Exercising is healthy, but it also puts strain on the heart. During physical exertion, the protein troponin is released—a biomarker indicative of cardiac damage. New research from Radboudumc involving a thousand athletes shows that elevated troponin levels after exercise are not due to coronary atherosclerosis. This suggests that the cause of elevated troponin levels after exertion lies elsewhere.

The findings have been published in the Journal of the American College of Cardiology.

It’s a paradox: regular exercise is healthy and reduces the risk of cardiovascular disease, yet it also places significant stress on the heart. During both physical exertion and cardiac damage, signaling substances are released, including the protein troponin. That’s why troponin levels in the blood are checked when a heart attack is suspected.

Troponin levels in the blood also increase during intense physical activity. However, the amount of troponin released after exercise varies from person to person.

Radboudumc previously conducted research among participants of the Nijmegen Four Days Marches. It showed that long-distance walkers with high troponin levels following the exercise bout were more likely to suffer a heart attack, stroke, or premature death in the following years than those with low troponin levels.

A thousand athletes

In a new study, researchers aimed to determine the cause of elevated troponin levels in athletes. They examined a group of over a thousand cyclists, walkers, and runners to see whether participants with very high troponin levels were more likely to have coronary atherosclerosis.

First author Sylvan Janssen explains, “We measured the troponin levels of all athletes, both before and after the sporting event. We then compared the heart health of athletes with the highest levels to those with the lowest levels. In both groups, we used CT scans to visualize the coronary arteries.”

There turned out to be no difference between the two groups: the group with the highest troponin levels had just as many coronary artery issues as the group with the lowest levels. “A striking result,” says lead researcher Thijs Eijsvogels. “Coronary atherosclerosis does not lead to elevated troponin levels in the blood.”

With completion of this large-scale investigation, the TREAT study, one hypothesis for high troponin levels after exercise, has been ruled out. “At least now we know what doesn’t cause the elevated troponin levels,” says Eijsvogels.

Now that the blood vessels are no longer considered the cause, Eijsvogels wants to look at the heart muscle itself. “Intense exertion causes damage to the heart muscle—that’s known. So maybe that’s where we should look for the cause.”

Previous research showed that heart muscle cells in marathon runners can leak, allowing small molecules such as troponins to escape into the bloodstream.

Athletes with early-stage heart disease may be less able to cope with the strain of intense exercise, resulting in more leakage and thus higher troponin levels in the blood. The thousand participants in the study will continue to be monitored for years to better understand the link between elevated troponin levels after exercise and the risk of heart problems, and to enable early detection.