The Impact Of Training Status On Cardiac Biomarkers: The Role Of Ace Gene I/d Polymorphism

PURPOSE: This study aimed to investigate the effects of exercise mode on cardiac damage in young men and to test the contribution of training status and Angiotensin-Converting Enzyme insertion/deletion (ACE-I/D) polymorphism to exercise-associated cardiac damage. METHODS: We measured circulating levels of cardiac Troponin I (cTnI) and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) in 29 trained and 27 untrained soccer players before and after moderate-intensity continuous exercise (MICE) and high-intensity interval exercise (HIIE) running tests. ACE-I/D polymorphism was evaluated from circulating leukocyte-derived DNA. RESULTS: Compared to untrained, trained soccer players had higher cTnI levels - independently of exercise mode (pre-exercise: 0.014 ± 0.007 vs. 0.010 ± 0.005 ng/mL; post HIIE: 0.031 ± 0.008 vs. 0.0179 ± 0.007 ng/mL and post MICE: 0.030 ± 0.007 vs. 0.018 ± 0.007 ng/mL in trained vs. untrained, respectively). No group differences were found in the NT-proBNP response to exercise. No within training-status group differences were found in cTnI levels across the three ACE-I/D polymorphism categories for trained (DD: 0.015 ± 0.008 ng/mL; ID: 0.015 ± 0.007 ng/mL; II: 0.014 ± 0.008 ng/mL) and their untrained counterparts (DD: 0.010 ± 0.004 ng/mL; ID: 0.011 ± 0.004 ng/mL; II: 0.010 ± 0.006 ng/mL). CONCLUSION: Training status but not exercise mode nor ACE-I/D polymorphism affected circulating markers of cardiac damage in young healthy men. Additionally, ACE genotype did not impacted biomarkers of cardiac damage in response to HIIE and MICE, suggesting that the ACE gene does not play a significant role in exercise-induced cardiac damage in young healthy men.