Exercise-Induced Athletic Heart Syndrome: Good or Bad? The Truth Explained

Exercise-induced cardiac remodeling, known as athletic heart syndrome, is a benign physiological response characterized mainly by ventricular hypertrophy and bradycardia. It is also called athlete’s heart, physiological cardiac hypertrophy, exercise-induced cardiac remodeling, or exercise-related cardiac remodeling. This phenomenon comes with normal cardiac systolic and diastolic function, but its features may overlap with certain pathological conditions.

In some athletes, these changes can make the heart look similar to a cardiomyopathy. Because cardiomyopathy is not harmless, healthcare providers need to understand the difference between athlete’s heart and cardiomyopathy.

Past research found that in athletes with different endurance and strength training, cardiac mass was about 35% higher than in non-athletes, and cardiac volume was 60% to 80% higher. Endurance exercise training led to a marked increase in volume while maintaining wall thickness and increasing cardiac mass, whereas strength training led to increased wall thickness and cardiac mass with smaller changes in volume.

Other research suggests the factors behind cardiac remodeling may relate to the severity of the hemodynamic challenge (exercise intensity) and the time the heart is exposed to that challenge (total exercise duration). Cardiac remodeling may be influenced more by total exercise load (intensity times time, often quantified with metrics such as MET-hours) than by the specific sport.

Epidemiology

• This adaptive change is fairly common among highly trained athletes, affecting about 2% of athletes.
• It may occur after many years of intense training and is more common in Black athletes than in people of other races.
• Cardiac remodeling has also been observed in moderately active adults who exercise 3 to 5 hours a week.
• It is easily mistaken for a pathological condition.
• Women are underrepresented in cardiology and in research.

Etiology and pathophysiology

• Changes in cardiac structure vary with the type of exercise.
• The increase in heart size rarely exceeds the upper limit of normal.
• Relatively dynamic exercise (for example, long-distance running and swimming):
  • Increased heart rate, increased stroke volume, and decreased systemic vascular resistance.
  • An adaptive response driven by increased volume load and systolic pressure.
  • Increased left ventricular end-diastolic diameter, with a proportional increase in the thickness of the interventricular septum and the free wall.
• Relatively static exercise (for example, weightlifting and bodybuilding):
  • Increased peripheral resistance, with smaller increases in heart rate and cardiac output.
  • Increased thickness of the interventricular septum and the free wall, but no clear change in left ventricular end-diastolic diameter.
• Combined dynamic-static exercise (for example, cycling and rowing):
  • Very large volume and pressure load.
  • The greatest increase in left ventricular end-diastolic diameter and in the thickness of the interventricular septum and the free wall.

Risk factors

• Long-term endurance exercise
• Genetics

History

• There are usually no symptoms.
• Some athletes may report palpitations or a skipped beat, but most are asymptomatic.
• Take a detailed exercise history, including training volume, training intensity, and exercise type.
• The medical history should rule out any family history of early heart disease, sudden death, or other cardiac conditions.

Physical examination

• The physical examination is usually normal.
• Auscultation may reveal:
  • A slow heart rate (bradycardia)
  • A fourth heart sound (ventricular filling sound) compared with a normal person
  • A low-frequency systolic murmur
• Blood pressure is usually normal or on the low side.
• Watch for any abnormal heart murmur or other signs that suggest cardiac pathology.

Differential diagnosis

• Pathological cardiac hypertrophy:
  • Hypertrophic cardiomyopathy (HCM)
  • Aortic stenosis
  • Hypertensive heart disease
• Arrhythmias:
  • Long QT syndrome
  • Atrial fibrillation
• Other pathological causes:
  • Myocarditis
  • Pericardial disease

Diagnostic tools

• Electrocardiogram (ECG)
  • May show sinus bradycardia, premature beats, or other nonspecific changes.
  • Common athlete features include early repolarization and signs of left ventricular hypertrophy.
• Echocardiography
  • Used to distinguish exercise-induced physiological changes from pathological cardiac hypertrophy.
  • Left ventricular wall thickness is usually no more than 13 mm.
  • Functional indices (such as ejection fraction) are usually normal.
• Cardiac MRI
  • Can serve as a secondary tool when echocardiography does not provide enough information.
• Exercise testing
  • Assesses cardiac function during exercise.

Initial management

• No specific treatment is needed, because this is a physiological change.
• After ruling out other pathological causes, the athlete can safely continue exercising.
• Educate the athlete and family to ease concerns.

Medication

• Medication is usually not needed, because this is a non-pathological condition.
• If an accompanying pathological arrhythmia or cardiovascular disease is confirmed, treatment should target the specific problem.

Additional management

• Observation and education:
  • Explain the benign nature of athlete’s heart.
  • Educate the athlete and family about the normal range of cardiac remodeling and its positive effect on exercise capacity.
• Regular check-ups:
  • Provide regular cardiac health monitoring for high-risk athletes, especially those in high-intensity or extreme sports.

Surgery

• Surgery is usually not needed, because this syndrome is a physiological adaptive change.
• If atypical structural or functional abnormalities are detected (such as heart valve disease), further intervention may need to be considered.

Follow-up

• Regular cardiac health assessment:
  • Athletes should have a yearly cardiac check-up, including ECG and echocardiography.
• Athletes with a family history or concern for cardiac disease need closer follow-up.
• If new symptoms appear (such as palpitations, syncope, or reduced exercise tolerance), they should be evaluated promptly.
• In most people, the heart returns to normal size about three months after excessive training stops. However, one study found that 20% of former athletes still had a larger left ventricle five years later.

Prognosis

• This physiological change generally has a good prognosis and does not require limiting exercise.
• It has a positive effect on cardiac function and exercise performance.
• After ruling out pathological heart disease, athletes can safely continue high-intensity training and competition.

References

• https://my.clevelandclinic.org/health/diseases/23920-athletes-heart
• https://stanfordhealthcare.org/medical-conditions/blood-heart-circulation/athletes-heart.html
• J Am Coll Cardiol. 2022 Oct 4;80(14):1346-1362.
• Bosn J Basic Med Sci. 2008 May;8(2):116–120.
• Heart. 2017 Mar;103(6):463-473.

Further reading

• Runner topic
• Sports injury overview
• PRP prolotherapy
• Rehabilitation exercise prescription
• Pain management