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Background: Troponin I and T are biomarkers to diagnose myocardial infarction and damage. Studies indicate that strenuous physical activity can cause transient increases in these troponin levels, typically considered physiological. However, current data show differences in the exercise-induced increase in troponin I and T in elite athletes. Method: This prospective clinical study aimed to determine troponin I and T levels in 36 top cross-country skiers of the German national team (18 male, 18 female) after a standardized competition load over two days. All study participants underwent a comprehensive sports medical and cardiological evaluation, including ECG and echocardiography. A multivariable regression analysis was utilized to identify possible predictors of increased troponin I levels. Results: Only three male athletes (8.1%) showed an isolated increase in Troponin I (Ø 112.49 ng/L, cut off < 45.2 ng/L), while no increase in troponin T in the study population was detected. Conclusions: The analysis suggested several potential predictors for increased troponin I levels, such as height, weight, weekly training hours, and indications of an enlarged sports heart, though none achieved statistical significance. Knowing the different exercise-induced detectability of the various troponins in the clinical setting is essential. [ABSTRACT FROM AUTHOR]

Asthma is defined as a chronic inflammatory disorder of the airways with bronchial hyperresponsiveness and variable bronchoconstriction, and is one of the most common diseases in childhood and adolescence. Exercise-induced asthma-like symptoms and asthma are also frequently seen in highly trained athletes. Exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are found in 8%-10% of healthy school-aged children and in 35% of children with asthma. Highly increased ventilation, inhalation of cold, dry air and air pollutants (eg, chlorine) are thought to be important triggers for EIA and EIB. EIA is often experienced concurrently with vocal cord dysfunction, which needs to be considered during the differential diagnosis. The pharmacological treatment of EIA is similar to the treatment of asthma in nonexercising adolescents. The therapy is based on anti-inflammatory drugs (eg, inhaled glucocorticosteroids) and bronchodilators (eg, β2-agonists). The treatment of EIB is comparable to the treatment of EIA and leukotriene modifiers offer a new and promising treatment option, particularly in EIB. Generally, athletes may not use β2-agonists according to the prohibited list of the World Anti-Doping Agency (WADA). However, the WADA list contains specific β2-agonistic substances that are permitted to be used by inhalation. [ABSTRACT FROM AUTHOR]