rates. Changes in the QRS Complex No significant change was observed during or after exercise in the QRS duration. However, the duration of the S wave in leads X and Y increased from a mean of 14 (range 0-52), and 18 msec (0-50) respectively at a heart rate of 70 to 21 (10-52) and 24 (0-52) msec at a 572 SIMOONS, HUGENHOLTZ ms PPK-O The magnitude of the T wave decreased gradually from 516 ± 97 ,uV at rest to 415 ± 176 ,uV at maximum exercise (P < 0.01). Its spatial orientation did not change. In the first minute of the recovery period the T wave spatial magnitude increased markedly to 629 ± 154 ,uV (P < 0.01). The differences between the time normalized vectors at rest and during exercise have been plotted in figure 5. This figure shows that the direction of the changes was independent of heart rate. The magnitude of the changes gradually increased during exercise. The changes of the ST vectors were similar in direction to the changes of the terminal QRS vectors. The whole ST segment as well as the T wave in leads X and Y was shifted downward during exercise. 200+ X) -m 100o pp*- 200t ORS m v JLR YAM., 2-5, 100+ - , Regression Analysis Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 G-TPK ,A 300+ X .4+t + + 200+ . + 01, - 100 100 x * t50 200 HEART RATE BEATS/ MIN. REST EXERCISE v RECOVERY Figure 1 Plots of PPK-Q interval (point of maximum amplitude of P wave until QRS onset), QRS duration, and Q-TPK interval (QRS onset until maximum spatial magnitude of T wave), against heart rate. x: measurements at rest, sitting on the bicycle; +: exercise; v: recovery period. Regression lines have been drawn (see table 3). heart rate of 170 beats per minute (fig. 2). The R wave duration shortened by the same amount. No significant changes were observed in the magnitudes of the time-normalized QRS vectors during exercise. Also the spatial orientation of the maximum QRS vectors did not change (fig. 2). However, the initial and terminal parts of the QRS complex shifted rightward and superiorly. This shift caused a heart rate dependent right axis deviation in the ECG. ST-T Segment Changes The Q-TPK interval shortened during exercise and increased again in the recovery period. The ST segment shifted toward the right, superior, and posterior. These changes were also linearly dependent on heart rate (fig. 4). The results of the linear regression analysis of 32 parameters at rest and during exercise with heart rate as the independent variable are summarized in table 3. A significant (P : 0.05) reduction of the standard errors of the amplitudes ST-1/8, ST-2/8, ST-3/8, ST30 and the standard errors of the negative ST integrals in X and Y were obtained when adjustment for heart rate was made. Predictions which adjusted for both heart rate and age by linear multiple regression analysis did not yield better results than prediction from heart rate alone. Regression analysis with heart rate expressed as a fraction of the maximal heart rate, or with workload as the independent variable, did not reduce the standard errors. Discussion Comparison with Other Studies The results of the current study confirm and extend earlier observations of changes of various ECG measurements during and after exercise in normal individuals. However, these studies' 12 each describe a small number of ECG measurements. A systematic analysis of the entire ECG waveform was performed in the present investigation. The spatial magnitude of the P wave increased gradually during exercise, while the PPK-Q interval shortened. This is in agreement with earlier findings during3' 4, 12 and after'1 exercise. However, Irisawa et al.3 report immediate reduction of the P amplitude in the standard leads after mild exercise, while a further augmentation of the P magnitude was observed in the first minutes of the recovery period in the present study (fig. 3). In an earlier study from this laboratory,14 a small, but statistically significant shortening of the QRS complex of 2.7 ± 2.0 msec was found in young individuals, using the same waveform analysis algorithms. In the present study the QRS duration did not change, a finding also described by Rautahariu et al.