2026-02-13
A practical look at HCM in young athletes
Cardiology and Vascular Medicine
By Carolina Lima | Published on February 13, 2026 | 3 min read
Hypertrophic cardiomyopathy (HCM) remains a major concern in sports cardiology because it is among the leading causes of sudden cardiac death (SCD) in young competitive athletes. In a large US registry of 1,866 athlete deaths, HCM accounted for nearly 40% of cases, most occurring in adolescents still in high school. More than 80% of these individuals were asymptomatic prior to collapse, underscoring how difficult it is to identify HCM before catastrophic events occur.
A consistent challenge in evaluating young athletes is distinguishing physiological left‑ventricular hypertrophy (LVH), the result of intensive training, from the pathological hypertrophy characteristic of HCM.
Endurance training remodels the heart through increased LV wall thickness, cavity enlargement and enhanced diastolic filling. Up to 20% of young athletes develop LVH, though most remain below the 12 mm threshold considered normal for athletic adaptation. However, a subset—particularly male endurance athletes and African American athletes—may develop wall thickness between 13–16 mm. This “grey zone” provides limited diagnostic clarity.
Unlike LVH, HCM is marked by asymmetric septal hypertrophy (≥15 mm), a small LV cavity, impaired relaxation and potentially left ventricule outflow tract obstruction (LVOTO), a narrowing of the outflow tract during systole increasing the pressure gradient between the LV and the aorta. LVOTO contributes to symptoms such as exertional chest pain, dyspnea, dizziness and syncope and may be present in one‑third of patients at rest and in up to 70% during exercise. Importantly, such obstructive physiology is not observed in athletes with purely LVH.
Electrocardiography is one of the most helpful first‑line diagnostic tools. T‑wave inversion (TWI) is the most common ECG hallmark of HCM, appearing in over 75% of athletes with the condition. Importantly, healthy athletes do not show pathological TWI, ST depression or Q waves.
Echocardiography also plays a central role. Physiological LVH is typically symmetric, accompanied by a significantly enlarged LV cavity (55–70 mm), whereas HCM usually presents with smaller cavity dimensions (<50 mm). An LV cavity size >54 mm has been shown to effectively distinguish athlete’s heart from HCM, though a small minority of athletes with HCM may still exceed this value.
Cardiac MRI (CMR) provides an additional tips for diagnostic and is the gold standard for structural assessment, particularly with its ability to detect fibrosis and measure extracellular volume (ECV). Elevated ECV and T1 values suggest pathological hypertrophy. An ECV threshold >22.5% offers excellent sensitivity and specificity for distinguishing HCM from athletic remodeling.
Exercise physiology
Functional assessment further highlights the contrast between physiological and pathological remodeling.
Athletes with LVH typically achieve high peak oxygen consumption (VO₂max >50 ml/kg/min). In contrast, individuals with HCM often fail to augment stroke volume appropriately during exercise. Exercise testing may reveal abnormal blood-pressure responses, ST‑segment changes or ventricular arrhythmias in HCM.
These exercise‑induced limitations help explain why some individuals with HCM, despite appearing structurally similar to athletes, cannot perform athletically at an elite level.
Detraining studies provide additional insight: LVH regresses with weeks of reduced activity, whereas HCM-related abnormalities persist, offering a practical diagnostic strategy when uncertainty remains.
Implications for sports eligibility
Given the unpredictable risk of arrhythmogenic events in HCM, both American and European guidelines traditionally advise against participation in moderate and high‑intensity sports for phenotype‑positive individuals. Genotype‑positive but phenotype‑negative athletes remain more controversial: European guidelines adopt a more conservative posture, while US recommendations permit full participation with structured follow‑up.
A structured evaluation—integrating ECG, echocardiography, CMR, and exercise physiology—remains essential to prevent misdiagnosis and reduce the risk of sudden cardiac death in young athletes.
Read next : Cardiovascular diseases: the leading cause of death among women in France
À propos de l’auteure – Carolina Lima
Docteure spécialisée en anesthésiologie Carolina est spécialiste en anesthésiologie et nourrit une profonde passion pour l’apprentissage et le partage des connaissances médicales. Dévouée à l’avancement de sa discipline, la Dre Lima s’efforce d’apporter à la communauté médicale des perspectives nouvelles fondées sur les données probantes. Considérant la médecine non pas simplement comme une profession, mais comme un parcours d’apprentissage continu tout au long de la vie, la Dre Lima s’engage à rendre l’information complexe claire, pratique et utile pour les professionnels de santé du monde entier.
Hypertrophic cardiomyopathy (HCM) remains a major concern in sports cardiology because it is among the leading causes of sudden cardiac death (SCD) in young competitive athletes. In a large US registry of 1,866 athlete deaths, HCM accounted for nearly 40% of cases, most occurring in adolescents still in high school. More than 80% of these individuals were asymptomatic prior to collapse, underscoring how difficult it is to identify HCM before catastrophic events occur.
Physiological vs Pathological
A consistent challenge in evaluating young athletes is distinguishing physiological left‑ventricular hypertrophy (LVH), the result of intensive training, from the pathological hypertrophy characteristic of HCM.
Endurance training remodels the heart through increased LV wall thickness, cavity enlargement and enhanced diastolic filling. Up to 20% of young athletes develop LVH, though most remain below the 12 mm threshold considered normal for athletic adaptation. However, a subset—particularly male endurance athletes and African American athletes—may develop wall thickness between 13–16 mm. This “grey zone” provides limited diagnostic clarity.
Unlike LVH, HCM is marked by asymmetric septal hypertrophy (≥15 mm), a small LV cavity, impaired relaxation and potentially left ventricule outflow tract obstruction (LVOTO), a narrowing of the outflow tract during systole increasing the pressure gradient between the LV and the aorta. LVOTO contributes to symptoms such as exertional chest pain, dyspnea, dizziness and syncope and may be present in one‑third of patients at rest and in up to 70% during exercise. Importantly, such obstructive physiology is not observed in athletes with purely LVH.
ECG and imaging clues
Electrocardiography is one of the most helpful first‑line diagnostic tools. T‑wave inversion (TWI) is the most common ECG hallmark of HCM, appearing in over 75% of athletes with the condition. Importantly, healthy athletes do not show pathological TWI, ST depression or Q waves.
Echocardiography also plays a central role. Physiological LVH is typically symmetric, accompanied by a significantly enlarged LV cavity (55–70 mm), whereas HCM usually presents with smaller cavity dimensions (<50 mm). An LV cavity size >54 mm has been shown to effectively distinguish athlete’s heart from HCM, though a small minority of athletes with HCM may still exceed this value.
Cardiac MRI (CMR) provides an additional tips for diagnostic and is the gold standard for structural assessment, particularly with its ability to detect fibrosis and measure extracellular volume (ECV). Elevated ECV and T1 values suggest pathological hypertrophy. An ECV threshold >22.5% offers excellent sensitivity and specificity for distinguishing HCM from athletic remodeling.
Exercise physiology
Functional assessment further highlights the contrast between physiological and pathological remodeling.
Athletes with LVH typically achieve high peak oxygen consumption (VO₂max >50 ml/kg/min). In contrast, individuals with HCM often fail to augment stroke volume appropriately during exercise. Exercise testing may reveal abnormal blood-pressure responses, ST‑segment changes or ventricular arrhythmias in HCM.
These exercise‑induced limitations help explain why some individuals with HCM, despite appearing structurally similar to athletes, cannot perform athletically at an elite level.
Detraining studies provide additional insight: LVH regresses with weeks of reduced activity, whereas HCM-related abnormalities persist, offering a practical diagnostic strategy when uncertainty remains.
Implications for sports eligibility
Given the unpredictable risk of arrhythmogenic events in HCM, both American and European guidelines traditionally advise against participation in moderate and high‑intensity sports for phenotype‑positive individuals. Genotype‑positive but phenotype‑negative athletes remain more controversial: European guidelines adopt a more conservative posture, while US recommendations permit full participation with structured follow‑up.
A structured evaluation—integrating ECG, echocardiography, CMR, and exercise physiology—remains essential to prevent misdiagnosis and reduce the risk of sudden cardiac death in young athletes.
Read next : Cardiovascular diseases: the leading cause of death among women in France
À propos de l’auteure – Carolina Lima
Docteure spécialisée en anesthésiologie Carolina est spécialiste en anesthésiologie et nourrit une profonde passion pour l’apprentissage et le partage des connaissances médicales. Dévouée à l’avancement de sa discipline, la Dre Lima s’efforce d’apporter à la communauté médicale des perspectives nouvelles fondées sur les données probantes. Considérant la médecine non pas simplement comme une profession, mais comme un parcours d’apprentissage continu tout au long de la vie, la Dre Lima s’engage à rendre l’information complexe claire, pratique et utile pour les professionnels de santé du monde entier.
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