The Extreme Exercise Hypothesis: Can Too Much Exercise Harm Your Heart? A Patient's Guide to Recent Research

Table of Contents

• Key Points
• Why This Research Matters
• How This Review Was Conducted
• Is There an Upper Limit to Exercise Benefits?
• Accelerated Coronary Artery Calcification in Athletes
• Heart Muscle Scarring (Myocardial Fibrosis)
• Exercise and Atrial Fibrillation (Irregular Heartbeat)
• Sudden Cardiac Death: How Real Is the Risk?
• What This Means for Patients
• Limitations of the Current Evidence
• Recommendations for Active Individuals
• Frequently Asked Questions
• Source Information

Key Points

• Regular exercise is overwhelmingly beneficial; the extreme exercise hypothesis is unproven and may affect only a tiny minority.
• The most compelling concern is a higher atrial fibrillation risk in the highest-volume exercisers.
• Sudden cardiac death in young athletes is rare, at 0.76 cases per 100,000 athletes per year.
• Athletes may have more coronary calcium, but their plaques tend to be stable calcified types.
• No clear upper limit for exercise benefits has been identified; current evidence is largely circumstantial.

Why This Research Matters

The health benefits of exercise are well established. The World Health Organization (WHO) recommends that adults aged 18–64 engage in at least 150 minutes per week of moderate-intensity aerobic activity, or 75 minutes per week of vigorous-intensity aerobic activity, or an equivalent combination of the two. In addition, muscle-strengthening activities involving major muscle groups should be performed on two or more days each week.

Regular aerobic exercise and resistance training are associated with a reduced risk of cardiovascular disease and death. The relationship between exercise volume—which largely reflects the duration and intensity of physical activity—and health benefits is usually described as curvilinear. This means the most dramatic health improvements occur at the beginning of the curve.

In other words, a person who goes from being sedentary to walking a few times per week gains enormous heart-health benefits. The WHO's guidance that "more exercise is better" appears to hold true, and it is estimated that maximal cardiovascular health benefits are obtained at exercise volumes roughly 3 to 4 times the current recommendations.

But what happens when people exercise far beyond that level? That question is at the heart of the "Extreme Exercise Hypothesis." This hypothesis proposes that the relationship between exercise volume and heart health may not be a straight upward line of benefit, but rather a U-shaped or reverse J-shaped curve. In plain terms, the idea is that health risks decrease as you go from no exercise to moderate exercise, but may start to rise again once you reach very high volumes of intense, long-term training.

This topic is hotly debated in sports cardiology. Researchers have valid concerns that suggesting high-volume, high-intensity exercise could potentially harm the heart might discourage a physically active lifestyle among the general population, and thus contribute to the already high prevalence of physical inactivity.

The goals of this review were to: (1) summarize recent findings that support or refute the "Extreme Exercise Hypothesis," and (2) interpret the potential effects of exercise-induced heart changes on cardiovascular health outcomes.

How This Review Was Conducted

This article is a review paper, not a new clinical study. The authors—Thijs M. H. Eijsvogels, MD, PhD, from Radboud University Medical Center in the Netherlands, Paul D. Thompson, MD, from Hartford Hospital in Connecticut, and Barry A. Franklin, PhD, from William Beaumont Hospital in Michigan—systematically examined recently published epidemiological studies, cross-sectional imaging studies, biomarker studies, and large population-based cohort studies related to extreme exercise.

They focused on five specific areas of concern in veteran endurance athletes: the identification of a potential upper limit of exercise benefits, accelerated coronary artery calcification (plaque buildup in heart arteries), increased myocardial fibrosis (scarring of heart muscle), atrial fibrillation (an irregular heartbeat), and sudden cardiac death. They also reviewed the tools used to detect these conditions, including computed tomography (CT) scans for coronary artery calcification and cardiac magnetic resonance imaging (MRI) for fibrosis.

Is There an Upper Limit to Exercise Benefits?