`5 Circulation. Volume 52, October 1975 57t3 ECG CHANGES DURING & AFTER EXERCISE Table 2 Measurements from the Electrocardiograms Used in this Study* Explanation Units PPK-Q QRS Q-TPK P-1/8 ... P-8/8 msec msec msec AV QRS-1/8 ... QRS-8/8 ST-1/8. .. ST-8/8 IV ST-30 ... ST-90 AV SXA JV mV X msec Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 *The mean amplitude 20-10 Interval spatial maximum P wave - onset QRS complex QRS duration Interval onset QRS complex - spatial maximum T wave 8 time-normalized amplitudes of the P wave, with the maximal spatial magnitude or the P wave and QRS onset as reference points P-3/8 corresponds to the maximal spatial magnitude of the P wave 8 time-normalized amplitudes of the QRS complex 8 time-normalized amplitudes of the ST-T segment, with the end of the QRS complex and the maximal spatial magnitude of the T wave as reference points ST-8/8 corresponds to the maximum spatial magnitude of the T wave Amplitudes of the ST segment at 30, 50, 70, and 90 msee after the end of the QRS complex Area of the negative part of the ST segment msec before the onset of the QRS complex is the baseline for all measurements. measurements increased at higher heart rates. This was caused by the gradual shortening of the Q-TPK interval. At a heart rate of 60, ST-90 corresponds approximately to ST-4/8, while it corresponds to ST-6/8 at a heart rate of 180 beats/min. Also the slopes measured at fixed intervals after the QRS complex became steeper during exercise. On the other hand the slopes of the time-normalized ST segment hardly changed during exercise (fig. 2), a finding which is in agreement with the results obtained with Chebychev waveform vectors for the description of the STsegment changes during moderate exercise.`2 There is no apparent explanation for this discrepancy, other than the differences in the populations studied. The observed shift of the QRS and ST-T vectors toward the right and superiorly during exercise is in agreement with data published by Blomqvist8 and by Rautaharju et al. 12 This shift results in a depression of the QRS-ST junction followed by an ascending ST segment. This junctional depression has often been reported in different leads2 16f and is generally considered as a normal response to exercise. The junctional depression proved to be linearly related to heart rate.2 It should be noted that, while all timenormalized amplitudes in leads X and Y decreased during exercise, the amplitudes at ST-70 and ST-90 increased (table 3). Also the variances of these Possible Cause of ECG Changes During Exercise The factors which may contribute to the changes of - REST EXERCISE 90* API__ p .\-~~~~~~~~,. W9A Circulation, Volume 52, October 1975 Figure 2 Means of time-normalized instantaneous P, QRS, and ST vectors at rest and during exercise at heart rate of 160-180 beats/min. The Cartesian coordinates (X, Y, Z) have been plotted as well as the polar coordinates (M = magnitude; a = angle in the frontal plane; AP = angle toward the frontal plane). Vertical calibration of X, Y, Z, M is in mV; angles in degrees. a = 0: x-axis; + = vectors pointing toward inferior; A: vectors pointing anterior; P: posterior. SIMOONS, HUGENHOLTZ 574 mV Tz + 0.25+ X + + + + + HR + + + + 1 + .1. +~~~~~~~+ ++ -I +++0 +, + +~~ ~ HR -0 24 + y + +o +++++ as + ' + ++ + Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 HR RECOVERY EXERCISE HR Figure 3 Plots of X, Y, Z components, and magnitude (M) of the maximal P vectors at rest and during exercise, and the magnitude in the recovery period against heart rate. Regression equations are presented in table 3. (P - 3/8) mV +0.25 X I + + + + ;++HR 0 1, + + o0 .-At HR .0 *m44PT` r ++ + + - ++ ++# * 'p' + ++ -0 .254- M y + HR + IF +4Y HR Iuu 150 200 Figure 4 Plots of instantaneous 2/8 ST vectors during exercise against heart rate. Regression equations are presented in table 3. Circulation, Volume 52, October 1975 575 ECG CHANGES DURING & AFTER EXERCISE mV mV .2 0.251 |M X i , Figure 5 a-180, Plots of differences between rest and exercise ECGs. Means have been plotted of the records when the heart rate during exercise was 30-50 (thin line), 60-80 (dotted line), and 90-110 (heavy line) beats per minute higher than at rest. See legend figure 2. Note the gradual augmentation of the magnitude of the changes (M), while the mean directions of the changes (a, AP) are the same at different heart rates. +180 Z 90 p 9CA Table 3 Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 Regression Analysis of ECG Measurements and Heart Rate During Exercise Parameter PPK-Q QRS Q-TPK P -3/8 X Y Z QIiS-7/8 X Y Z ST -1/8 X Y Z ST -2/8 X Y Z ST -3/8 