By Aria Afsharian

Graphic design by Vicky Lin

In the lead-up to the 2026 FIFA World Cup, eyes were on Danish footballer Christian Eriksen after he collapsed on the field from cardiac arrest during a match against Ukraine. This was not new for Eriksen, as he suffered a similar incident in 2021.¹ While Eriksen recovered from both incidents, highly publicized cardiac events have fueled concerns about the safety of vigorous exercise. Understanding when exercise benefits the heart—and when it may be harmful—is a major focus of Dr. Jack Goodman, Professor Emeritus of Cardiac Health and Exercise in the Faculty of Kinesiology at the University of Toronto and adjunct scientist in the Mount Sinai Hospital Division of Cardiology.

Dr. Goodman’s early research aimed to understand how cardiovascular health impacts exercise performance and heart function. He initially investigated how cardiovascular disease affects the body’s response to exercise.^2,3 Now, Dr. Goodman examines how sustained vigorous exercise influences the heart, distinguishing normal physiological adaptations from pathological changes. 

In a 2010 study, Dr. Goodman and his team assessed the effects of acute exercise on heart function.⁴ Participants performed 150 minutes of high- and low- intensity exercise while heart function was assessed with echocardiography, in which ultrasound is used to image the heart. Following high-intensity exercise, participants showed reduced ventricular contractility, lower left ventricular ejection fraction (i.e., blood pumped out from the ventricle), and reduced ventricular wall deformation, indicating a temporary reduction in cardiac efficiency known as “cardiac fatigue.” 

To explore the mechanistic explanation for this effect, the team examined whether changes in hormonal responsiveness contribute to reduced contractility during exercise. Catecholamines like norepinephrine increase heart rate and contractility by acting on β-adrenergic receptors, enhancing cardiac output (CO) during stress.⁴ To assess β-adrenergic responsiveness, participants were administered the synthetic catecholamine dobutamine before and after exercise, with heart function assessed via echocardiography. Pre-exercise dobutamine treatment produced the expected increase in CO, while post-exercise dobutamine did not, suggesting that high-intensity exercise leads to cardiac fatigue partially through dampened β-adrenergic sensitivity. Importantly, this phenomenon appears to be a temporary physiological adaptation with Dr. Goodman emphasizing that, “there is still no evidence that these responses have long-term adverse cardiac consequences.”

To further understand the distinction between acute physiological change and lasting pathology, Dr. Goodman also investigated whether high-intensity exercise has clinically relevant, long-term effects on cardiac structure. Athlete’s heart (AH) refers to a set of morphological changes to the heart in athletes who engage in long-term intensive training, including enlargement of ventricular chambers, increased wall thickness, and lower resting pulse.⁵ Despite similarities to some forms of heart disease, AH is typically a normal adaptation and not pathological.⁵ 

To investigate whether long-term exercise-induced cardiac remodelling carries clinical consequences in middle-aged athletes, Dr. Goodman and colleagues performed a comprehensive study comparing long-standing (>10 years) endurance athletes who exercised for the recommended amount to a control group of recreational athletes with similar long-standing history.⁶ Both groups received a physical examination, underwent graded exercise testing and echocardiogram (ECG) assessment, along with cardiac imaging to assess cardiac structure and function. Endurance athletes showed cardiac remodelling, but there were substantial heterogeneity and variability within and between groups. Given past reports of exercise inducing ventricular fibrosis in athletes, cardiac MRI was used to determine if fibrosis was present in either group.⁷ Indeed, there was evidence of ventricular fibrosis in 25% of athletes, regardless of training history, but all had perfectly normal cardiac function. Their overarching findings were that cardiac adaptation to long-term exercise is not uniform across individuals, even those with similarly high training exposure, and that presence of focal fibrosis in some areas are unlikely to have clinical relevance but may simply be a ubiquitous physiological outcome of long-term exercise warranting further study. Endurance training promotes cardiac remodelling, but these changes are highly individualized. Whether these structural changes lead to adverse clinical outcomes remains unknown. 

Another avenue of research that attempts to bridge the effects of intensive exercise and adverse cardiac outcomes is atrial fibrillation (AF), the most common age-related cardiac arrhythmia that causes rapid abnormal contractions of the upper heart chambers.⁸ AF is associated with well-established risk factors such as hypertension and obesity. Surprisingly, it is also more prevalent among endurance athletes who lack traditional risk factors. Studies by Dr. Goodman and collaborators suggest that AF in athletes may be linked to elevations in proinflammatory markers (e.g., IL6 and TNFα), in addition to markers for extracellular matrix remodelling and atrial fibrosis.⁹ Studies suggest an exercise-dependent increase in some of these markers, but a direct cause-and-effect model between prolonged exercise, AF and cardiac pathology is yet to be uncovered. Dr. Goodman suggests that numerous factors are likely at play, and much more research is required to understand all of the potential mechanisms.

How can we make sense of exercise-related cardiac events and provide the public a sensible and reassuring message that vigorous exercise is healthy, yet also answer the fundamental question ‘how much is too much?’ Dr. Goodman says that “Far more people die at home in their chair from sudden cardiac death, than they do playing sports” adding that “there is irrefutable evidence that adhering to an active lifestyle that includes vigorous exercise is the single largest influencer in reducing all-cause mortality, cardiovascular disease and certain forms of cancer.” Sudden cardiac events in athletes are extremely rare and typically occur in individuals with known or occult cardiac conditions. Exercise may act as a trigger, but it is not the underlying cause. While there are certainly cardiac conditions where exercise must be used judiciously, the claim that exercise poses a risk because of incidents like Eriksen’s greatly misrepresents the overall risk-benefit profile of physical activity, overlooking its significant cardio-protective effects.

References

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