Exercise is widely recognised as beneficial for cardiovascular health, yet it also places stress on the heart. During physical exertion, the heart releases troponin, a protein typically associated with cardiac injury. While elevated troponin levels are a key marker for heart attacks, new research from Radboudumc involving over 1,000 athletes suggests that post-exercise spikes in troponin are not caused by coronary atherosclerosis.
This apparent paradox—exercise both strengthening and stressing the heart—has long intrigued researchers. When someone experiences a heart attack, troponin levels rise significantly, signalling cardiac damage. However, similar elevations occur after prolonged or intense physical activity, raising questions about their clinical significance.
Previous studies, including one conducted during the Nijmegen Four Days Marches, found that participants with higher post-exercise troponin levels were more likely to experience adverse cardiovascular events, such as heart attacks, strokes, or premature death, in the years that followed.
In the new study, Radboudumc researchers examined over a thousand endurance athletes—cyclists, walkers, and runners—to investigate whether those with the highest post-exercise troponin levels also had more coronary artery disease. They measured troponin levels before and after a sporting event and used CT scans to examine the coronary arteries of athletes with the highest and lowest levels.
The results were surprising: there was no difference in the prevalence of coronary artery disease between the two groups. This finding clearly shows that coronary atherosclerosis is not responsible for elevated post-exercise troponin levels.
With coronary disease ruled out, researchers are now turning their focus to the heart muscle itself. It is already known that intense exertion can cause subtle injury to the heart muscle. One possibility is that this strain causes temporary leakage of troponin from heart cells into the bloodstream.
Previous studies have shown that heart muscle cells in endurance athletes, such as marathon runners, can become permeable during extreme exertion. In individuals with early-stage heart conditions, this leakage might be more pronounced, leading to higher troponin readings.
To better understand this phenomenon, the research team will continue to monitor the study’s participants over time. Their goal is to uncover the precise mechanism behind exercise-induced troponin release and to determine whether it signals hidden heart vulnerability. Ultimately, the findings may lead to earlier detection and improved prevention of heart disease in active individuals.
Source: Radboud University Medical Center
Image Credit: iStock
References:
Janssen SLJE, van Everdingen WM, Saalmink WBJ et al. (2025) Relationship Between Exercise-Induced Cardiac Troponin Elevations and Occult Coronary Atherosclerosis in Middle-Aged Athletes. Journal of the American College of Cardiology. 85 (24) 2370–2382.