X Y Z ST -4/8 X Y Z ST -8/8 X Y Z ST - 30 X Y Z ST - 90 X SXA Y Z X Y N 356 405 404 3X56 356 356 405 405 405 404 404 404 404 404 404 404 404 404 404 404 404 404 404 404 405 405 405 405 405 405 404 404 Mean SD A 92 19 133 8 84 81 230 31 330 55 41 9 176 62 54 24 56 23 -90 162 200 -22 106 106 331 39,5 183 -30 51 108 -14 43 90 -12 34 -47 -16 46 94 - 8 39 77 -42 42 -90 2 47 94 3 38 73 -59 51 -109 26 52 106 81 18 40 -81 63 -130 275 118 384 142 76 221 -240 159 -277 -15' 45 78 66 -7 37 -43 43 -68 96 98 -58 12 50 58 -145 124 6 -1.7 2.3 3.4 -1.2 2.0 2.6 B -0.34 0.02 -0.81 0.1.5 0.95 -0.34 -2.35 -1.03 0.52 -1.12 -0.84 0.29 -0.89 -0.69 0.39 -0.75 -0.57 0.41 -0.6.5 -0. 51 0.40 -0.88 -0.69 0.30 -0.75 -0.59 0.21 1.25) 0.31 -1.22 -0.04 -0.03 r SEE 0.58 16* 0.09 8 0.88 15** 0.20 40 0.51 52* 0.21 55 0.49 142 0.33 100 0.10 0.74 0.67 0.28 0.6.5 0.61 0.31 0.54 0.50 0.27 0.42 0.43 0.21 0.25 0.28 0.06 0.57 0.53 0.16 0.43 0. 18 0.33 0.61 0.51 182 34** 32** 33 35** 31** 40 40* 33* 49 47 37 61 114 73 159 36* 32* 42 88 57 117 1.8** 1.8* *SEE < SD (P . 0.05). **SEE < SD (P . 0.01). Regression analysis of 32 selected ECG parameters with heart rate as independent variable (Y = A + B * X) in rest and exercise records. List of parameters in table 2. P-3/8 and ST-8/8 correspond to the maximum spatial magnitude of the P and T wave. Results of regression analysis of all ECG measurements during exercise and recovery can be obtained from the authors. Abbreviations N = number of records used; SD = standard deviation; A, B = regression parameters-intercept and slope; r = correlation coefficient; SEE = standard error of estimate. Circulation, Volume 52, October 1975 the P wave, the QRS complex, and the T wave during exercise include different positions of the recording electrodes relative to the heart at rest and during exercise; alterations of the action potentials or the atrial and ventricular activation patterns;3' 12 augmentation of the atrial repolarization wave (Ta);'6 temporarily increased serum potassium levels;'6 increased hematocrit,'8 and changes in the intracardiac blood volume.'122 However, none of these can account for all ECG changes during exercise, as will be shown below, and little is known about the combined effect of these factors. It is unlikely that the ECG changes are caused largely by differences in the position of the heart because the spatial orientation of the maximum P, QRS and T vectors remained constant (fig. 2). Alterations in the shape of the action potentials occur when the heart rate increases, and these may contribute to the ECG changes during exercise.3 It has been suggested3 that the augmentation of the P wave is caused by a more synchronous activation of the right and left atrium during exercise. However, the duration of the QRS complex did not change during or after exercise, and we observed no shortening of the P wave at heart rates from 60 to 120 beats/min, which makes this mechanism unlikely. It is striking that the changes of the QRS complex and the ST-T segment during exercise have similar spatial orientations and magnitudes. This suggests that one mechanism is responsible for both the QRS and the ST-T changes. Lepeschkin'6 indicated that the lowering of the R wave as well as a depression of the initial part of the ST segment may be caused by an augmented atrial repolarization wave. This Ta wave usually is opposite in direction to the P wave and becomes more negative when the P wave increases. During exercise, however, the most striking changes of the P amplitude were seen in the Y lead, while the largest changes of the ST vectors occurred in lead X. Also the ST-T SIMOONS, HUGENHOLTZ 576 changes were continuous from the terminal part of QRS until the peak of the T wave, which is far beyond the end of the Ta wave (fig. 5). Consequently, this mechanism can explain only part of the observations. Lepeschkin16 also suggested that temporarily increased serum potassium levels may be responsible for the T wave changes during exercise. However, Simonson did not find a correlation between the serum potassium levels and T wave amplitudes during strenuous work.'7 Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 The P waves observed during exercise in the present study correspond to the pattern of predominant right atrial overload which has been described recently by Ishikawa et al.23 It is generally accepted that changes in the intracardiac