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Electrocardiography In Elite Athletes
F. CARRE and J.C. CHIGNON*
Department of Physiology, Pontchaillou Hospital
35003 Rennes, France
*National Institute of Sports, 11 Avenue du Tremblay,
75012 Paris, France.
Electrocardiographic (ECG) features commonly observed in top
ranking sportsmen were first described in 1929 by Hoogerwerf. The
development of new non-invasive exploration methods (i.e. cardiac
echocardiography and magnetic resonance imaging) in the early
1970s offered physiologists the means of investigating the so-called
"Athlete's Heart Syndrome" recognized by its specific ECG features.
Standard ECG tracings have the advantage of low cost, ready
availability and ease of use and remain an essential investigation
tool. In trained subjects, ambulatory ECG monitoring and stress
testing ECG are particularly important as they provide
supplementary information to the classical 12-ECG which records
only a brief period of cardiac electrical activity.
The features of the athlete's ECG basically reflect the heart's
normal physiological adaptation to repetitive physical training.
However several unusual patterns appear to be quite similar to
pathological aspects occurring in different heart diseases. It is thus
essential to acquire a full understanding of the ECG patterns in the
elite athlete.
2
Interpretation of the athlete's ECG
A highly trained athlete is usually defined as a subject who
practices at least ten hours a week at a level of intensity reaching at
least 60 percent of his maximal oxygen consumption (Use Word 6.0c or later to
view Macintosh picture.
O2max).
Consequently, and athlete's ECG must always be interpreted in light
of his individual level of training, both qualitatively and
quantitatively, and in accordance with the physical examination,
functional signs and his personal and familial cardiovascular risk
factors, including age.
The most common ECG features described in elite athletes can
be observed in all age groups and in both men and women, however
they are not always found in every elite athlete. They result from
physiological adaptations to physical conditioning and should not be
immediately interpreted as markers of heart disease. The
mechanisms underlying the disturbances observed on the athlete's
ECG are not yet fully understood although modifications in
autonomic nervous system tone and cardiac hypertrophy are often
proposed as significant explanations.
Modifications in autonomous nervous system tone have been
described in the athlete's heart syndrome on the basis of
biochemical and pharmacological tests. Another way of evaluating
the effect of changes in parasympathetic and sympathetic tone is to
study heart rate variability. Characteristically, there is an increase in
parasympathetic tone and a decrease in sympathetic tone (perhaps
through the effect of lower baroreceptor sensitivity). At rest,
vagotonia appears to predominate whereas during exercise the
3
deceased sympathetic drive results in the slower heart rate observed
in athletes compared with untrained subjects performing the same
work load.
Cardiac hypertrophy in the athlete was first suspected by
Henschen in 1899 on the basis of chest percussion and has been
confirmed by non-invasive morphology investigations including
radiology, echocardiography and more recently magnetic resonance
imaging. It is described as a four-chamber harmonious wall
hypertrophy-chamber dilation which can be observed at all ages and
appears to be totally reversible after deconditioning.
There is some controversy in the literature as to the real
incidence of ECG disturbances. For example, in two studies based on
a large sample population (Venerando published a series of 12,000
subjects and in our own personal unpublished work we investigated
6,487 subjects) the global prevalence of ECG disturbances was found
to be 13 and 44 percent respectively. This difference could be
explained by differences in methodology in the training level since
the ECG criteria for diagnosis of cardiac hypertrophy have not been
standardized.
The mean ± SD values of classical ECG criteria as observed in
our study are given in Table I in comparison with the ranges
classically described in a standard population. In general, the ECGs of
athletes lie within standard limits. A few trends which increase with
training level can however be seen. The durations of the PR interval,
the QRS complex and the corrected QT interval increase with the
Sokolow-Lyon Index and frontal QRS axis turns to the left. Even
though the ECGs of elite athletes lie within normal limits, different
patterns of ECG disturbances have been described.
4
For the purposes of this review, we have divided these changes
into rhythm disorders, atrio-ventricular conduction impairment,
cardiac hypertrophy related ECG criteria and disturbed
repolarization. Finally, we shall try to specify the potential differences
observed in endurance versus resistance in the trained athlete.
Changes in cardiac rhythm
Hypokinetic Arrhythmias
The respective incidences of changes in cardiac rhythm and
hypokinetic arrhythmias are summarized in Table II.