Only a few studies have had enough participants to explore whether there is a "ceiling" or an upper limit beyond which additional exercise no longer helps—and may even hurt.

The Arem study: 661,137 people. One landmark study by Arem and colleagues combined leisure-time physical activity data from six large population-based cohorts in the USA and Europe, creating a study population of 661,137 individuals. The researchers found that the maximal reduction in all-cause mortality occurred at an exercise volume of 3 to 5 times current exercise recommendations (hazard ratio [HR]: 0.61, 95% confidence interval [CI]: 0.59–0.62). This translates to about a 39% lower risk of dying from any cause compared to inactive people.

Individuals who performed physical activity at volumes 10 times or more above current recommendations still had a lower mortality risk compared to the inactive reference group (HR: 0.69, 95% CI: 0.59–0.78), but the health benefit was notably smaller—a 31% risk reduction versus the optimal group's 39% risk reduction.

The Lear study: 130,843 people from 17 countries. More recently, Lear and colleagues analyzed a cohort of 130,843 individuals from 17 low-, middle-, and high-income countries to explore the effect of physical activity on mortality and cardiovascular disease. Individuals in the high physical activity group had a substantially reduced risk of all-cause mortality (HR: 0.65) and major cardiovascular events (HR: 0.75) compared to the low physical activity group.

Interestingly, recreational physical activity at about 112 minutes per week yielded the largest risk reductions for the combined endpoint of mortality and major cardiovascular disease (HR: 0.89, 95% CI: 0.82–0.95). However, those significant health benefits were lost at physical activity volumes above 255 minutes per week.

These observations challenge the notion that more exercise is always better. However, the review authors caution that it remains difficult to tell the difference between:

1. A genuine finding that supports the "Extreme Exercise Hypothesis," versus
2. A loss of health benefits due to statistical factors produced by the relatively small number of individuals in the most active groups

This second possibility is supported by the large confidence intervals for the risk estimates, which indicate a high degree of statistical uncertainty. Based on the limited current evidence and numerous potential confounders, the authors conclude that it is difficult to pinpoint an exact upper limit for the benefits of physical activity at this time. Future studies should combine data from large cohorts—including highly active amateur athletes—to determine the health effects of the highest volumes of physical activity.

Accelerated Coronary Artery Calcification in Athletes

Atherosclerotic coronary artery disease (CAD)—a condition where plaque builds up in the arteries that supply blood to the heart—is the largest cause of cardiovascular disease. Regular physical activity and exercise training are known to reduce several cardiovascular risk factors, including lipid (cholesterol) levels, blood pressure, and inflammation.

Coronary artery atherosclerosis can be detected using several imaging techniques. A coronary artery calcification (CAC) score, derived from computed tomography (CT) images, is an excellent predictor of future cardiac events. The higher the score, the greater the amount of calcium in the artery walls, and the higher the risk.

Striking findings in marathon runners. One of the most frequently cited observations comes from Möhlenkamp and colleagues, who found a higher prevalence of CAC scores of 100 or higher (measured in Agatston units) among 108 marathon runners (36%) compared to an age- and risk factor-matched control group from the general population (22%).

The Aengevaeren study: 284 male amateur athletes. A more recent study examined the association between lifelong physical activity volumes and the prevalence and characteristics of coronary atherosclerosis in 284 male amateur athletes. The most active athletes routinely exercised at volumes equal to four times current recommendations, whereas the least active athletes exercised at the currently recommended volume.

Results showed that the most active athletes had a higher CAC prevalence than the least active athletes (68% versus 43%, odds ratio [OR]: 3.2, 95% CI: 1.6–6.6). This sounds alarming—until you look at the type of plaque. The most active athletes actually had a lower prevalence of mixed plaques (48% versus 69%; OR: 0.35, 95% CI: 0.15–0.85) and more often had only calcified plaques (38% versus 16%; OR: 3.57, 95% CI: 1.28–9.97) compared with the least active athletes.