blood volume, as well as hematocrit changes, influence the apparent electric forces of the heart according to the Brody effect.23 Since the atrial depolarization fronts are largely tangentially oriented,25 an increased right atrial volume should cause a decrease in the right atrial forces, which is contradictory with the P wave pattern in right atrial overload.23 It is not clear how this dilemma can be explained. The study of Braunwald et al.P9 of the left ventricular volume in man during mild supine exercise, as well as recent data obtained during isometric exercise20 and in animal experiments,21, 22 shows a reduction of the left ventricular end-systolic volume during exercise. This may contribute to the lowering of the T wave during exercise, because the repolarization vectors are radially oriented. 26 The augmentation of the T wave after exercise may then be explained by a return of the end-systolic volume to resting levels, or even by a temporary overshoot of this volume immediately after exercise. The increased hematocrit caused by fluid loss during exercise"' may contribute to the augmentation of the P wave magnitude, as shown in animal experiments.27 However, as hematocrit increases only 10% during strenuous exercise, this factor may account for only 5-20% augmentation of the P wave. Nelson et al.28 have shown that the magnitude and orientation of the QRS vectors are altered by increased hematocrit. According to the Brody effect, the tangentially-oriented depolarization fronts in the right ventricle would be enhanced by this factor while the radially-oriented left ventricular forces25 would be reduced. This may explain the shift toward the right and superiorly of the QRS complex during exercise. While all these mechanisms need further analysis, it is attractive to consider the concept that the ECG changes during exercise are, in part, dependent on the hemodynamic performance of the heart. This concept is supported by the recent observation that patients with a manifest reduction of the R amplitude during exercise have benefited more from physical training than others who do not show such ECG changes.29 Clinical Implications The data presented in this study show that the P, QRS, and T waves in the ECG change gradually, in a predictable manner, during a multistage exercise procedure. In particular, the amplitudes of the P wave and the first half of the ST segment appeared to be linearly related to heart rate during exercise. The detailed analysis of the exercise ECG which permitted these observations was only possible after noise reduction by computer processing of the ECG signal. These findings imply that the diagnostic value of exercise ECGs may be improved when ST-segment measurements, obtained by digital computer techniques in a given subject, are compared with those in a control group at the same heart rate. As the measurements in the recovery period were different from those at corresponding heart rates during exercise, separate criteria should be used for analysis of exercise and recovery records. Preliminary results from our laboratory30 indicate that the sensitivity of the exercise ECG for detection of ischemic heart disease is indeed considerably enhanced when these principles are employed for interpretation of ECG measurements during exercise. References 1. SIIONSON, E: Effect of moderate exercise on the electrocardiogram in healthy young and middle-aged men. J Appl Physiol 5: 584, 1953 2. SJOSTRAND T: The relationship between the heart frequency and the S-T level of the electrocardiogram. Acta Med Scand 138: 201, 1950 3. IRISAWA H, SEYAMA I: The configuration of the P wave during mild exercise. Am Heart J 71: 467, 1966 4. BLOMQVIST CG: The Frank lead exercise electrocardiogram; quantitative study based on averaging technic and digital computer analysis. Acta Med Scand 178 (suppl 440) 1965 5. BRUCE RA, MAZZARELLA JA, JORDAN JW JR, GREEN E: Quantitation of QRS and ST segment responses to exercise. Am Heart J 71: 455, 1966 6. HORNSTEN TR, BRUCE RA: Computed ST forces of Frank and bipolar exercise electrocardiograms. Am Heart J 78: 346, 1969 7. SMITH RF: Quantitative exercise stress testing in the naval aviator population and in the projected Apollo spacecraft experiment MO-18. In Measurement in Exercise Electrocardiography. The Ernst Simonson Conference, edited by BLACKBURN H. Springfield Ill, C C Thomas, 1969, p 