By Michael H. Crawford, MD, Editor
Synopsis: In middle-aged competitive recreational athletes, increases in cardiac troponin levels with exercise competitions were not infrequent. In a subgroup, coronary artery calcium by computed tomography was found in almost two-thirds, but the prevalence and magnitude of calcium was not associated with the exercise troponin response.
Source: Janssen SLJE, van Everdingen WM, Saalmink WBJ, et al. Relationship between exercise-induced cardiac troponin elevations and occult coronary atherosclerosis in middle-aged athletes. J Am Coll Cardiol. 2025;85(24):2370-2382.
Elevated troponin levels have been observed in middle-aged athletes after strenuous exercise. Although generally considered benign because these athletes are healthy individuals without symptoms, these investigators from the Netherlands conducted the Improving the Interpretation of Troponin Concentrations Following Exercise and Their Clinical Significance (TREAT) study, which hypothesized that high levels of troponin post-exercise would indicate the presence of occult coronary artery atherosclerosis (or coronary artery disease [CAD]) compared to their peers with low post-exercise troponin levels.
Competitive athletes ≥ 40 but < 70 years of age who participated in walking (≥ 30 km), cycling (≥ 100 km), or running (≥ 15 km) events were recruited and had pre-event and immediate post-event high sensitivity troponin I and T levels measured. Ten percent of this group was selected for cardiac computed tomography (CCT) performed within three months of the event, which included coronary artery calcium (CAC) score, categorized as no/mild/moderate/severe/extensive (Coronary Artery Disease-Reporting and Data System [CAD-RADS] 1-5), coronary angiography, and measures of fractional flow reserve (FFR) if lesions with ≥ 25% to < 90% occlusion were found. Baseline and post-event troponin levels were rank ordered, and those selected for CCT were those with highest troponin levels (top 7%) and lowest troponin levels (lower 3%) in a 2:1 ratio. A total of 1,017 subjects (497 long-distance walkers, 122 cyclists, and 398 runners) were recruited between 2022 and 2023, and 994 completed the pre-event and post-event troponin level measurements (mean age 56 years, 63% men).
CCT was performed in 68 high troponin and 34 low troponin athletes. Cardiac troponin T (cTnT) increased from a baseline mean of 5.8 ng/L to 14.3 ng/L post-exercise (57% above the upper limit of normal [ULN]) and cardiac troponin I (cTnI) increased from 2.0 ng/L to 7.4 ng/L (16% above the ULN). CAC ranged from 0 to 5,503 Agatston units (AU), with a median of 7 AU. Coronary plaque was found in 62%, but only 11% were categorized as obstructive. Plaque type and distribution were the same in the high and low responders.
The prevalence and magnitude of the CAC score was not different between the high and low troponin responders (P = 0.24). However, CAD-RADS correlated with cTnT at rest (P = 0.003) and the change post-exercise (P = 0.042) but only correlated with the change in cTnI with exercise (P = 0.022).
In the 35 subjects with FFR performed, 12% of the high troponin responders and 6% of the low responders had an FFR ≤ 0.75 (adjusted odds ratio [OR], 1.03; 95% confidence interval [CI], 0.67-1.60).
The authors concluded that in middle-aged individuals competing in recreational aerobic athletic competitions, many experienced significant increases in troponin levels, with up to half exhibiting cTnT and 16% exhibiting cTnI levels above the ULN. However, the presence of CAC and the magnitude of CAC did not differ between the high- and low-troponin responders to exercise.
Commentary
Since cardiac troponin levels usually are not measured in middle-aged participants after exercise competitions, one might question the relevance of this study. However, not infrequently, such athletes experience symptoms, from gastrointestinal upset to syncope, after exercise and are referred for medical evaluations, which often include measuring troponin because such symptoms could be caused by myocardial injury or infarction. If the troponin comes back elevated, this may lead to a cardiac testing spiral that could end in an invasive coronary angiogram. Thus, the TREAT study is of interest and suggests that, in general, elevated troponin levels with exercise cannot be attributed to occult CAD.
Of course, this does not mean that it could not be. In fact, the CAD-RADS score was related to the change in troponin with exercise by both assays (cTnT and cTnI). It is reassuring that, although the presence of CAC was common, obstructive disease was infrequent in the TREAT subjects. However, 25% of the low-troponin response to exercise subjects had a CAC score > 100 and 10% had a CAD-RADS score ≥ 3 (obstructive disease). So, the nature of the symptoms, electrocardiogram (ECG) findings, echocardiography, and clinical judgment are required in individual cases.
There are limitations to the TREAT study. The population was homogeneous regarding race/ethnicity, since all the participants were described as being Dutch. The sample size for the CCT part of the study was small. Only the acute change in troponin with exercise was measured, with no further measurements to look at the time course of any elevations. High-sensitivity troponin assays are known for their low specificity, and there was a considerable difference between the results of the two assays used. These differences make interpreting the results somewhat challenging. Finally, ECGs were not done, and no imaging was done to see if there were wall motion abnormalities.
In summary, the TREAT study shows that the magnitude of exercise-induced troponin elevations in middle-aged competitive recreational athletes is not necessarily the result of occult CAD but is probably caused by other factors not elucidated in this study.
Michael H. Crawford, MD, is Professor Emeritus of Medicine and Consulting Cardiologist, UCSF Health, San Francisco.