This distinction matters clinically. Mixed plaques are associated with a higher probability of future cardiovascular events (38%) compared with calcified plaques (6%). In other words, the type of plaque an athlete develops may be more stable and less dangerous.

English veteran athletes study. Similar findings were reported in an English cohort of 152 veteran athletes and 92 sedentary controls. Male athletes more often had atherosclerotic plaques (44% versus 22%; p = 0.009) and a higher prevalence of high CAC scores above 300 (11% versus 0%; p = 0.009) compared to age- and risk factor-matched sedentary controls. Again, veteran athletes predominantly had calcified plaques, whereas mixed plaques were more prevalent among the sedentary controls.

What does this all mean? Taken together, these data suggest that long-term exercise training is associated with accelerated coronary artery atherosclerosis, but that accelerated plaque calcification may outweigh the cardiovascular risks normally associated with increased CAC scores. In plain language, athletes may build up more calcium in their arteries, but their plaques appear to be of the "stable," lower-risk variety. Additional longitudinal studies are needed to confirm this hypothesis.

The Race Across the USA study. Lin and colleagues assessed changes in plaque characteristics among 8 participants of the Race Across the USA, an event covering 140 race days and 3,080 miles. Four runners had no evidence of coronary artery disease on CT angiography before or after the race. However, in the four runners who had coronary atherosclerosis before the race, luminal stenosis (narrowing of the artery) and plaque volume (ranging from 4.8 to 94 mm³) increased. The change in plaque volume was mainly attributed to an increase in non-calcified plaque.

Notably, the researchers also observed increases in high-sensitivity C-reactive protein (CRP), a marker of inflammation, suggesting that exercise-induced inflammation may contribute to accelerated plaque progression. Whether the initial increase in non-calcified plaque later transforms into calcified plaque during recovery is unknown.

The review also describes some possible biological mechanisms: previous studies have demonstrated that exercise increases parathyroid hormone, decreases vitamin D3, and decreases magnesium levels. All of these are involved in calcium-phosphate metabolism, which could affect vascular calcification. Future studies examining these mechanisms may provide insight into how to stabilize plaques in vulnerable patient populations.

Heart Muscle Scarring (Myocardial Fibrosis)

Exercise-induced increases in cardiac biomarkers—substances released into the blood when the heart is stressed or damaged—are common in athletes after endurance exercise. These include troponin, a marker of cardiomyocyte (heart muscle cell) damage, and B-type natriuretic peptide (BNP), a marker of myocardial stress.

Newer biomarkers of fibrosis. Recent studies have explored the impact of endurance exercise on newer cardiac biomarkers:

• Galectin-3, a marker of myocardial fibrosis (scarring)
• Soluble suppression of tumorigenicity-2 (sST2), a marker of extracellular matrix remodeling and fibrosis

Resting levels of galectin-3 were higher in athletes (n = 21) compared to controls (n = 21), and significant increases were observed following a 30-km run, with levels rising from 12.8 ± 3.4 to 19.9 ± 3.9 ng/ml (p < 0.001). Similarly, sST2 concentrations increased following a marathon, from 34.2 to 54.2 ng/ml (p < 0.001), with 68 of 79 athletes (86%) demonstrating a concentration above the upper reference limit. Complete normalization of sST2 levels occurred within 48 hours.

These biomarker elevations are modest and transient, but their long-term clinical implications are unknown. The review authors note that long-term exercise training and competition, with repetitive exposure to prolonged vigorous exercise, may increase the risk of cardiac fibrosis.

How is fibrosis detected? Cardiomyocyte damage can lead to myocardial fibrosis, which is characterized by collagen infiltration in the extracellular matrix (the structural support around heart muscle cells). The presence and extent of myocardial fibrosis can be determined via microscopic analysis of cardiac muscle obtained by postmortem biopsy, or via cardiac magnetic resonance imaging (MRI) with gadolinium contrast. Newer T1 mapping techniques can detect more diffuse fibrosis.

