Thijs M H Eijsvogels1, Maurits D Hoogerwerf2, Martijn F H Maessen2, Joost P H Seeger3, Keith P George4, Maria T E Hopman2, Dick H J Thijssen3. 1. