What happens if you do too much exercise?

28th July 2025, A/Prof Chee L Khoo

We have explored the association between intensive endurance athletes and cardiovascular events in the past. Data on the dose–response relationship between long-term intensive endurance exercise and coronary heart disease has been rather conflicting over the years. While early studies suggest that regular endurance athletes have lower ischaemic heart disease (1), later studies reported an increased prevalence of coronary atherosclerotic plaques amongst highly trained athletes in comparison to healthy non-athletes (2–4). As a runner, I am comforted by the studies which show that most of these plaques in the intensive endurance athletes are of the stable calcified type. What about the risk of arrhythmias amongst these athletes?

Regular physical exercise is in pretty much every recommended guideline for optimal cardiovascular health. Regular exercise improves blood pressure control and lipid profiles, reduces the incidence of diabetes and myocardial infarction, and increases life expectancy (5-8). However, high-intensity exercise over an extended duration can result in cardiac structural changes such as chamber enlargement, increased compliance, and electrical remodelling (the athlete’s heart) (1). These changes are thought to be benign, adaptive, and reversible but long-term high-intensity exercise has also been associated with increased risk of atrial fibrillation and myocardial fibrosis (1).

In patients with cardiomyopathy, myocardial fibrosis have been associated in a dose-response manner with ventricular arrhythmias. We are able to identify diffuse myocardial fibrosis and scarring using cardiac MRI (CMR) and late gadolinium enhancing imaging (LGE). The VENTricular arrhythmia and cardiac fibrOsis in endUrance eXperienced athletes (VENTOUX) study prospectively assessed the incidence of ventricular arrhythmias in longstanding masters endurance athletes and correlated events to imaging evidence of myocardial fibrosis by CMR (9). The findings will have implications in our understanding of the impact of high intensity exercise on cardiovascular health.

A highly selected cohort of 106 males >50 years old who have exercised (cycling or triathlon) at least 10 hours a week for the last 15 years and were free of cardiovascular disease or symptoms at baseline. Baseline investigations included resting ECG, CMR and LGE imaging. Controls were age-matched men who exercised for less than 3 hours a week. All participants wore implantable loop recorders for arrythmia detection.

Results

Compared with controls, high intensive endurance athletes had more non-ischaemic myocardial fibrosis (47.2% vs 11.2%). Most commonly affected segment involved is in the inferolateral segment of the left ventricle. There were signs of cardiac remodelling. Athletes with myocardial fibrosis (n=50) were older and had more frequent and atypical PVCs during exercisethan athletes without fibrosis (n=56).

The incidence of ventricular arrhythmias (≥ episode of non-sustained ventricular tachycardia (NSVT) was low. 18% of athletes had at least one episode of NSVT and 3% have at least one episode of VT. The presence of myocardial fibrosis was associated with a 4.7-fold increased risk (95% CI 1.7 – 12.7) in the incidence of ventricular arrhythmia. The vastmajority of participants with detected ventricular arrhythmias had myocardial fibrosis (100% ofthose with sustained VT, 91% with recurrent NSVT, and 78% with any VT). While there were no significant differences in training volume between athletes with and without fibrosis or arrhythmia, athletes with ventricular arrhythmias tended to have less cumulative training years (15y vs. 20y). Perhaps, athletes who start training later in life adapt less effectively.

The mechanisms underlying the development of myocardial fibrosis in athletes remain uncertain. Vigorous exercise acutely increases cardiac strain and wall stress and can cause detectable cardiomyocyte damage.1 Repetitive trauma can progress to fibrosis over time. The high prevalence of myocardial fibrosis was unexpected but the authors suggested that perhaps, it may be in part, related to the selected older patient.

Implications

Endurance exercise appears clearly associated with pathologic cardiac remodelling and ventricular arrhythmias in some individuals. From this study, it would seem that myocardial fibrosis increases the risk of ventricular arrythmias.

We have an increasing number of patients who are or were intensive endurance athletes who are now getting older. Perhaps, a CMR may be a good risk stratification tool especially in those who have demonstrated NSVT, PVCs, or atypical PVCs on resting ECG or during exercise testing. We might be picking up more of these patients as wearable technology becomes more common place and affordable.

NSVT has been shown to meaningfully increase the risk of adverse cardiovascular outcomes including sudden cardiac death in patients with underlying heart disease. However, its clinical significance in asymptomatic, healthy individuals remains unclear, as the absolute risk of cardiac events in these populations tends to be quite low (10–12).

References:

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