Background: Physical exercise induces changes in cardiac biomarkers associated with cardiac injury and inflammation.Theability of these changes to identify subjects at risk of sport-related cardiac events islargely unknown. This project aimed to identify the physiological pattern and predictors of the exercise-induced cardiac troponin(cTn)and C-reactive protein (CRP) response to exercise.Apotential pathological responseto exercise was exploredin a subset of subjects. Methods: The exercise-induced increase in cTnand CRP were studied in two cohorts of presumably healthy recreational athletes; The North Sea Race Endurance Exercise Study (NEEDED) 2013 (n=97) and 2014 (n=1002). Bothstudies obtained databefore and within 24 hours after a 91-kilometrecycling competition ("The North Sea Race"). Coronary computed tomography angiography was used in a subset of subjectsto identify a possible association between exercise-induced cTn elevationand underlying coronary artery disease. Results: In Paper 1(n=97), we determined themagnitude andtime-dependent changes in cTnI following the North Sea Race. There was a continued increase in cTnI between immediately after the race and 3 hours following the race. This findingwas important for the design of the main study. Also, three of the four subjects with highest exercise-induced cTnI values had significant coronary artery pathology. In Paper 2 (n=1002), 84-92 % of subjects exceeded the 99th percentile of the cTn assay 3 hours post-race. At 24 hours post-race, 18-30 % still had cTn values above the 99th percentile.Lower race duration and higher systolic blood pressure were predictors of theexercise-inducedcTn increase. In Paper 3 (n=120), subjects were assessed by coronary computed tomography angiography (CCTA). Subjects with obstructive CAD (n=9) had significantly higher cTn levels at 24 hours after the race, but not at 3hours after the race. In paper 4 (n=97), the CRP response to exercise was determined. In this study, CRP continuedto increase until 24 hours following the race. Physical fitness was found to significantly attenuate the exercise-induced CRP response. There was no association between exercise-induced levels of CRP and cTnI. Conclusion: The present work identified the physiological pattern and predictors of exercise-inducedcTn and CRP. More than84 % of subjects had cTn levelsabove the 99thpercentile cut-off. This finding supports the hypothesis that exercise-induced cTn increase is a physiological response in most subjects. Lower race duration and higher systolic blood pressure were consistent predictors of the exercise-induced cTn response. In a subsetof subjects,aprolonged elevation of cTn was associated with occult obstructive CAD, suggesting a pathologicalpattern ofcTn increase in these subjects. Lastly,physical fitness was inversely associated with the exercise-inducedCRP response. No associationbetween exercise-induced cTn-and CRP increase wasidentified.
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