Abstract
It is well established that regular physical activity reduces cardiovascular disease risk; however, numerous studies have demonstrated postexercise elevations in cardiac troponin (cTn), indicative of cardiac injury in apparently healthy individuals. The prevalence of these findings in different exercise settings and population groups, as well as potential underlying mechanisms and clinical significance of exercise‐induced cTn release are not yet quite determined. The present review will discuss the cTn response to exercise in light of developing cTn assays and the correlation between postexercise cTn release and cardiac function. Additionally, recent data regarding the potential link between strenuous endurance exercise and its relationship with unfavorable cardiac effects in athletes, as well as the management of patients presenting at emergency care after sport events will be briefly reviewed.
Highlights
Studies carried out since 1987 using early experimental troponin (Tn) assays have shown that prolonged exercise may induce detectable increase in circulating troponins.[1]
The introduction of the high-sensitivity troponin assays, unsurpassed in sensitivity to detect low levels of myocardial damage[5] has allowed better characterization of exercise-induced cTn elevation. This has led to the Abbreviations: ACS, acute coronary syndrome; CAD, coronary artery disease; myocardial band isoform of creatine kinase (CK-MB), creatine kinase-myocardial band; cMRI, cardiovascular magnetic resonance; CTCA, computed tomography coronary angiography; cTn, cardiac troponin; cTnI, cardiac troponin I; cTnT, cardiac troponin T; LV, left ventricular; MI, myocardial infarction; RV, right ventricular; Tn, troponin
Exercise-induced cTn elevation is important to understand in the management of athletes presenting with chest pain at emergency care after sport events, since in many relevant studies cTn levels exceeded the 99 percentile of the method formally fulfilling the criteria for acute MI.[15]
Summary
Studies carried out since 1987 using early experimental troponin (Tn) assays have shown that prolonged exercise may induce detectable increase in circulating troponins.[1]. Observation that measurable changes in cTn are common, with extreme levels of exercise, such as marathon,[6] but even following normal physical activity,[7] or a treadmill test.[8] The origin of this biomarker release and whether it reflects a physiological or pathological process, remains a contentious issue.[9] The clinical implications are worthy of study for a number of reasons This issue may be of relevance to the controversy surrounding the long-term prognosis of athletes presenting with postexercise cTn elevations and the possible role of high level exercise as a cause of cardiac disease in some individuals.[10] the beneficial effect of moderate duration exercise on cardiovascular health in the general population is well recognized,[11] it has been postulated that participation in multiple extreme endurance events may lead to right ventricular (RV) dysfunction,[12] accelerate coronary atherosclerosis,[13] or even promote cardiac fibrosis.[14] Second, exercise-induced cTn elevation is important to understand in the management of athletes presenting with chest pain at emergency care after sport events, since in many relevant studies cTn levels exceeded the 99 percentile of the method formally fulfilling the criteria for acute MI.[15]. Clinical significance, and the management of patients with cTn elevation after exercise will be briefly discussed
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