Resting sinus bradycardia is the most common finding among
trained athletes. It is difficult to determine the real incidence of
athlete's bradycardia due to the lack of a common definition of
bradycardia. The incidence varies from 8 to 85% in studies using the
cut-off of 60 beats per minute, and in our study, we found only 9% of
our athletes with a resting heart rate below 50 beats per minute.
Controlled Holter recordings have shown a significantly lower mean
hourly heart rate. Training undoubtedly affects the incidence of
bradycardia but the role of individual sensitivity and the mechanisms
of training-induced bradycardia have yet to be established.
Classically, the alterations in the autonomous nervous system
described above would have an effect, but some studies have shown
that lower intrinsic heart rate is also related to athlete's bradycardia.
In most cases, the bradycardia is benign as confirmed by normal
rhythms recorded during stress testing and also by the persistence of
physiological circadian variations (lower nocturnal heart rate) on
Holter recordings. Rarely, the bradycardia is associated with
5
dizziness, syncope or hyperkinetic arrhythmias due to vagal tone. In
general, these symptoms disappear with deconditioning. Electrical
stimulation is rarely needed and usually concerns older athletes in
whom a latent sinus node disease is unmasked by the increased
vagal tone. The resting heart rate in individuals with athlete's
bradycardia correlates with their individual level of peak training,
and is used as a criteria for evaluating their level of training although
it is not well correlated with performance or Use Word 6.0c or later to
view Macintosh picture.
O2max. A better index
of training level would be the heart rate recovery curve. The rapidity
at which the heart rate returns to the basal level (or near basal level)
would be an indication of a good level of training. An unusual
disturbance of the resting sinus rate which cannot be explained by a
change in the training regimen, is commonly considered to be a
feature of overtraining.
Other hypokinetic dysrhythmias also concern the sinus rhythm
and are related to altered autonomous tone. They disappear during
stress training. These modifications are frequently observed on
ambulatory ECG recordings, particularly at night. They are of no
prognostic significance.
The prevalence of sinus dysrhythmia , the so-called
"respiratory arrhythmia", would appear to be significantly higher in
athletes than in the standard population, but in fact the apparent
sinus dysrhythmia disappears when the variability of R-R interval as
a function of basal heart rate is taken into account (R-R interval
variation increases with decreasing heart rate). This is a well-
recognized ECG pattern on ambulatory ECGs where the sinus pauses
during both awake and (especially) sleeping hours are significantly
longer on athlete's recordings than on control recordings.
6
Ectopic atrial rhythm including the wandering atrial pacemaker
or coronary sinus rhythm have also been described.
Nodal rhythm is more frequent in elite athletes. The escape threshold
varies from 45 to 65 beats per minute and in some cases (in 15% of
the subjects in our study) escape rhythm totally disappears only
above 100-120 beats per minute.
Idioventricular rhythm (Figure 1) is the event of a low sinus
rate and/or of sinus pauses. This cardiac rhythm originates in
pacemaker cells at a rate of 40 to 100 beats per minute.
Hyperkinetic Arrhythmia
Hyperkinetic arrhythmia involves premature supraventricular
and ventricular beats. These disorders can be detected on the
resting ECG but most of the studies have used Holter monitoring to
best quantify these episodes of arrhythmia. A training session during
the monitoring period is useful because ECG stress training does not
always produce significant episodes. It is important to study
arrhythmia during exercise and during recovery to clarify the links
with autonomous tone and the epinephrine effect.
Supraventricular Arrhythmias
The incidence of premature supraventricular beats observed in
trained athletes (37.1 to 100%) is similar to, or higher than, that
seen in the standard population (20-80%). Some authors relate
premature supraventricular arrhythmias to training level and suggest
athlete's bradycardia could be an explanation. Most often, these
premature beats are isolated and infrequent (less than 15 to 20 per
24 hours). They are asymptomatic and may disappear during
7
exercise. Complex supraventricular tachyarrhythmias which provoke
palpitations are rarely described (0.5 to 5%) and suggest an
underlying heart disease such as the Wolff-Parkinson-White
syndrome or prolapsus of the mitral valve. The role of vegetative
imbalance has been suggested in cases of paroxysmal atrial
fibrillation.
