Exercise and the Heart: The Good, The Bad, and The Ugly — What Patients Need to Know

Table of Contents

• Key Points
• Introduction: Why This Research Matters
• The Good: How Exercise Protects Your Heart
• The Athlete's Heart: What Happens to the Heart with Intense Training
• The Athlete's ECG: Electrical Changes from Training
• Cardiac Dimensions: How Much Can a Heart Grow?
• Upper Limits of Normal Cardiac Size in Athletes
• Distinguishing Athlete's Heart from Heart Muscle Disease
• The Bad: Sudden Cardiac Death in Sport
• Can Exercise Damage a Previously Normal Heart?
• Atrial Fibrillation and Sinus Node Disease in Athletes
• Adverse Cardiac Remodelling and Ventricular Arrhythmias
• The Ugly: Performance-Enhancing Drugs and the Heart
• Limitations of the Current Research
• Recommendations: What Does This Mean for You?
• Frequently Asked Questions
• Source Information

Key Points

• Moderate exercise of about 2 hours weekly lowers cardiovascular mortality; each MET of exercise gives a 12–20% reduction.
• Athlete's heart includes 10–20% thicker left ventricular wall and 10–15% larger cavities; usually benign and reversible with detraining.
• In 102 veteran marathon runners, 12% showed myocardial fibrosis on MRI compared with 4% of controls, suggesting extreme endurance exercise may harm some.
• Endurance athletes have a 5-fold higher atrial fibrillation risk per a meta-analysis of 655 athletes; more training hours raise the risk.
• Anabolic steroids and cocaine can cause heart attacks, heart failure, arrhythmias, and sudden death; no safe dose exists.

Introduction: Why This Research Matters

Exercise is universally recommended for heart health, but this review by Dr. Sanjay Sharma and colleagues from St George's University of London and the University of Barcelona tackles a more complex question: is there a point where exercise stops being helpful and starts becoming harmful?

The authors divide sports cardiology into three categories. The "good" covers the well-proven benefits of moderate exercise. The "bad" refers to the rare but tragic occurrence of sudden cardiac death in athletes with undiagnosed heart conditions. The "ugly" describes two concerning trends: emerging evidence that decades of extreme endurance exercise may damage otherwise normal hearts, and the dangerous use of performance-enhancing drugs in competitive sports.

The Good: How Exercise Protects Your Heart

The cardiovascular benefits of regular exercise have been recognized for decades. Exercise helps control blood pressure, improves the blood lipid (fat) profile by raising "good" HDL cholesterol and lowering "bad" LDL cholesterol, and increases insulin sensitivity, which helps prevent type 2 diabetes.

In the 1950s, researcher Morris and colleagues made a landmark observation: active bus workers and postal workers had a 50% lower rate of coronary artery disease (CAD) events compared with their less active colleagues—sedentary bus drivers and clerical postal workers. A more recent study of over 44,000 professional men followed for 475,755 person-years confirmed that regular exercise reduces coronary event rates by a similar magnitude.

How much exercise is needed to achieve these benefits? Surprisingly little. The research shows that just 2 hours of exercise per week at an intensity of 6–10 metabolic equivalents of task (METS)—think of a brisk walk, a gentle jog at 6.4–8 km/h, or cycling at 15–20 km/h—divided over three exercise sessions is enough. Even lower-intensity exercise provides meaningful protection compared with being completely sedentary. For every single MET of exercise achieved, there is a 12–20% reduction in cardiovascular mortality.

For patients who already have heart disease, exercise is still powerful medicine. A systematic review and meta-analysis of 34 randomized controlled trials looking at exercise-based cardiac rehabilitation after a heart attack found a lower risk of a second heart attack, lower cardiac mortality, and lower all-cause mortality in patients who participated in structured exercise programs. In patients with heart failure, regular physical activity improves functional capacity and modestly reduces hospitalizations and death from all causes.