131 8. BLOMQVIST CG: Variations of the electrocardiographic response to exercise under different experimental conditions; deconditioning, reconditioning and high altitude. In Measurement in Exercise Electrocardiography. The Ernst Simonson Conference, edited by BLACKBURN H. Springfield Ill, C C Thomas, 1969, p 299, p 323 9. SHEFFIELD LT, HOLT JH, LESTER FM, CONROY DV, REEVES TJ: On-line analysis of the exercise electrocardiogram. Circulation 40: 935, 1969 10. BRUCE RA: Exercise testing of patients with coronary heart disease. Ann Clin Res 3: 323, 1971 Circulation, Volume 52, October 1975 ECG CHANGES DURING & AFTER EXERCISE Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 11. BRUCE RA, Li YB, DOWER GE, NILSON K: Polarcardiographic responses to maximal exercise and to changes in posture in healthy middle-aged men. J Electrocardiol 6: 91, 1973 12. RAUTAHARJU PM, PUNSAR S, BLACKBURN H, WARREN J, MENOTTI A: Waveform patterns in Frank-lead rest and exercise electrocardiograms of healthy elderly men. Circulation 48: 541, 1973 13. BAART J: De oudere havenwerker, aspekten van zijn cardiorespiratoire conditie. Thesis. Rotterdam, 1973 14. SIMOONS ML, BOOM HBK, SMALLENBURC E: On-line processing of orthogonal exercise electrocardiograms. Comput Biomed Res 8: 1975 15. RAUTAHARJU PM, WOLF H, BLACKBURN H, WONG A: The accuracy of computer measurements from the Frank lead exercise electrocardiograms. In Aktuelle Probleme der Vektorkardiographie, herausgegeben von Wenger R. Stuttgart, G Thieme, 1968, p 375 16. LEPESCHKIN E: Physiological factors influencing the electrocardiographic response to exercise. In Measurements in exercise electrocardiography. The Ernst Simonson Conference, edited by BLACKBURN H. Springfield Ill, C C Thomas, 1969, p 363 17. SIMONSON E: Discussion on physiological factors influencing the electrocardiographic response to exercise. Op. cit., p. 386 18. DE LANNE R, BARNES JR, BROUHA L: Hematological changes during muscular activity and recovery. J Appl Physiol 15: 31, 1960 19. BRAUNWALD E, SONNENBLICK EH, Ross J JR, GLICK G, EPSTEIN SE: An analysis of the cardiac response to exercise. Circ Res 40 (suppl I): 1-44, 1967 20. LUDBROOK P, KARLINER JS, O ROURKE RA: Effects of submaximal isometric handgrip on left ventricular size and Circulation, Volume 52, October 1975 577 wall motion. Am J Cardiol 33: 30, 1974 21. ERICKSON HH, BISHOP VS, KARDON MB, HOWITz LD: Left ventricular internal diameter and cardiac function during exercise. J Appl Physiol 30: 473, 1971 22. HORWITZ LD, ATKINS JM, LESHIN SJ: Role of the Frank-Starling mechanism in exercise. Circ Res 31: 868, 1972 23. ISHIKAWA K, KINI PM, PIPBERGER HV: P wave analysis in 2464 orthogonal electrocardiograms from normal subjects and patients with atrial overload. Circulation 48: 565, 1973 24. BRODY DA: A theoretical analysis of the intracavitary blood mass influence on the heart-lead relationship. Circ Res 4: 731, 1956 25. DURRER D, VAN DAM RT, FREUD GE, JANSE MJ, MEIJLER FL, ARZBAECHER RC: Total excitation of the isolated human heart. Circulation 41: 899, 1970 26. ABILDSKOV JA, MILLAR K, BURGESS MJ, GREEN L: Characteristics of ventricular recovery as defined by the vectorcardiographic T loop. Am J Cardiol 28: 670, 1971 27. HEIKKILX J, HUGENHOLTZ PG, TABAKIN BS: Prediction of left heart filling pressure and its sequential change in acute myocardial infarction from the terminal force of the P wave. Br Heart J 35: 142, 1973 28. NELSON CV, RAND PW, ANGELAKOS ET, HUGENHOLTZ PG: Effect of intracardiac blood on the spatial vectorcardiogram. I. Results in the dog. Circ Res 31: 95, 1972 29. KENTALA E, HEIKKILX J, PYORXLX K: Variation of QRS amplitude in exercise ECG as an index predicting result of physical training in patients with coronary heart disease. Acta Med Scand 194: 81, 1973 30. SIMOONS ML, SMALLENBURG E, ZEELENBERC C, ENGELSE W: On-line processing of exercise ECG's. In Proceedings, Computers in Cardiology. Washington DC, 1974 (in press) Gradual changes of ECG waveform during and after exercise in normal subjects. M L Simoons and P G Hugenholtz Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017 Circulation. 1975;52:570-577 doi: 10.1161/01.CIR.52.4.570 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1975 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/52/4/570 Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. 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