Ventricular arrhythmias
On resting ECG recordings, the incidence of ventricular
arrhythmias in trained athletes is similar to or much higher (0.5 to
4%) than in the standard population (0.6 to 0.7%). On the basis of
Holter studies, most authors conclude that the incidence in athletes
(30 to 45%) is the same as in untrained subjects (16-55%) but in one
controlled study, the incidence was higher in athletes (70%).
Generally, premature ventricular beats are unifocal, isolated,
infrequent (less than 50 per 24 hours), asymptomatic and disappear
at the onset of exercise.
In our clinical experience with regularly screened athletes, we
distinguished (Figure 2) between old asymptomatic arrhythmia,
which disappears during exercise and reappears during the slow
phase of recover and which we consider to be benign, and a newly
occurring, often symptomatic (unexplained decline in performance)
ventricular arrhythmia which usually persists or becomes worse
during stress testing. This situation, which suggests catecholamine
sensitive focal arrhythmia, always requires a complete cardiac
examination to eliminate a latent heart disease. Overtraining, which
sometimes provokes hyperkinetic arrhythmias through changes in
8
biological mechanisms, must be suspected only if the cardiac
examination is normal.
Other complex ventricular arrhythmias such as multifocal or
repetitive premature ventricular beats, ventricular tachycardia and R
on T phenomena appear to have the same incidence in trained and
untrained individuals. Some authors have observed paroxysmal
ventricular tachycardia in 0 to 7.5% of athletes (ventricular
tachycardia is classically nocturnal but sometimes appears in
daytime) and in 0 to 5.7% in untrained subjects. Here again some
authors describe a higher incidence of complex arrhythmias in
trained subjects and explain their controversial results by the
training level in the general population. For these authors regular
moderate physical training could protect against ventricular
arrhythmias while very intensive training could favor them, perhaps
through a prolonged QT interval. In contrast with cases of
pathological cardiac hypertrophy, no study has been able to
demonstrate a correlation between ECG or echocardiographic cardiac
hypertrophy and hyperkinetic arrhythmia in athletes.
In concluding this chapter, it can be stated that hypokinetic
arrhythmias in athletes are common and benign. The discovery of an
episode of hyperkinetic arrhythmia, particularly ventricular
hyperkinetic arrhythmia, in an athlete often raises the question as to
how many single extra beats should be tolerated. This is especially
true in high level trained subjects who undertake maximal exercise
regularly and often encounter the well-known adrenergic stress. It
would appear that the prevalence of hyperkinetic arrhythmia is
nearly the same in trained and untrained people and that cardiac
adaptation to intensive training itself is not a determinant cause of
9
malignant arrhythmia. Therefore the discovery of a recent or serious
episode of hyperkinetic arrhythmia in an elite athlete would require a
full cardiac examination with Holter monitoring, stress testing,
echocardiography, and if necessary an electrophysiologic study.
Impaired atrio-ventricular conduction
First or second (with a Luciani-Wendkeback period, see Figure
3) degree atrio-ventricular block is relatively common in athletes
(Table III). Inversely, third degree functional block is rarely described
and until now the Mobitz type II and higher degree atrio-ventricular
blocks must be considered as pathological and require cardiologic
screening. These disorders result mainly from changes in
autonomous tone and disappear during stress testing and or
pharmacological tests.
Their higher, although intermittent (nocturnal predominance),
incidence in Holter studies (Table III) would confirm their functional
character. A correlation with training intensity has been reported.
Although the same physiological explanations have been proposed
as for hypokinetic arrhythmia and conduction disorders in athletes, it
must be noted that no real correlation has yet been described linking
the two phenomena.
The prevalence of the pre-excitation syndrome (i.e. the Wolff-
Parkinson-White syndrome and the short PR syndrome) in athletes is
nearly the same as in the standard population (0.16 to 1%) even
though changes in autonomous tone could unmask accessory
pathways. The discovery of a pre-excitation syndrome in trained
subjects always requires a full cardiac exploration.
10
Ecg Disturbances Partly Related To Cardiac Hypertrophy
As noted above, cardiac hypertrophy in the athlete is described as a
classical "physiological" example of adaptative increase in heart
volume. Many different ECG criteria have been proposed for the
diagnosis of athlete's cardiac hypertrophy based on isolated voltage
criteria (i.e. the Sokolow-Lyon Index) or voltage and non-voltage
criteria (i.e. the Romhilt-Estes Point Score System) such as
intraventricular conduction delays and/or repolarization disturbances.
