This results in eccentric hypertrophy with a more
pronounced increase in wall thickness than expected.- The strength-trained athlete adapts by developing a
concentric hypertrophy with an increase in absolute
and relative wall thickness without significant
changes in end-diastolic diameter.
PHYSICAL EXAMINATION
- The heart rate of well-conditioned athletes is usually
between 40 and 60 bpm, secondary to enhanced vagal
tone and decreased sympathetic tone. Normal sinus
arrhythmia may be more noticeable. - The physiologic splitting of S2 may be slightly
delayed during inspiration. An S3 may be noted in
endurance-trained athletes secondary to the increased
rate of left ventricular filling associated with the rela-
tive left ventricular dilatation (Zeppilli, 1988). - While an S4 may be noted in strength-trained athletes
secondary to concentric hypertrophy, its presence
always warrants clinical evaluation. Functional mur-
murs may be noted in 30–50% of athletes on careful
examination (Huston, Puffer, and Rodney, 1985).
ELECTROCARDIOGRAPHIC CHANGES
•Several minor electrocardiogaphic variations have
been commonly noted in highly trained athletes and
are considered to be consistent with the athlete’s heart
syndrome (Huston, Puffer, and Rodney, 1985; Oakley
and Oakley, 1982) (Tables 25-1 and 25-2).
- More significantly abnormal appearing electrocardio-
gram(EKG) patterns have also been identified in other-
wise normal athletic hearts. In a recent Italian study
(Pelliccia et al, 2000), 1005 athletes were consecu-
tively assessed with EKGs and echocardiograms. The
study found that 40% of the athletes had abnormal
EKGs, not including the minor alterations associated
with the athlete’s heart syndrome mentioned above. Of
these athletes, 36% had distinctlyabnormal patterns. Of
those with the distinctly abnormal patterns, only 10%
actually had evidence of structural cardiac disease,
suggesting that the EKG manifestation of the normal
athletic heart is much more variable than previously
believed.
SUDDEN DEATH IN EXERCISE- While there is considerable net cardiovascular benefit
to exercise, there is also a clear risk for susceptible
individuals. Indeed, as Barry J. Maron (Maron, 2000)
has clearly shown, there is a “paradox of exercise”
that requires a clinical assessment of risk prior to the
initiation of a vigorous program.
•Overall risk of sudden death during exercise is low.
Estimates from various studies (Siscovick et al, 1984;
Ragosta et al, 1984; Thompson et al, 1982; Maron,
Poliac, and Roberts, 1996; Van et al, 1995; Maron,
Gohman, and Aeppli, 1998) range from 1:15,000 jog-
gers per year (Siscovick et al, 1984; Thompson et al,
1982) to 1:50,000 marathon participants (Maron,
Poliac, and Roberts, 1996). For high school and col-
lege-aged athletes the range is estimated at 1:200,000
to 1:300,000 per academic year (Van camp et al, 1995;
Maron, Gohman, and Aeppli, 1998). - The specific etiologies contributing to sudden cardiac
death are most closely related to age. Generally, the
dividing age is 35 (Basilico, 1999). This primarily stems
from the observation that for sudden deaths over age 35,
over 75% are associated with coronary artery disease.
The high prevalence of atherosclerosis in this age group
clearly predominates as an etiology. - In younger athletes, nonobstructive hypertrophic car-
diomyopathy(HCM) is the most common etiology.
Coronary artery anomalies, myocarditis, premature
atherosclerotic disease, and dilated cardiomyopathy
are next most common, at least in the United States.
In European studies (Tabib et al, 1999; Firoozi et al,
2002; Priori et al, 2002), arrhythmogenic right ven-
tricular cardiomyopathy(ARVC) is more commonly
recognized as an etiology than it is in the United
States. Other less common etiologies include aortic
rupture from Marfan’s syndrome, genetic conductive
system abnormalities, idiopathic concentric left ven-
tricular hypertrophy, substance abuse (cocaine or
steroids), aortic stenosis, mitral valve prolapse,
TABLE 25-2 Rhythm Disturbances on Resting
Electrocardiograms of the General Population and Athletes
GENERAL
ARRHYTHMIA POPULATION (%) ATHLETES (%)
Sinus bradycardia 23.7 50–85
Sinus arrhythmia 2.4–20 13.5–69
Wandering atrial pacemaker — 7.4–19
First degree block 0.65 6–33
Second degree block — —
Mobitz I 0.003 0.125–10
Mobitz II 0.003 Not reported
Third degree block 0.0002 0.017
Nodal rhythm 0.06 0.031–7
Ventricular pre-excitation 0.1–0.15 0.15–2.5
Atrial fibrillation 0.004 0–0.063142 SECTION 3 • MEDICAL PROBLEMS IN THE ATHLETE
TABLE 25-1 Common ECG Findings in Athletic
Heart Syndrome
Sinus bradycardia Sinus arrhythmia
First-degree AV block Wenckebach AV block
Incomplete RBBB Notched P waves
RVH by voltage criteria LVH by voltage criteria
Repolarization changes QTc interval at upper limit
Tall, peaked and inverted t waves