Athlete’s heart

1. Which of the following ECG findings is most characteristic of Athlete’s Heart?
A. ST-segment elevation in V1-V3
B. Prolonged QT interval
C. Sinus bradycardia
D. Pathological Q waves
Explanation: Sinus bradycardia is a hallmark finding in well-trained athletes due to increased vagal tone. It is considered a physiological adaptation.
2. Which echocardiographic feature best differentiates Athlete’s Heart from hypertrophic cardiomyopathy (HCM)?
A. Left ventricular wall thickness of 14 mm
B. Preserved diastolic function
C. Normal or increased cavity size
D. Left atrial enlargement
Explanation: Athlete’s heart typically shows increased LV cavity size, while HCM presents with smaller LV cavity and abnormal diastolic filling.
3. Which hormone plays a major role in cardiac remodeling seen in Athlete’s Heart?
A. Cortisol
B. Aldosterone
C. IGF-1 (Insulin-like Growth Factor-1)
D. Epinephrine
Explanation: IGF-1 mediates physiological hypertrophy through the PI3K-Akt pathway, promoting adaptive cardiac remodeling in athletes.
4. In Athlete’s Heart, what happens to the resting stroke volume?
A. Increases
B. Decreases
C. Remains unchanged
D. Becomes erratic
Explanation: Resting stroke volume increases due to enhanced cardiac compliance and chamber dilation, contributing to lower resting heart rate.
5. Which of the following is TRUE about left ventricular (LV) mass in Athlete’s Heart?
A. LV mass decreases with endurance training
B. LV mass always indicates pathology
C. LV mass increases proportionally with body size and training load
D. LV mass does not change with athletic training
Explanation: Physiological adaptation includes proportional LV mass increase with training intensity and athlete body size.
6. What structural cardiac adaptation is most typical in endurance athletes?
A. Eccentric left ventricular hypertrophy
B. Concentric hypertrophy
C. Right atrial stenosis
D. Myocardial fibrosis
Explanation: Endurance training leads to eccentric hypertrophy due to increased volume load, resulting in chamber dilation and mild wall thickening.
7. Which of the following is LEAST likely in an athlete with physiological cardiac adaptation?
A. Increased LV end-diastolic dimension
B. Sinus arrhythmia
C. Increased stroke volume
D. Reduced ejection fraction (<45%)
Explanation: A reduced ejection fraction <45% is not typical in athlete’s heart and suggests pathology. Physiological adaptations maintain or slightly increase EF.
8. What is the significance of early repolarization pattern on ECG in athletes?
A. It indicates ischemia
B. It is a benign finding in athletes
C. It warrants immediate electrophysiology study
D. It indicates ventricular tachycardia risk
Explanation: Early repolarization with J-point elevation is common and benign in athletes, often reflecting increased vagal tone.
9. Which imaging modality is most useful to distinguish athlete’s heart from HCM?
A. Chest X-ray
B. ECG
C. Holter monitor
D. Cardiac MRI
Explanation: Cardiac MRI provides detailed structural assessment and tissue characterization, helping differentiate physiological from pathological hypertrophy.
10. Athlete’s heart is more likely to regress with:
A. Beta-blocker use
B. ACE inhibitor therapy
C. Deconditioning and cessation of training
D. Diuretics
Explanation: Athlete’s heart regresses with detraining or deconditioning, confirming its reversible and physiological nature.
11. What is the expected pattern of left atrial size in athlete’s heart?
A. Marked enlargement with dysfunction
B. Mild to moderate enlargement with preserved function
C. Normal size only
D. No change at all
Explanation: Athlete’s heart may include mild to moderate LA enlargement due to increased preload, but function remains preserved.
12. The typical heart rate variability in athletes is:
A. Increased
B. Decreased
C. Normal
D. Fixed
Explanation: Trained athletes often have increased heart rate variability due to autonomic balance favoring parasympathetic tone.
13. Which demographic is more likely to develop marked athletic cardiac remodeling?
A. Male endurance athletes
B. Female sprinters
C. Children in school sports
D. Non-athletes with active lifestyle
Explanation: Male endurance athletes have the highest degree of physiological remodeling due to training intensity and hormonal factors.
14. Which change is seen in the right ventricle of endurance athletes?
A. Dilatation with normal function
B. Constriction with low pressure
C. Fibrosis and aneurysm formation
D. No change
Explanation: The right ventricle may show mild dilatation with preserved function, part of the balanced physiological adaptation in athletes.
15. What is a red flag for pathological hypertrophy rather than athlete’s heart?
A. Mild concentric LVH
B. Asymmetrical septal hypertrophy
C. Mild LV dilatation
D. Normal diastolic function
Explanation: Asymmetrical septal hypertrophy is characteristic of HCM and not seen in physiological athletic adaptations.
16. Which ECG change would raise suspicion of underlying pathology in an athlete?
A. Sinus bradycardia
B. T-wave inversion in lateral leads
C. First-degree AV block
D. Incomplete RBBB
Explanation: T-wave inversion in lateral leads may indicate cardiomyopathy or other pathology, not typical for benign athletic adaptations.
17. What physiological effect allows trained athletes to have lower resting HR?
A. Increased sympathetic tone
B. Enhanced vagal tone
C. AV nodal block
D. Beta-blocker use
Explanation: Resting bradycardia in athletes results from increased parasympathetic (vagal) activity and high stroke volume.
18. VO2 max is typically:
A. Lower in athletes
B. Higher in athletes
C. Not affected by training
D. Unrelated to cardiac adaptation
Explanation: VO2 max increases with aerobic training due to improvements in cardiac output, capillary density, and mitochondrial efficiency.
19. Athlete’s heart most commonly affects which chambers?
A. Left atrium and right atrium only
B. Both ventricles and atria
C. Right heart only
D. Left ventricle only
Explanation: Cardiac remodeling in athlete’s heart often affects all four chambers, especially in endurance sports.
20. After how many weeks of detraining can athlete’s heart begin to regress?
A. 1 week
B. 4–6 weeks
C. 6 months
D. 1 year
Explanation: Reversal of cardiac adaptations can begin as early as 4–6 weeks of detraining, confirming its physiological nature.

21. In athlete’s heart, which echocardiographic feature is most commonly observed?

A. Increased left ventricular cavity size

B. Decreased ejection fraction

C. Right ventricular hypokinesia

D. Thickened mitral valve leaflets



22. Which of the following is typically absent in athlete’s heart but present in pathological hypertrophy?

A. Diastolic dysfunction

B. Mild LV wall thickening

C. Resting bradycardia

D. Increased stroke volume



23. A key differentiating test between athlete’s heart and cardiomyopathy is:


A. Deconditioning with repeat imaging

B. Chest X-ray

C. Serum troponin level

D. 24-hour urine protein



24. Athlete’s heart typically shows which pattern on ECG?


A. Sinus bradycardia and voltage criteria for LVH

B. Prolonged QT interval

C. Frequent ventricular ectopy

D. Delta wave


25. Which of the following supports a diagnosis of athlete’s heart over hypertrophic cardiomyopathy?


A. Symmetric wall thickening with normal diastolic function

B. Family history of sudden cardiac death

C. Asymmetric septal hypertrophy

D. Presence of late gadolinium enhancement on MRI



20-Point Summary Table: Athlete’s Heart


🔢 No.📘 TopicAthlete’s heart🧠 Key Point
1️⃣DefinitionAthlete’s heart is a benign, adaptive increase in cardiac size and function due to long-term endurance or strength training.
2️⃣CausePhysiological remodeling from regular intensive aerobic or anaerobic exercise.
3️⃣Types of TrainingEndurance (e.g., running) → volume overload; Strength (e.g., weightlifting) → pressure overload.
4️⃣LV CavityDilated in endurance athletes; concentric hypertrophy in strength athletes.
5️⃣LV Wall ThicknessMildly increased, but usually ≤13 mm.
6️⃣RV ChangesRight ventricular enlargement may occur, often proportional to LV changes.
7️⃣Resting Heart RateOften bradycardia (<60 bpm) due to high vagal tone.
8️⃣ECG FindingsSinus bradycardia, 1st-degree AV block, early repolarization, voltage criteria for LVH.
9️⃣VO₂ MaxIncreased significantly due to better cardiac output and peripheral efficiency.
🔟Stroke VolumeIncreased both at rest and during exercise.
1️⃣1️⃣Diastolic FunctionNormal or enhanced; helps differentiate from pathological hypertrophy.
1️⃣2️⃣LA EnlargementMild left atrial enlargement may be seen due to increased preload.
1️⃣3️⃣Ejection Fraction (EF)Normal or mildly reduced at rest, but increases with exercise.
1️⃣4️⃣NT-proBNP/TroponinMay be mildly elevated post-exercise but returns to normal—distinguishes from pathology.
1️⃣5️⃣ReversibilityChanges regress within 3–6 months of detraining.
1️⃣6️⃣Differentiation from HCMNo family history, symmetric hypertrophy, normal diastolic function, regression with detraining.
1️⃣7️⃣SymptomsUsually asymptomatic; no exertional syncope, angina, or breathlessness.
1️⃣8️⃣Echocardiography RoleKey tool to differentiate from cardiomyopathy—assesses wall thickness, cavity size, function.
1️⃣9️⃣MRI FindingsNormal tissue characteristics, no fibrosis or LGE (Late Gadolinium Enhancement).
2️⃣0️⃣PrognosisExcellent; associated with reduced cardiovascular risk and improved longevity.

Athlete’s Heart vs Hypertrophic Cardiomyopathy (HCM) — Comparison Table


🔢 No.🔍 Feature🏃‍♂️ Athlete’s HeartHypertrophic Cardiomyopathy (HCM)
1️⃣EtiologyPhysiological adaptation to trainingGenetic disorder (AD; MYH7, MYBPC3 mutations)
2️⃣LV Wall ThicknessMild increase (usually ≤13 mm)Often >15 mm (especially septal)
3️⃣Pattern of HypertrophySymmetricalAsymmetrical (septal > posterior wall)
4️⃣LV Cavity SizeNormal or increasedNormal or decreased
5️⃣Diastolic FunctionNormal or enhancedOften impaired
6️⃣Systolic FunctionNormal EF, ↑ during exerciseNormal or hyperdynamic EF, ↓ with obstruction
7️⃣Regression with DetrainingYes (within months)No regression
8️⃣ECG FindingsBradycardia, voltage criteria for LVH, early repolarizationLVH, T-wave inversion, Q waves, arrhythmias
9️⃣Family HistoryNegativePositive in ~60%
🔟SymptomsAsymptomaticMay have syncope, angina, palpitations, dyspnea
1️⃣1️⃣Risk of Sudden Cardiac Death (SCD)Very lowHigh, especially in young athletes
1️⃣2️⃣Fibrosis on Cardiac MRIAbsentOften present (Late Gadolinium Enhancement)
1️⃣3️⃣NT-proBNP / Troponin LevelsMild transient rise post-exerciseMay be persistently elevated
1️⃣4️⃣LA SizeMildly enlargedOften enlarged
1️⃣5️⃣LVOT ObstructionAbsentMay be present (dynamic)
1️⃣6️⃣Response to ExerciseNormal or supernormalLimited by obstruction or arrhythmia
1️⃣7️⃣Genetic TestingNot indicatedUseful for diagnosis and family screening
1️⃣8️⃣Tissue Doppler ImagingNormal E’ velocity↓ E’ velocity (diastolic dysfunction)
1️⃣9️⃣ManagementReassurance, monitor if unclearLifestyle restriction, beta-blockers, ICD if needed
2️⃣0️⃣PrognosisExcellent, improves fitness and longevityRisk of SCD; lifelong monitoring needed


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