Athlete’s heart syndrome
Why very fit hearts can often appear diseased
by Leonard Schwartz, MD
Vol.17, No.05, May 2009

More and more adults are participating in athletics, particularly aerobic sports such as cycling and running. This can lead to cardiovascular adaptations that — while physiological — may be difficult to distinguish from disease, particularly demonstrated by electrocardiography and rhythm. This pattern of changes is commonly referred to as athlete’s heart syndrome.

Heavy exercise can bring cardiovascular changes that may be misinterpreted as pathological, leading to anxiety or invasive investigation. They can conversely be misread as benign when in fact they’re indicative of underlying disease.

Sir William Osler had an interesting perspective on exercise and the older patient:

Golf and bicycle have in the past few years materially lowered the average incomes which doctors in this country can derive from persons under forty. From the senile contingent — those above this age — the average income has for a time been raised by these exercises, as a large number of persons have been injured by taking up sports which may be vigorously pursued with safety only by those with young arteries.1

This is consistent with Osler’s attitude to chronological age. He felt that the real work of life is done before the 40th year and that after the 60th it would be best for the world and for men themselves if they rested from their labours.2

Times have changed

In 1953, Jeremy Morris and colleagues, who compared postmen to mail sorters and bus drivers to conductors, for the first time linked a sedentary occupation with a higher incidence of cardiovascular events.3

Since then it’s been shown that physical fitness is an independent predictor of a lower mortality from any cause.4 Physical inactivity is now accepted as a coronary risk factor5 and aerobic exercise has been embraced by the health-minded public as a ticket to longevity.

There’s been considerable interest in cardiac findings in the young competitive athlete.6 Less attention has been given to the older noncompetitive athlete who nevertheless may present with abnormalities — particularly electrocardiographic — which may be misinterpreted as indicating underlying heart disease. The converse can also occur, with findings incorrectly assumed to be physiologic and due to exercise when in fact they’re due to organic heart disease.

Below I describe four patients who were joggers for 15 to 50 years averaging 30 to 70 kilometres a week. All presented with electrocardiographic abnormalities, which were misdiagnosed as pathological in three of the cases, and misdiagnosed as athlete’s heart syndrome in the fourth case, delaying a correct diagnosis of apical hypertrophic cardiomyopathy.

Case 1: A 66-year-old man had no prior history of heart disease but had had intermittent epigastric pain for many years. Endoscopy in the past had shown esophageal inflammation and he had been on intermittent lanzoprasole. He was an avid runner and exerciser, averaging 50 kilometres a week for 40 years with additional indoor training.

In February 2006, he was on a cruise around South America when his epigastric pain worsened. He disembarked and flew back to Toronto.

He presented to my office shortly afterwards with persistence of epigastric and low sub-sternal chest pain. Physical examination was normal. The ECG (Fig. 1) showed sinus bradycardia, a PR interval at the upper limit of normal (194 msecs), ST elevation in V2 and V3, T inversion in V2 and a more marked T inversion in V3, which was terminal and asymmetric. ECGs over 3 days showed the same pattern with occasional T inversion in V4. Old ECGs were obtained and proved similar, although the depth of T inversion had grown with time. He was admitted to hospital. The diagnosis was repolarization ECG changes and epigastric pain not yet diagnosed. An acute coronary syndrome was considered. Cardiac enzymes weren’t elevated. An echocardiogram was unremarkable with normal contractility and no evidence of hypertrophic cardiomyopathy. The left ventricular (LV) wall dimensions were 8 mm and 9 mm for the septum and posterior wall, respectively. Left ventricular end-diastolic dimension (LVEDD) was at the upper limit of normal at 50 mm (normal ≤ 56 mm). A coronary angiogram was performed and revealed completely normal epicardial coronary arteries, normal LV contractility and a normal LV end diastolic pressure of 11 mm Hg. The diagnosis was the athlete’s heart syndrome.

He was discharged from hospital. Gastrointestinal endoscopy 2 weeks later revealed a small hiatus hernia and reflux. Small bowel biopsies were taken and were negative. Colonoscopy was normal. He was started on rabeprazole 10 mg a day and has been asymptomatic since.

Figure 1: 12 lead ECG in Case #1 showing terminal T inversions in leads V1 to V3

Case 2: A 43-year-old woman, an avid aerobic exerciser running 30 km a week for 15 years, developed abdominal pain during her second pregnancy after an amniocentesis and presented to an emergency department (ED). Her pain remitted and she had an uneventful pregnancy but an electrocardiogram in the ED showed a junctional rhythm (Fig. 2), which remained throughout her pregnancy and afterwards. This information caused some personal and family anxiety. She had no cardiac symptoms and her physical exam was normal. A 48-hour Holter monitor showed a constant junctional rhythm at 48 to 131 bpm and no other arrhythmia. An echocardiogram was normal with LVEDD of 47 mm, LV end systolic dimension (LVESD) of 25 mm, an interventricular septum of 9 mm, a LV posterior wall of 9 mm and grade 1 LV contractility. No further investigation was performed and she has remained well.

Figure 2: 12 lead ECG in Case #2 showing a junctional rhythm

Case 3: A 42-year-old man had an episode of syncope in the distant past but no other symptoms. He’s been an avid runner since the age of 12, averaging 40 km a week. His application for life insurance was denied because of an ECG (Fig. 3) which was interpreted as Brugada’s syndrome. The ECG shows ST elevations in leads V2 and V3 with terminal asymmetric T inversions which are in fact a normal variant seen in healthy athletic men.7

A report was sent to the insurance company stating that he did not have Brugada’s syndrome which requires a wide terminal r wave in leads V1 to V3 followed by ST elevation beginning at the top of the terminal r wave and downsloping.8 On echocardiography, the LVEDD was normal at 43 mm, the width of the interventricular septum was minimally increased at 11 mm (normal = < 11 mm), the posterior wall was at the upper limit of normal at 10 mm (normal = < 11 mm) and LV systolic function was normal. His application for life insurance was reconsidered and granted but with higher premiums.

