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Transcript
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
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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
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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
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*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 +
'
+ ++
+
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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
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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
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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
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Circulation. 1975;52:570-577
doi: 10.1161/01.CIR.52.4.570
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