Cardiac troponins T and I, due to their cardiospecificity, are the basic laboratory test for the detection of cardiomyocyte necrosis. In addition to daily use in the diagnosis of acute myocardial infarction, elevated cardiac troponin values have been observed in other cardiac and noncardiac conditions (myocarditis, pulmonary embolism, hypothyroidism, cytostatic cardiotoxicity) and even in a healthy population. The impact of physical activity on troponin increase in healthy individuals was lately intensively investigated. Many studies and meta-analyzes have been conducted with the intention to detect the underlying mechanism of cardiac troponin increase after physical activity and whether troponin increase after physical activity is a physiological or pathological phenomenon. There is growing evidence that troponin rise after physical activity is not due to irreversible necrosis, and a "physiological" leakage through the transient permeable cell membrane is increasingly mentioned as a underlying mechanism. The dynamics of increase and decrease of troponin after physical activity does not correspond to the dynamic observed after acute coronary syndrome and the absolute values are several thousand times lower. The intensity of physical activity is currently the most consistent predictor of absolute and relative increase in troponin after physical activity. Also, heart rate and basal troponin value are likely to have at least a partial impact. Professional athletes have higher deviations of troponin than recreational athletes but this observation is more likely a consequence of more intense activity required by professional sports and not the result of longer and more frequent physical activity. From a clinical point of view, it is important to recognize this phenomenon, as it can easily lead to misdiagnosis into everyday clinical practice. Larger and longer studies are needed to clarify and confirm the benign nature of this phenomenon and to investigate the possible long-term impact on cardiovascular health.