Figure 3: 12 lead ECG in Case #3 showing ST elevation in leads V2 and V3 with terminal T inversions

Case 4: This 67-year-old man presented at the age of 40 years with mild hypertension and an abnormal ECG but was asymptomatic. At that time he ran 48 to 64 km a week and conducted five exercise classes a week at the YMCA. The ECG showed deep T inversions in the anterior and lateral leads (Fig. 4). The echocardiogram was reported as a normal study. The diagnosis was the athletic heart syndrome. He has remained asymptomatic but more recent echocardiograms suggested the possibility of apical hypertrophic cardiomyopathy with apical widths measuring 14 to 17 mm. This was confirmed with contrast echocardiography (Fig. 5).

Figure 4: 12 lead ECG in Case #4 showing asymmetric T inversions in leads V1 to V6.

The thickening heart

Repetitive long-term aerobic exercise increases myocardial wall stress, which is normalized by an increase in wall thickness. Our first three patients had wall thicknesses and end diastolic dimensions in the upper range of normal and the wall dimensions were symmetrical (i.e. posterior wall and interventricular septum were equal) in contrast to the asymmetrical hypertrophy one sees in certain variations of hypertrophic cardiomyopathy. Another distinguishing point is that physiological hypertrophy regresses with deconditioning, whereas pathological hypertrophy doesn’t. Echocardiography is pivotal in distinguishing physiological hypertrophy from pathological hypertrophy caused by hypertension or by hypertrophic syndromes. Our 4th case illustrates the ongoing improvement of echocardiographic techniques and consoles. The first ECG was performed in 1981 and was reported as normal even though he almost certainly had apical hypertrophic cardiomyopathy then, since the ECG was classical for this condition. Even now, in centres with less experience in hypertrophic syndromes or with older machines, apical hypertrophy can be missed because of difficulty in visualizing the apex.

Benign arrhythmias are common in athletes but may trigger concern and anxiety, as in our second case. Sinus bradycardia is present in about 70% of athletes with an average lowest heart rate of 37 bpm, and ventricular preexcitation is more common than in the general population.9 Ambulatory monitoring has demonstrated that athletes have a high prevalence of certain arrhythmias. This includes sinus pauses of > 2.0 seconds in 37%, 2nd degree AV block (usually Mobitz I) in 31%, and a junctional rhythm in 20%.9 The issue in our second patient was the finding of a junctional rhythm. Most of these arrhythmias are a consequence of excessive vagal tone, a so-called vagotonic state, which in turn results from the high stroke volume. But the causes go deeper than a vagotonic state, as it’s been shown that trained subjects have consistently lower intrinsic heart rates even after temporary chemical denervation with atropine and propanolol.10

ST elevation occurs in 10% of athletes.11 It’s usually most prominent in leads V2 to V4, as in our second case, and can be incorrectly mistaken for Brugada’s syndrome. Brugada’s is also characterized by ST-segment elevation in the right precordial leads but with a coved not concave configuration as occurs in the athlete. Also, in Brugada’s syndrome there’s a large terminal delayed r prime wave.8

T inversions are common in athlete’s heart syndrome and are usually terminal and asymmetric. The T inversions of our first case fit this description, in contrast to pathological T wave inversions, which, are more symmetrical and not terminal.9 The difference may not be obvious, however. The morphology of the physiological T inversions in our first case weren’t dissimilar from the pathological inversions of our 4th case with apical HCM.

Our four patients had enthusiastically pursued exercise training for most of their lives. The causality can never be certain, but it seems that adaptations of the cardiovascular system to repetitive long-term aerobic exercise resulted in rhythm and electrocardiographic changes that in three of the cases resulted in either invasive investigation, undue anxiety or insurance problems, while in the fourth case they hid a significant underlying cardiac condition. Adults who exercise a lot — and their medical providers — should be aware of these issues. These patients should be provided with copies of their electrocardiograms to carry with them so that future health encounters will have the benefit of a baseline tracing.


The author would like to thank Dr. Shemy Carassos for performing the contrast echocardiogram on the 4th case.

Leonard Schwartz, MD, FRCP, FRCPC is a cardiologist at the University Health Network — Toronto General Hospital, Toronto, ON.
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Figure 5: A contrast echocardiogram in Case #4 showing apical hypertrophy.


  1. Osler W. Aequaminitas (2nd Edition) 1906; p 258. McGraw-Hill.
  2. Osler W. Aequaminitas (2nd Edition) 1906; Preface. McGraw-Hill Company Ltd New York, Toronto, London.
  3. Morris JN, et al. Lancet 1953;2:1053.
  4. Sandvik L, et al. NEJM 1993;328:533-7.
  5. Fletcher GF, et al. Circulation 1996;94:857.
  6. Spirito P, et al. Am J Cardiol 1994;74:802-6.
  7. Wang K, et al. NEJM 2003;349:2128-35.
  8. Brugada J, et al. Circulation 2002;105:73-8.
  9. Huston TP, et al. NEJM 1985;313:24-31.
  10. Badeer HS. Cardiovascular adaptations in the trained athlete. In: Lubich T Venerando A, eds. Sports cardiology. Bologna: Aulo Gaggi 1980;3-12.
  11. Luckman J, et al. Arch Intern Med 1973; 132:763-70.
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