Unfortunately, the different ECG parameters of cardiac hypertrophy
observed in athletes are poorly correlated with the results of non-
invasive investigations such as echocardiography or with those of
invasive or anatomic studies. This can be explained, at least
partially, by the fact that these populations are comprised of young
and physically fit individuals. Thus the ECG does not appear to be an
extremely useful tool for the assessment of cardiac hypertrophy in
the athlete.
Nevertheless, it is essential to recognize the features of elite
athletes' ECGs. Increased P wave amplitude, with or without
notching, can be observed although several studies failed to
demonstrate any significant difference compared with matched
controls. Right ventricular hypertrophy, based on the classical
Sokolow-Lyon Index (RV1 + SV5), has been reported in 4.5 to 6.9% of
athletes.
In heterogeneous and small samples of athletes, the incidence
of left ventricular hypertrophy based on a Sokolow-Lyon Index (SV1
+ RV5 or RV6) > 35 mm has been reported to vary from 8 to 85%
11
compared with 5% in the general population. Inversely, in our study
of a large population of trained subjects (Table I), and in the study by
Venerando et al. (12,000 subjects), there was no real enhancement
of the Sokolow-Lyon Index.
The use of new cardiac hypertrophy ECG criteria, including
total QRS amplitude in 12-lead ECGs, appears to be helpful and in
our own study (Table IV) we found that this sum (mean: 192 ± 40
mm) was higher than the classical sedentary sum (< 128 mm) but
clearly less than the sums described in heart diseases (aortic
stenosis > 244 mm; aortic regurgitation > 246 mm). Based on
vectocardiographic criteria, the prevalence of left ventricular
hypertrophy is about 40% (37-46%).
Electrical wave delays have also been studied in athletes. The
incidence of right and left atrial hypertrophy is low. The duration of
QRS complexes is correlated with the size of the heart chambers and
many authors suggest that the best criteria for right ventricular
hypertrophy in the athlete is the presence of intraventricular
conduction delay. This delay, which appears on the ECG tracing as a
notching or slurring of the QRS complex on D3, aVF and on the right
precordial leads, is often observed (3.2 to 70%). These features
suggest, as does the well-known incomplete right bundle branch
block (prevalence 1.7 to 51%), an asymmetrical cardiac hypertrophy
with right ventricular predominance. Though vectrocardiographic
studies have also noted a high frequency of right ventricular
hypertrophy (18 to 30%) this explanation is questionable since
echocardiographic data do not offer a confirmation. Incomplete right
bundle branch block does not appear to be linked to changes in
autonomous tone since it persists during stress testing. Ventricular
12
apical thickness may be involved. Complete right bundle branch
block is much rarer (0.08 to 0.31%) and left bundle branch block is
normally not observed in the elite athlete.
Unlike cardiac patients, and in spite of these cardiac
hypertrophy ECG criteria, the QRS axis is often normal. A vertical
QRS axis may be observed (10 to 27%) and left deviation is seldom
reported (10 to 12%). Similarly, associated pathological
repolarization is not common.
In summary, trained athletes show a high incidence of cardiac
hypertrophy based on ECG criteria. These phenomena, including
right bundle branch block, are related to physical training since the
incidence decreases significantly with deconditioning. Nevertheless,
these features cannot be fully explained by cardiac hypertrophy
alone. Besides anatomic heart adaptation, other factors including
age, body weight, body surface area, fat-free weight and depth of
the heart in the chest may also play a role. ECG criteria of cardiac
hypertrophy are however, as are echocardiographic features, quite
different in elite athletes as compared with those described in the
patients with heart diseases.
Repolarization disturbances
Repolarization disturbances are a striking feature observed in
"athlete's heart syndrome". These phenomena lie between a
physiologic and pathologic state (i.e. pericarditis, ischemia,
metabolic disturbances.…). It is difficult to give a precise assessment
of their prevalence partly because of seasonal and career variations.
Holter monitoring is less useful than stress testing in this situation.
13
No single explanation has been proposed for these disturbances,
although changes in autonomous tone and/or cardiac hypertrophy
and/or electrolyte abnormalities have been proposed. These
repolarization disturbances are generally asymptomatic.
Several classifications have been proposed. We think the most useful
is the descriptive classification developed by Zeppilli and Caselli.
These authors propose four criteria. Criteria (a) and (b) are
classically described asminor repolarization abnormalities.
Criteria (a), the so-called "early repolarization syndrome" is
the most frequent (10-100%). The top of the ST-T segment
elevation often has a dip in the initial portion. It has been
speculated that changes in autonomous tone could be the cause.
Sympathetic tone decrease reveals inherent a non-homogeneity
phase of the ventricular repolarization, the epicardium
repolarizing first. The ECG pattern, well-correlated with duration
and training level is age-dependent and benign. This is supported
by the fact that it disappears either at the onset or early during
stress testing.
Criteria (b) is classically characterized as negative T waves
in inferior (D2, D3 or aVF) or right precordial (V1-V3) leads; low
amplitude or flat T waves can also be observed. Described in 3-
31% of the trained population, they regress as a general rule
during exercise. They must be related to vagotonic-induced
heterogeneity of the myocardial action potential. They are
sometimes associated with echocardiographic criteria for cardiac
hypertrophy.
14
Criteria (c) and (d) are described as marked repolarization
disturbances. In our experience as in that of Venerando, the
prevalence is relatively low (0.6-2.8%). A complete cardiac work-up is
always needed.
Criteria (c) is defined as JT segment depression with positive
low-voltage isoelectric or diphasic T waves. This feature which
evokes subepicardial ischemia is a questionable physiological
adaptation and must be assessed carefully because it disappears
inconsistently during stress testing or after a long period of
deconditioning.
Criteria (d) is defined as T wave inversion in the left
precordial leads (V4 - V6) which also disappears inconsistently
during stress testing (Figure 4).
In a study involving 98 athletes who presented features (b), (c)
and (d), Zeppilli et al. reported no demonstrable heart disease in
53%, prolapsus of the mitral valve in 37%, hyperkinetic heart
syndrome in 3% and hypertrophic cardiomyopathy in 4%. More
recently certain authors have stressed that negative T waves on the
right precordial leads in athletes, especially when associated with
incomplete right bundle branch block or premature ventricular beats
with a left bundle branch block configuration, may reveal right
ventricular dysplasia.
Other repolarization disturbances have been described in the
elite athlete including the common and benign evident U wave
(especially in precordial leads) and a prolonged corrected QT interval
(prevalence 10 to 15%) which could be explained by changes in
15
autonomous tone and for which, in trained subjects, no real
relationship with ventricular arrhythmias has been observed.
Thus the prevalence of ECG and vectocardiography patterns of
repolarization disturbances, especially minor abnormalities, is higher
in trained individuals than in the untrained population. No
unequivical explanation has been proposed. These features vary
spontaneously and are not correlated with physical fitness. Their
interpretation must take into account different factors including age,
ethnic origin, training level and symptoms. Venerando has stressed
the criteria of benign disturbances: healthy and totally asymptomatic
athletes with good physical capacity (VO2max), normal duration of
QRS complex and lack of (or constantly reversible) spontaneous
(exercise) or induced (pharmacodynamic tests) ECG abnormalities.
In the present state of the art, the recent discovery of marked
repolarization abnormalities requires a compete cardiac work-up,
including at least stress testing and echocardiography.
Comparison Of "Endurance" And "Power"
Physiological adaptation is generally divided into two
categories resulting from the effects of two types of training
methods: aerobic and anaerobic. Actually, the results of both ECG
and echocardiographic studies are rather controversial. This can be
explained, at least in part, by the fact that most athletes undertake
both types of training simultaneously.
In our personal study (Figure 5) we found that the prevalence
of bradycardia and incomplete right bundle branch block was higher
in endurance than in power athletes. Inversely, premature
16
ventricular beats occurred more frequently in power athletes. Some
authors stress the fact that sinus pauses longer than 2,000 ms, ECG
criteria of left ventricular hypertrophy and prolongation of the
corrected QT interval are more frequent in endurance athletes. On
the other hand, some authors suggest that marked repolarization
disturbances tend to be associated more readily with isometric
training.
17
Suggested readings:
1- Carré F. and J.C. Chignon. Advantages of electrocardiographic
monitoring in top level athletes. Int. J. Sports Med. 12: 236-240, 1991
2- Ferst J.A. and B.R. Chaitman. The electrocardiogram of the athlete.
Sports Med. 1: 390-403, 1984
3- George K.P., L.A. Wolfe, G.W. Burgraff. The "Athletic Heart
Syndrome". Sports Med. 11: 300-331, 1991
4- Huston T.P., J.C. Puffer, W.M. Mc Millan-Rodney. The athletic heart
syndrome. New Eng. J. Med. 313: 24-32, 1985
5- Lichtman J., R.A. O'Rourke, A. Klein et al. E.C.G of the athlete.
Arch. Intern. Med. 1323: 763-770, 1973
6- Rost R.and W Hollmann. Athlete's heart- a review of its historical
assessment and new aspects. Int. J. Sports Med. 4: 147-165, 1983
7- Venerando A. Electrocardiography in sports medicine. J. Sports
Med and Phys. Fitness. 19: 107-128, 1979
8- Zeppilli P., A. Pelllicia, M.M Pirrami et al. Ethiopathogenetic and
clinical spectrum of ventricular repolarization disturbances in
athletes. J. Sports Cardiol. 1: 41-51, 1984
18
Figure Legends
Figure 1. Intermittent idioventricular rhythm in a long distance
runner. Precordial lead V3, amplitude divided by two.
Figure 2. Two typical cases of isolated premature ventricular beats
observed on 24-hour Holter recordings in athletes.
Subject 1 was a soccer player with old, asymptomatic, isolated
premature ventricular beats. Hourly frequency of premature beats
does not vary.
Subject 2 was a weight lifter with recent, symptomatic, isolated
premature ventricular beats. A peak frequency occurred during two
training sessions (T)
h = hours of monitoring, nb•h-1 = number of premature ventricular
beats per hour.
Figure 3. Asymptomatic second degree atrio-ventricular block with a
Luciani-Wenckeback period observed in a cyclist during the
competition period. P waves are noted with an arrow ().
Figure 4. An asymptomatic, 35-year-old, well-trained long distance
runner.
Resting ECG shows incomplete right bundle branch block and a
negative T wave in the V5 lead.
Maximal exercise ECG shows a significant (2 mm) JT depression (V5).
Recovery ECG (5 min) showing a normalization of the T wave on V5.
19
Exercise thallium myocardial scintigraphy was normal and
echocardiography showed an asymmetrical septal hypertrophy (12
mm).
Figure 5. Respective prevalence of resting ECG features observed in
endurance athletes (n = 5,700) and power athletes ( n = 526) in our
own study. BRA = sinus bradycardia, AVB = atrio-ventricular block,
RBBI = incomplete right bundle branch block, SVPB = premature
supraventricular beats, VPB = premature ventricular beats.
20
Table Legends
Table I. Classical ECG criteria: comparison between trained
individuals and general population.
These data were obtained in men and women 15 to 40 years of age.
Data concerning trained individuals were observed in athletes
examined at the French National Institute of Sports. Three training
level groups were described: I (three to five hours per week), II (five
to ten hours per week), III (more than ten hours per week, national
team level).
Data concerning the general population were described by Blondeau
and Hiltgen, 1980 (15-19 years of age, n = 200; 20-29 years, n =
200; 29-39 years, n = 200).
* T wave amplitude measured on the precordial lead V5
** QT corrected for a heart rate of 60 beats per minute
*** QT corrected using the Bayes formula.
Table II. Incidence (%) of athlete's hypokinetic arrhythmia
Ranges are based on the highest and lowest values reported in the
literature and were observed in controlled and uncontrolled studies.
bpm = beats per minute
(--) = no data available.
Table III. Incidence of athlete's atrio-ventricular conduction
impairment
Ranges are based on the highest and lowest values reported in the
literature and were observed in controlled and uncontrolled studies.
21
* One study (Viitasalo et al., 1982) reported an incidence of 8.6% for
Mobitz II atrio-ventricular blocks which were, very probably, in fact
Luciani-Wenckebach type II atrio-ventricular blocks with a very small
increment in the PR interval duration (personal communication of the
authors).
Table IV. Comparison of two ECG criteria (mean ± SD) for cardiac
hypertrophy in trained subjects, (n = 730).
Three training level groups were described (see Table I).Use Word 6.0c or later to
view Macintosh picture.
O2max = maximal oxygen consumption.
S-L Index = Sokolow-Lyon Index (SV1 + RV5 or RV6).
Total QRS = sum of the QRS complex amplitudes in the twelve ECG
leads.