How common is fibrosis in athletes? Previous studies using MRI reported that the prevalence of myocardial fibrosis among athletes varied substantially—from 0% to 50% depending on the study population. A systematic review found evidence of myocardial fibrosis in 30 of 509 scanned athletes (5.9%). The fibrosis patterns were heterogeneous (varied) and most frequently located near the interventricular septum (the wall between the heart's two lower chambers) and the right ventricular insertion points. Importantly, the presence of myocardial fibrosis was strongly associated with cumulative exercise dose—that is, how much exercise the athlete had done over a lifetime.

Contrasting studies. Not all studies found high rates of fibrosis. Bohm and colleagues found no difference in left and right ventricular function parameters between 33 competitive elite male master endurance athletes and 33 controls matched for age, height, and weight, and myocardial fibrosis was observed in only 1 athlete. Similarly, Abdullah and colleagues compared left ventricular characteristics across groups of long-term exercisers (2–3, 4–5, and 6–7 exercise sessions per week) and found a stepwise improvement of cardiac structure and function with increasing doses of physical activity. Among the 92 study participants, delayed gadolinium enhancement was observed in only 1 exerciser in the 2–3 sessions-per-week group.

On the other hand, Wilson and colleagues used delayed gadolinium enhancement on cardiovascular MRI to describe diverse patterns of myocardial fibrosis in 6 of 12 highly trained veteran endurance athletes. The authors note that the discrepancy in prevalence rates between studies may be due to differences in the age and training status of the study populations, or to survival bias (i.e., athletes who died or became ill may not have been included in the studies).

T1 mapping and diffuse fibrosis. Gormeli and colleagues used T1 mapping—a newer MRI technique—to quantify diffuse fibrosis. They found that athletes had significantly higher native T1 values in the left ventricle (LV) (1230 ± 39 ms versus 1174 ± 36 ms, p < 0.001) and in the interventricular septum (IVS) (1268 ± 48 ms versus 1180 ± 27 ms, p < 0.001) compared to matched sedentary controls. Furthermore, native T1 values of both the LV and IVS were significantly higher in athletes who had trained 5 years or more compared to those training less than 5 years, and the highest values of LV end-diastolic volume and IVS wall thickness were found in those athletes who had trained the longest. These data suggest that more training results in greater cardiac remodeling—but potentially also more diffuse myocardial fibrosis.

Clinical consequences of fibrosis. The clinical consequences of myocardial fibrosis in athletes are largely unexplored, but some concerning findings have emerged:

• A German study found that coronary revascularization (a procedure to restore blood flow to the heart) was more common in athletes with fibrosis than without fibrosis—25% versus 1%, respectively.
• Schnell and colleagues reported a case series of serious cardiac complications in Belgian athletes with isolated subepicardial fibrosis, including non-sustained ventricular arrhythmias, symptomatic ventricular tachycardia (a dangerously fast heart rhythm), and progressive left ventricular dysfunction.
• British veteran athletes with myocardial fibrosis demonstrated normal cardiac function overall, but co-localized regional cardiac dysfunction was found in the fibrotic areas, substantiated by evidence of an attenuated cardiac strain and base-to-apex gradient (a measure of how well the heart muscle squeezes).

These observations suggest that the presence of myocardial fibrosis requires appropriate clinical follow-up to evaluate the possibility of future adverse cardiovascular outcomes.

Exercise and Atrial Fibrillation (Irregular Heartbeat)

Atrial fibrillation (AF) is a heart rhythm disorder characterized by an irregular and often abnormally fast heartbeat. The relationship between physical activity, cardiorespiratory fitness (CRF—measured in mL O₂/kg/min or metabolic equivalents [METs], where 1 MET = 3.5 mL/kg/min), and atrial fibrillation is complex.

Conflicting findings. Two recent studies reported that higher cardiorespiratory fitness was associated with a graded reduction in the risk of AF. However, this observation contrasts with a prospective observational study in older adults and a large cohort study of long-distance cross-country skiers, which found that individuals participating at the highest intensities and/or volumes of exercise were at greater risk of developing AF.

Meta-analysis of athlete risk. A systematic review and meta-analysis of case-control studies found that the overall risk of AF was significantly higher in athletes than in controls, with an odds ratio of 5.29 (95% CI: 3.57–7.85; p = 0.0001). Other researchers have reported that practicing endurance sports increases the probability of experiencing AF by two- to tenfold, even after adjusting for potential confounding variables and associated risk factors. The lifetime-accumulated hours of vigorous endurance training—specifically 2,000 or more hours—was identified as the most powerful predictor of exercise-induced AF.

Why does this happen? The potential mechanisms for AF induced by long-term strenuous endurance exercise include a combination of autonomic, structural, and hemodynamic effects of high-volume, high-intensity aerobic exercise, repeated over time. Additional pathophysiologic mechanisms may include:

• Derangements in sympathetic/parasympathetic tone (the balance between the "fight-or-flight" and "rest-and-digest" nervous systems)
• Recurrent fluid and electrolyte shifts during and after exercise

The other side of the coin. For the general population, increased cardiorespiratory fitness is associated with a reduced risk of AF. There is also at least one non-randomized study demonstrating that increases in CRF achieved by a physician-led exercise program reduce the recurrence of AF in obese patients, even when weight loss is minimal. These findings suggest that the relationship between physical activity and incident AF is best summarized by a reverse J-shaped curve: light-to-moderate amounts of exercise decrease the risk of AF, but larger volumes of exercise potentially increase the risk.

Sudden Cardiac Death: How Real Is the Risk?

High-intensity exercise can acutely—albeit transiently—increase the risk of sudden cardiac arrest (SCA) or sudden cardiac death (SCD) in individuals with underlying cardiac disease. The cause of death is usually different for young versus older athletes.

• Young individuals (≤ 40 years) die during exercise primarily from inherited or congenital cardiac conditions, such as hypertrophic cardiomyopathy (HCM, a disease in which heart muscle becomes abnormally thick), coronary artery anomalies, and right ventricular cardiomyopathy (RVCM, a disease affecting the right heart chamber).
• Older individuals (> 40 years) die primarily from atherosclerotic coronary artery disease (ASCAD), the same plaque buildup disease that causes heart attacks.

The Canadian study. A Canadian study of athletic participants aged 12–45 years found 74 cases of sudden cardiac arrest over the course of 18.5 million person-years of observation, yielding an incidence of 0.76 cases per 100,000 athletes per year. A total of 16 SCA cases occurred during competitive sports, of which 44% survived, whereas 58 cases occurred during non-competitive sports, of which 44% also survived.

More importantly, genetic structural abnormalities such as HCM and RVCM were uncommon causes of SCA in this study—accounting for only 8% and 5% of cases, respectively. This is in contrast to some primarily older studies that identified HCM as the predominant cause of SCD in young athletes. The review authors suggest that early risk identification of gene carriers for conditions such as HCM and RVCM, and subsequent exercise restriction, may have contributed to this apparent change in the causes of SCD in young athletes.

The Australian/New Zealand study. Another study from Australia and New Zealand found a similar incidence of SCD (1.3 cases per 100,000 persons per year) in children and young adults, but this study included all deaths, not just exercise-related deaths. SCD incidence increased with age and was highest for individuals aged 31–35 years (3.2 cases per 100,000 persons per year).

The Australian study reported that most SCD cases occurred during sleep (28%) and rest (20%), with relatively few cases occurring during light physical activity (14%), exercise (8%), or post-exercise (3%). However, the investigators did not correct SCD incidence for exposure time, which makes it difficult to accurately assess the relative risks of exercise. Here's the key insight: since most people spend far more time asleep than exercising, the fact that 25% of SCDs occurred during all intensities of exercise combined actually suggests that exercise does increase the risk of SCD compared to non-exercise activities.

The bottom line on SCD. The exercise-induced risk of SCA and SCD is only transient, and there is strong evidence that regular exercise training is associated with an overall decreased risk of adverse cardiovascular outcomes. In other words, the temporary spike in risk during and immediately after vigorous exercise is far outweighed by the long-term protection that regular exercise provides.

What This Means for Patients

Based on the evidence reviewed, the authors reached several important conclusions:

1. There is limited evidence supporting the "Extreme Exercise Hypothesis." The most compelling evidence relates to the increased risk of atrial fibrillation at high volumes of exercise. For most people, the risk of harm remains quite small.
2. Cardiac anomalies may be present in a small proportion of the most active veteran athletes. These include coronary artery calcification, myocardial fibrosis, and arrhythmias.
3. The combination of high-intensity physical activity in the presence of known or hidden (occult) cardiovascular disease appears to be the major cause of exercise-related fatalities.
4. Sudden cardiac arrest and death are infrequent among exercising young individuals, with an estimated incidence rate of just 0.76 per 100,000 person-years.

For patients, the practical takeaways are: exercise is still one of the best things you can do for your heart. But for veteran endurance athletes who have accumulated many years of high-volume training, it may be wise to have a cardiovascular check-up, including discussion of symptoms such as palpitations, unusual shortness of breath, or chest discomfort.

The finding about atrial fibrillation deserves special attention. If you are a long-term endurance athlete and experience heart palpitations, an irregular heartbeat, or unexplained fatigue, these should not be ignored. AF can be managed effectively when detected early.

Limitations of the Current Evidence

The review authors are careful to note several important limitations in the research base:

• Circumstantial evidence: Much of the support for the "Extreme Exercise Hypothesis" is based on cross-sectional studies (which look at a single point in time) rather than long-term prospective studies (which follow people forward over time).
• Small numbers in extreme exercise groups: In large epidemiological studies, the number of people exercising at volumes 10 times the recommendations is small, making it difficult to draw firm conclusions. This is reflected in the large confidence intervals for risk estimates.
• Potential confounders: Athletes who exercise at extreme volumes may differ from the general population in many other ways—including diet, supplement use, medication use, and genetics—that could influence heart health.
• Survival bias: Studies of veteran athletes may inadvertently exclude those who became ill or died from heart conditions, potentially making athletes appear healthier than they truly are.
• No clear threshold: Despite the data, there is no clearly defined upper limit for exercise-induced health benefits at this time.
• Conflicting findings on fibrosis: Prevalence rates of myocardial fibrosis varied dramatically (0% to 50%) across studies, likely due to differences in age, training status, and imaging techniques used.

These limitations mean that the "Extreme Exercise Hypothesis" remains a hypothesis, not a proven fact. Future studies combining data from large cohorts—including highly active amateur athletes—are needed to determine the true health effects of the highest volumes of physical activity.

Recommendations for Active Individuals

Based on the findings of this review, here is practical advice for different groups of people:

For the general population (including most patients reading this article):

• Continue to follow the WHO guidelines: at least 150 minutes of moderate-intensity or 75 minutes of vigorous-intensity aerobic exercise per week.
• Do not be discouraged by headlines about extreme exercise. The evidence strongly shows that regular exercise reduces cardiovascular risk and mortality.
• Aim for the "sweet spot" of 3 to 5 times the current recommendations if you are healthy and enjoy exercise—this is where maximal mortality risk reduction (about 39%) was observed.

For veteran endurance athletes (> 40 years old with many years of high-volume training):

• Consider a cardiovascular evaluation, including discussion with your doctor about your exercise history.
• Be aware that coronary artery calcification is more common in veteran athletes—but the plaques tend to be more stable (calcified) and less likely to rupture than the mixed plaques seen in sedentary individuals.
• Pay attention to symptoms like palpitations, irregular heartbeats, or reduced exercise tolerance, as these may signal atrial fibrillation, which is the most compelling exercise-related concern.
• If you have been diagnosed with heart disease, work with your cardiologist to determine a safe exercise program.

For young athletes (≤ 40 years):

• Sudden cardiac death during exercise is extremely rare: about 0.76 cases per 100,000 athletes per year.
• Inherited conditions like hypertrophic cardiomyopathy are now less commonly the cause of SCD, likely because of better screening and risk identification.
• If you have a family history of heart conditions or unexplained fainting, seek evaluation before engaging in competitive sports.

For everyone: The overall message is that the benefits of exercise vastly outweigh the risks for the vast majority of people. The "Extreme Exercise Hypothesis" may apply to a very small subset of individuals who push their bodies to extraordinary limits for decades—but it should not discourage anyone from being physically active.

Frequently Asked Questions

Is too much exercise bad for your heart?

Research suggests that extremely high volumes of intense, long-term exercise may be linked to heart abnormalities such as atrial fibrillation, coronary artery calcification, and rare heart muscle scarring. However, the evidence is largely circumstantial, and regular exercise remains overwhelmingly beneficial for most people. The risks appear limited to a small subset of extreme athletes.

What is the extreme exercise hypothesis?

The extreme exercise hypothesis proposes that the relationship between exercise volume and heart health may be U-shaped. Going from no exercise to moderate exercise lowers health risks, but risks may rise again at very high volumes of intense, long-term training. This idea is hotly debated, and researchers stress it remains a hypothesis, not proven fact.

Does extreme exercise increase the risk of atrial fibrillation?

Yes. A meta-analysis found athletes had a significantly higher risk of atrial fibrillation, with an odds ratio of 5.29 compared to controls. Training for 2,000 or more lifetime hours was the strongest predictor. However, light-to-moderate exercise reduces the risk. If you experience palpitations or an irregular heartbeat, seek medical evaluation.

How common is sudden cardiac death in athletes?

A Canadian study found 0.76 cases of sudden cardiac arrest per 100,000 athletes per year, which is extremely rare. In young athletes, causes are often inherited conditions; in older athletes, plaque buildup is the main cause. Although exercise transiently increases risk, regular training lowers overall cardiovascular risk.

Does endurance exercise cause coronary artery calcification?

Some studies show veteran athletes have more coronary artery calcium than non-athletes. For example, in a study of 284 male amateur athletes, the most active had a higher prevalence of calcification, but they had more stable calcified plaques and fewer dangerous mixed plaques. This suggests the plaques may be less likely to rupture.

Can extreme exercise cause heart muscle scarring?

MRI studies have found myocardial fibrosis in some veteran athletes. A systematic review identified scarring in 5.9% of 509 scanned athletes, and it was linked to lifetime exercise dose. However, reported prevalence varied widely from 0% to 50% across studies. The long-term consequences of such scarring remain uncertain.

What should veteran endurance athletes do?

Veteran endurance athletes should consider a cardiovascular evaluation, especially if they have many years of high-volume training. Pay attention to symptoms like palpitations, irregular heartbeats, or reduced exercise tolerance, as these may signal atrial fibrillation. Exercise is still beneficial, but discussing your history and symptoms with a doctor is wise.

Source Information

Original Article Title: Extreme Exercise Hypothesis

DOI: 10.1007/s11936-018-0674-3

Journal: Current Treatment Options in Cardiovascular Medicine (2018) 20:84

Published: August 28, 2018, as part of the Topical Collection on Sports Cardiology

DOI: 10.1007/s11936-018-0674-3

Disclosures: Dr. Eijsvogels and Dr. Franklin declared no potential conflicts of interest. Dr. Thompson reported serving on speakers' bureaus for Regeneron, Sanofi, Amgen, and Amarin; consulting for Amgen, Regeneron, Esperion, and Sanolfi; receiving research support from Sanofi, Regeneron, Esperion, Amgen, and Amarin; owning stock in Abbvie, Abbott, CVS, General Electric, Johnson & Johnson, Medtronic, and Sarepta; and providing legal consultation on exercise-related cardiac events and statin myopathy.

This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition.