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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.

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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

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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.

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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

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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.

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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

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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

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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

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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.

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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%

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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

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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.

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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.

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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

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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

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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.

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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

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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.

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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.

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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.

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* 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.