The benefits go beyond the heart. Regular exercise reduces the risk of prostate and breast cancer, prevents osteoporosis (bone thinning), and may delay the onset of dementia. Exercise also improves stamina, boosts self-confidence, and is widely considered an antidepressant. In terms of longevity, people who exercise regularly live at least 3 years longer than their sedentary counterparts. The authors emphasize that exercise may be the most effective, accessible, and cheapest therapy a physician can prescribe—especially in an era of rising obesity rates approaching epidemic levels in some Western regions.

The Athlete's Heart: What Happens to the Heart with Intense Training

Current European and American guidelines recommend a minimum of 150 minutes of moderate-intensity exercise per week for adults. But competitive athletes—and some dedicated recreational athletes—perform far beyond these recommendations, regularly engaging in over 20 hours of intense exercise (15 METS) per week.

This level of training demands a sustained 5-to-6-fold increase in cardiac output (the amount of blood the heart pumps per minute), sustained for long periods. To meet this demand, the heart undergoes a series of unique electrical, structural, and functional adaptations collectively known as the "athlete's heart".

In general, athletes develop a 10–20% increase in left ventricular (LV) wall thickness and a 10–15% increase in both left and right ventricular cavity size compared with non-athletes of similar age and size. Athletes also show enhanced cardiac filling during diastole (the relaxation phase of the heartbeat), maintain high stroke volume even at very rapid heart rates, and develop increased oxidative capacity and capillary density in skeletal muscle—all of which contribute to the high peak oxygen consumption seen in elite athletes.

The Athlete's ECG: Electrical Changes from Training

The electrocardiogram (ECG) of a trained athlete often looks quite different from a normal resting ECG. These changes fall into two broad categories: those caused by high vagal tone (the part of the nervous system that slows the heart) and those reflecting increased heart chamber size.

Common ECG patterns in athletes include:

• Sinus bradycardia (a slow resting heart rate)
• Sinus arrhythmia (irregular but normal heart rhythm)
• J-point elevation with ascending ST segments (a benign pattern)
• First-degree atrioventricular (AV) block (slight delay in electrical conduction)
• Voltage criteria for left and right ventricular hypertrophy (enlargement)
• Incomplete right bundle branch block (a partial delay in the heart's electrical system)

Some athletes even show a nodal rhythm or Mobitz type 1 second-degree AV block at rest, which resolves with mild exertion—both are considered normal in this population.

Importantly, ethnicity changes what is "normal" on an athlete's ECG. Athletes of African and Afro-Caribbean origin (black athletes) show more pronounced repolarization changes compared with white athletes. ST segment elevation is 6-fold greater in black athletes than white athletes. T-wave inversion—which would be considered abnormal in most adult white athletes—is present in up to 25% of black athletes. The most common pattern in black athletes is asymmetric deep T-wave inversion preceded by convex ST-segment elevation in leads V1–V4, which has not been shown to correlate with heart disease or poor outcomes. T-wave inversion in the inferior leads is probably also a normal variant in black athletes.

Axis deviation and voltage criteria for atrial enlargement are considered normal variants when they appear in isolation and do not require further investigation if the athlete has no symptoms, a normal physical examination, and no relevant family history.

Cardiac Dimensions: How Much Can a Heart Grow?

The increased preload and afterload associated with chronic intensive exercise leads to symmetrical enlargement of all four heart chambers. Up to 50% of male athletes show left and right ventricular cavity dimensions that exceed the predicted upper limits for the general population.

A study of over 1,300 white Italian Olympic athletes found that 45% had left ventricular cavity sizes exceeding predicted upper limits, and 14% had a cavity size greater than 60 mm—a dimension that could otherwise be consistent with dilated cardiomyopathy, a serious heart muscle disease.

A more recent study of almost 700 nationally ranked black and white athletes revealed that almost 40% of male athletes exhibited right ventricular enlargement similar to that observed in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), a genetic condition that predisposes to dangerous heart rhythms.

