8/12/2023 0 Comments Cardiovascular endurance sports![]() ![]() 13 Evidence also exists for the development of autoimmunity mechanisms against circulating cardiac proteins, triggering cardiomyopathy and arrhythmia in mice and potentially also humans. 11,12 Such fibrotic patches may be a plausible substrate for arrhythmias. 10 Furthermore, focal late gadolinium enhancement in cardiac magnetic resonance imaging was detected in the interventricular septum at the site of RV insertion in endurance athletes. 9 An increase of transforming growth factor-β1 expression, which can promote fibrosis, could for instance be observed in the atria and right ventricle (RV) of animal exercise models. 3 Repetitive cardiac micro-injuries due to endurance sports such as triathlons and marathons indicated by troponin release may play a role in developing cardiac maladaptation. Some studies reported an increased incidence of atrial fibrillation or arrhythmogenic right ventricular cardiomyopathy among endurance athletes. Whether the observed changes have pathological meaning remains an unanswered question. On the contrary, troponin elevation in myocardial infarction is due to cardiomyocyte necrosis and release of myofilament-bound troponin. Prolonged exercise can increase cardiomyocyte membrane permeability and secretion of cytoplasmic-free cardiac troponin. 7,8įigure 1: This shows the schematics of the troponin release after myocardial infarction versus endurance exercises. 6 Altogether, the evidence favours the "increase of membrane permeability" hypothesis as the cause in the majority of cases of cardiac troponin elevation after exercise. 3,5 On the other hand, the typically fast clearance (monophasic pattern) and kinetics do not resemble that observed in myocardial infarction (biphasic pattern). It also could represent genuine but subclinical cardiomyocyte apoptosis or necrosis. Several hypotheses have been proposed, such as transmembrane leakage of cytoplasmic-free cTnT and cardiac troponin I (cTnI) or decrease of troponin clearance from the plasma, both potentially caused by overload with free radicals, myocardial stretch, increased core temperature, or alteration of pH (Figure 1). ![]() The pathomechanism behind this increase is presently not well understood. In a recent meta-analysis, 3 we showed that high-sensitivity cardiac troponin T (cTnT) is elevated above the 99th percentile in approximately 83% of individuals after prolonged and intensive exercises. Several studies have shown significant cardiac troponin increases after different types of exercise. Increase of Cardiac Biomarkers After Strenuous Exercises 3 Keeping in mind that 25 out of 1,000 marathon runners seek medical attention after their races, 4 this issue is of clinical relevance when it comes to the interpretation of cardiac biomarkers in the context of an athlete presenting in your emergency unit. 2 Several studies have even demonstrated acute elevations of cardiac troponin after strenuous yet still physiological exercise. Although the current generation of high-sensitivity troponin assays is unmatched in its sensitivity to detect myocardial damage, elevations can occur in other acute or chronic cardiovascular disorders such as heart failure, pulmonary embolism, arrhythmias, or renal failure. 1 Cardiac troponins have become a key component of the universal definition of myocardial infarction and are indispensable for its early detection. Accurate diagnosis and risk stratification are pivotal because immediate therapeutic management of patients is associated with significant improvement of their prognosis. Acute coronary syndromes (ACS) are life-threatening cardiovascular emergencies.
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