While athletes show a slightly increased aortic root diameter compared with sedentary individuals, an aortic root larger than 40 mm is rare and should be considered abnormal.

Upper Limits of Normal Cardiac Size in Athletes

The upper limits for cardiac dimensions in athletes vary by ethnicity, age, and sex. The table below summarizes the key values from the research:

LVEDD = left ventricular end-diastolic diameter; LVWT = left ventricular wall thickness; RVD1 = basal right ventricular internal diameter; RVOT1 = right ventricular outflow tract.

In absolute terms, LV wall thickness in athletes is usually within the normal range for the general population (8–12 mm). Only 2% of Caucasian athletes show an LV wall thickness greater than 12 mm, and such dimensions are confined to male athletes. In contrast, LV hypertrophy above 12 mm is relatively common in black male athletes—up to 13% of black males and 3% of black females show an LV wall thickness of 12 mm or more. Regardless of ethnicity, an LV wall thickness greater than 16 mm is extremely uncommon and should raise concern for hypertrophic cardiomyopathy. These cardiac adaptations are smaller in adolescent athletes, who are generally less physically mature and have trained for shorter periods. The largest cardiac dimensions are typically found in male endurance athletes with large body surface areas, particularly rowers and long-distance cyclists.

Distinguishing Athlete's Heart from Heart Muscle Disease (Cardiomyopathy)

Here is the diagnostic challenge at the heart of sports cardiology: the same cardiac changes that occur naturally in response to training can also be signs of a cardiomyopathy—a disease of the heart muscle that can be life-threatening.

The electrical and structural changes in an athlete's heart are considered benign and generally reversible after a period of detraining. However, when LV hypertrophy combines with abnormal repolarization changes, or when an enlarged ventricular cavity coexists with a borderline low ejection fraction (the heart's pumping efficiency), the picture can overlap with a cardiomyopathy. This is especially relevant in black athletes, who have a higher prevalence of both LV hypertrophy and repolarization changes, and in endurance athletes, who may have very large ventricular cavities with borderline low ejection fractions.

To make the distinction, doctors use a combination of tests including ECG, echocardiography (ultrasound of the heart), cardiopulmonary exercise testing with exercise echocardiography, cardiac magnetic resonance imaging (CMRI), 24-hour Holter ECG monitoring, and genetic testing. An expert evaluation is essential because an erroneous diagnosis of cardiomyopathy may result in unnecessary disqualification from sport, while an erroneous diagnosis of "athlete's heart" in someone who actually has a cardiomyopathy may put a young life at risk.

Signs that strongly suggest a cardiomyopathy rather than athlete's heart include:

• ST segment depression in any lead
• T-wave inversion in the lateral leads
• Pathological q waves (Q/R ratio greater than 0.25)
• Left bundle branch block on the ECG
• Abnormal indices of diastolic function
• Reduced longitudinal systolic function
• Regional wall motion abnormalities
• Evidence of late gadolinium enhancement (scar tissue) on cardiac MRI
• Exercise-induced arrhythmias
• Complex ventricular arrhythmias on a Holter monitor
• Low peak oxygen consumption (below 50 mL/min/kg or below 120% of predicted)

In athletes with LV hypertrophy measuring 13–16 mm, the additional finding of a relatively small LV cavity (less than 50 mm) and dynamic LV outflow obstruction during exercise would point toward hypertrophic cardiomyopathy. In athletes with a dilated LV and borderline low ejection fraction, a failure to improve LV function or a peak oxygen consumption below 50 mL/min/kg (or below 120% of predicted) would favor dilated cardiomyopathy.

In an athlete with a dilated right ventricle, the following findings suggest arrhythmogenic right ventricular cardiomyopathy (ARVC): regional wall motion abnormalities or akinetic (non-moving) segments, T-wave inversion in leads V1–V3 with isoelectric ST segments or ST segment depression, epsilon waves (small deflections at the end of the QRS complex), low-amplitude QRS complexes in the limb leads, late potentials on signal-averaged ECG, and more than 1,000 extra-systoles (premature heartbeats) on monitoring.

The review also discusses left ventricular non-compaction (LVNC), a relatively newly recognized myocardial disorder characterized by increased LV trabeculation (a spongy appearance of the heart muscle), impaired systolic function, and a tendency toward fatal arrhythmias. The diagnosis is based on imaging showing a double-layered myocardial structure where the non-compacted-to-compacted layer thickness ratio is at least 2:1. The authors' experience reveals that almost 20% of young athletes show increased LV trabeculation, and 8% fulfill diagnostic criteria for LVNC on imaging. They propose that a pathological diagnosis of LVNC in athletes should only be made if there is reduced LV function, lateral T-wave inversion on ECG, low peak oxygen consumption, ventricular arrhythmias on exercise testing or Holter monitoring, or evidence of fibrosis on cardiac MRI.

When all investigations fail to resolve the diagnostic dilemma, a period of detraining for 6–8 weeks is advised to check whether the electrical and structural changes regress. Although this approach seems sensible, the authors note that convincing competitive athletes to detrain is difficult because it compromises fitness and team selection.

The Bad: Sudden Cardiac Death in Sport

Occasionally, an athlete dies suddenly during or immediately after competition. These tragedies are rare, but they strike young athletes harboring undiagnosed cardiomyopathies, coronary artery disease, accessory pathways (extra electrical connections in the heart), or ion channel disorders (conditions affecting the heart's electrical signaling). Middle-aged athletes who die suddenly typically have advanced coronary atherosclerosis (hardening and narrowing of the coronary arteries).

The prevalence of sudden cardiac death (SCD) varies depending on how data are collected, but the most reliable data reveal a prevalence of approximately 1 in 50,000 in young competitive athletes and in middle-aged marathon runners. Ninety percent of victims are male.

Although deaths in competitive athletes receive considerable media attention, over 90% of all exercise-related sudden cardiac deaths occur in recreational athletes—a crucial point that is often lost in the headlines.

Cardiovascular screening to identify athletes at risk of exercise-related SCD remains controversial because event rates are so low. However, data from a large prospective Italian study indicate that evaluating young athletes with a 12-lead ECG is effective in reducing the risk of SCD. The success of the Italian program is attributed to the ECG's ability to detect ion channel disease and accessory pathways, and because most patients with a primary cardiomyopathy exhibit an abnormal ECG. In contrast, most middle-aged athletes who die from coronary artery disease rarely show abnormalities on a resting ECG. Current recommendations for identifying middle-aged athletes at highest risk of SCD rely on an exercise stress test—but it is recognized that most abnormal exercise tests in asymptomatic middle-aged athletes are false positives and have low predictive accuracy.

Current data suggest that bystander cardiopulmonary resuscitation (CPR) and early use of an automated external defibrillator (AED) are the most effective methods of preventing SCD in this group. In most instances of SCD in sport, the reputation of exercise remains intact because exercise is considered a mere trigger for arrhythmias in predisposed individuals, rather than the cause of the underlying pathological condition.

Can Exercise Damage a Previously Normal Heart?

The past two decades have witnessed a surge in the number of people participating in grueling endurance events such as competitive cycling, marathons, triathlons, and Ironman races. In parallel, multiple studies have demonstrated raised blood concentrations of cardiac damage biomarkers (such as cardiac troponin) in a large number of these athletes after events.

The mechanism and consequences of elevated cardiac biomarkers after exercise are debated. The key question the authors raise: could repeated bouts of lifelong endurance exercise, in some individuals with an otherwise normal heart, cause enough heart muscle cell death (myocyte necrosis) to create an arrhythmogenic substrate through adverse myocardial remodelling and fibrosis (scarring)?

Evidence from animal models supports this theory. Benito and colleagues exercised rats on a treadmill for 16 weeks—which in human terms is equivalent to approximately 10 years. At the end of the study, the exercising rats had developed eccentric LV hypertrophy, diastolic dysfunction, and diffuse fibrosis in the atria and right ventricle. More importantly, ventricular tachycardia (a dangerous rapid heart rhythm) was inducible during electrophysiological studies in 42% of the exercising rats compared with only 6% of sedentary rats.

Human cross-sectional studies have also explored the role of chronic endurance exercise in myocardial fibrosis. Breuckmann and colleagues performed cardiac MRI on 102 men aged 50 years and older who had completed at least five marathons during the previous 3 years and had no history of heart disease or diabetes. Veteran marathon runners exhibited a 3-fold greater prevalence of late gadolinium enhancement (LGE)—an indicator of myocardial fibrosis or scar—compared with sedentary controls (12% vs. 4%).

Another study by Mohlenkamp and colleagues assessed coronary artery calcium scores in the same cohort and found that a larger proportion of marathon runners had coronary artery calcium scores above 100 Agatston Units (a measure of plaque buildup) compared with controls matched for age and Framingham risk factors (36% vs. 21%). The researchers implicated shearing forces within coronary arteries during high heart rates, circulating interleukins due to inflammation, and the production of free radicals as possible contributing factors.

Atrial Fibrillation and Sinus Node Disease in Athletes

Perhaps the most persuasive data suggesting that excessive endurance exercise could prove detrimental for some athletes comes from the higher-than-expected prevalence of atrial fibrillation (AF)—a common irregular heart rhythm—in middle-aged endurance athletes.

A meta-analysis of 6 studies involving 655 athletes engaged in chronic exercise reported a 5-fold higher risk of AF compared with the sedentary population. In a recent large study of 52,000 long-distance cross-country skiers, the risk of AF was related to the number of races competed in and faster finishing times.

Some studies have assigned specific exercise risk thresholds for developing AF:

• A lifetime sports practice exceeding 1,500 hours increases the risk
• More than 5 hours of intensive exercise per week starting at age 30 years and onward increases the risk of AF

The precise mechanism behind AF in athletes is not fully understood, but researchers have implicated vagally mediated shortening of the atrial refractory period (the time heart tissue needs to recover before it can beat again), atrial stretch, atrial inflammation, and scarring. Animal models support the theory that AF in athletes is a consequence of adverse atrial remodelling. One recent study demonstrated that rats subjected to intensive exercise for 1 hour per day for a total of 16 weeks displayed atrial dilatation, scarring, and an enhanced sensitivity to AF induction.

Athletes also show a higher prevalence of sinus node dysfunction (problems with the heart's natural pacemaker) and second- or third-degree AV block compared with non-athletes, though these are often benign in young athletes.

Adverse Cardiac Remodelling and Ventricular Arrhythmias

There is emerging evidence that ventricular arrhythmias (dangerous rhythms originating in the lower chambers of the heart) in an otherwise healthy athlete may have a more sinister prognosis than previously thought.

Heidbuchel and colleagues observed a high incidence of major arrhythmic events including sudden cardiac death (20%) in 46 young athletes presenting with frequent ventricular ectopy (extra heartbeats) or non-sustained ventricular tachycardia over a 5-year follow-up period. Notably, 80% of the ventricular arrhythmias were of right ventricular origin—pointing to the right side of the heart as a vulnerable area.

Subsequent studies from the same group suggest that chronic endurance exercise promotes adverse right ventricular remodelling. During exercise, invasive studies reveal that pulmonary artery pressures can reach as high as 80 mmHg, placing a heavy load (afterload) on the right ventricle. La Gerche and colleagues studied 40 healthy athletes at baseline and after an endurance race, revealing transient right ventricular enlargement associated with impaired right ventricular function on echocardiography. Cardiac troponin and B-type natriuretic peptide levels (blood markers of heart strain) were elevated and corresponded to the duration of exercise and the magnitude of reduction in right ventricular function.

The researchers postulated that repeated insults to the right ventricle of this type, following prolonged intense exercise, could lead to the concept of exercise-induced ARVC—a condition in which years of endurance training cause changes that mimic a genetic heart muscle disease. The dose of exercise required for this effect is probably more than 20 hours per week for more than 20 years.

The Ugly: Performance-Enhancing Drugs and the Heart

In the current era of celebrity athletes and lucrative sports contracts, several athletes have turned to performance-enhancing agents for success—with devastating consequences for cardiac health. The table below summarizes the effects of various performance-enhancing drugs on the heart:

LV = left ventricle; ✓ indicates a documented harmful effect on the heart.

Anabolic androgens (anabolic steroids) are particularly dangerous, as they can cause high blood pressure, arrhythmias, left ventricular hypertrophy (thickening of the heart muscle), coronary artery disease, heart attacks, heart failure, and sudden cardiac death. Cocaine is equally harmful across all categories. Amphetamines, ephedrine, and alcohol also carry significant cardiac risks, including heart attacks and sudden death.

Limitations of the Current Research

The authors are careful to point out the limitations of the evidence suggesting that extreme exercise can damage the heart. While there are mounting reports that regular participation in extremely intensive exercise may induce arrhythmogenic cardiac substrates in some athletes, these conclusions remain speculative. Much of the evidence is based on observational studies involving small, selected groups of symptomatic athletes who presented to medical professionals.

If such cases represented the "numerator" of athletes harboring exercise-induced arrhythmogenic substrates, the percentage of athletes affected would be minuscule when considering the likely "denominator" of approximately 10 million participants in marathons, triathlons, and Ironman events worldwide each year.

Importantly, a prospective study of 114 Olympic endurance athletes who had competed in 2–5 consecutive Olympic Games did not show any deterioration in cardiac function or increased risk of arrhythmias over time. Exercise also reduces age-related decreases in arterial compliance and elasticity, which may protect against cardiovascular disease in later life.

Furthermore, numerous studies have revealed that athletes engaging in the most grueling endurance events—including the Tour de France—live longer than inactive individuals. This longevity benefit may be attributed to their generally healthier lifestyle or genetic superiority, but it should not obscure the fact that years of intensive exercise were not associated with an increased risk of cardiac morbidity in these athletes.

Recommendations: What Does This Mean for You?

Based on this comprehensive review, here is what patients should take away:

1. Moderate exercise is powerfully protective. Aim for at least 150 minutes of moderate-intensity exercise per week (about 2 hours total), which can be divided into three sessions of 40–50 minutes each. Brisk walking, gentle jogging, or cycling all count.
2. Even small amounts help. Every single MET of exercise you achieve reduces cardiovascular mortality by 12–20%, and even light activity is better than being completely sedentary.
3. Exercise is medicine for existing heart disease too. Structured cardiac rehabilitation after a heart attack reduces the risk of future cardiac events and death, based on evidence from 34 randomized trials.
4. If you are an endurance athlete, know your body. While extreme endurance training appears safe for the vast majority, the data suggest a small subset of athletes may develop heart rhythm problems or structural changes with decades of very high-volume training (more than 20 hours per week for more than 20 years).
5. Pay attention to symptoms. Symptoms such as chest pain, fainting, palpitations, or unusual shortness of breath during exercise should never be ignored, especially in athletes with a family history of heart disease or sudden death.
6. If you are over 30 and exercising intensively, be aware of atrial fibrillation risk. More than 5 hours of intensive exercise weekly starting at age 30, or more than 1,500 cumulative lifetime hours of sports, has been associated with a higher risk of AF.
7. Never use performance-enhancing drugs. Substances like anabolic steroids and cocaine can cause catastrophic cardiac damage—including heart attacks, heart failure, and sudden death—with no safe threshold.
8. Black athletes should be evaluated with ethnicity-specific standards. ECG patterns and cardiac dimensions that would be concerning in white athletes may be completely normal in black athletes.

Frequently Asked Questions

How much exercise do I need to protect my heart?

Just 2 hours of moderate exercise per week, divided into three sessions, is enough. That means brisk walking, gentle jogging, or cycling. The benefit is clear: every single MET of exercise achieved reduces cardiovascular mortality by 12–20%. Even light activity is better than being sedentary.

What is athlete's heart and is it dangerous?

Athlete's heart is a combination of electrical, structural, and functional changes from intense training, including a 10–20% increase in left ventricle wall thickness and 10–15% larger chambers. It is generally benign and often reversible after detraining, but it can sometimes look like a heart muscle disease that needs expert evaluation.

Can extreme endurance exercise damage a previously normal heart?

In some studies, yes, there is concerning evidence. For example, 12% of 102 veteran marathon runners had heart scarring (fibrosis) on MRI, compared with 4% of sedentary controls. Also, animal studies show exercise-related scarring and arrhythmias. However, this appears rare, and most endurance athletes remain healthy and live longer.

What symptoms during exercise should never be ignored?

Chest pain, fainting, palpitations, or unusual shortness of breath during exercise should never be ignored, especially if you have a family history of heart disease or sudden death. These symptoms could signal an underlying heart condition, so see a doctor promptly for evaluation before continuing your training.

Why are black athletes evaluated differently for heart conditions?

Because normal heart changes from training differ by ethnicity. Black athletes often have more pronounced ECG repolarization changes, and up to 25% show T-wave inversion that is considered normal. Also, 13% of black male athletes have left ventricle wall thickness over 12 mm, which would be unusual in white athletes.

Are performance-enhancing drugs dangerous for the heart?

Yes, extremely dangerous. Anabolic steroids and cocaine can cause high blood pressure, arrhythmias, left ventricle hypertrophy, coronary artery disease, heart attacks, heart failure, and sudden cardiac death. These substances carry no safe threshold and should never be used for athletic performance or otherwise.

What is the link between endurance exercise and atrial fibrillation?

A meta-analysis of 6 studies covering 655 chronic endurance athletes found a 5-fold higher risk of atrial fibrillation compared with sedentary people. The risk increases with over 1,500 lifetime hours of sports or more than 5 hours of intensive exercise per week starting at age 30. This is more likely in middle-aged endurance athletes.

When should an athlete with ECG changes or enlarged heart chambers seek a second opinion to determine whether their heart is a normal athlete's heart or a cardiomyopathy?

An athlete should seek a second opinion when cardiac evaluation shows changes that could be either normal training adaptation or a serious heart muscle disease — for example, left ventricular wall thickness above 12 mm, T-wave inversion, or an enlarged right ventricle with abnormal function. These findings are common in athletes, especially black athletes, but when they coexist with symptoms or an abnormal ECG, the overlap with cardiomyopathy is significant. A mistaken diagnosis can cause unnecessary disqualification from sport or leave a dangerous condition undetected. A second opinion from experts in sports cardiology can clarify whether further testing or detraining is needed. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

This patient-friendly article is based on peer-reviewed research published in the European Heart Journal.

• Original title: "Exercise and the heart: the good, the bad, and the ugly"
• Authors: Sanjay Sharma, Ahmed Merghani, and Lluis Mont
• Journal: European Heart Journal (2015), Volume 36, Issue 23, Pages 1445–1453
• DOI: 10.1093/eurheartj/ehv090
• Affiliations: Department of Cardiovascular Sciences, St George's, University of London, UK; and Institut del Torax, Hospital Clinic, Universitat de Barcelona, Spain
• Published: Received 11 January 2015; accepted 4 March 2015; online publish-ahead-of-print 3 April 2015

This patient-friendly article is based on peer-reviewed research and is intended for educational purposes. It does not replace professional medical advice. Always consult your doctor before making changes to your exercise routine, especially if you have known heart disease or risk factors.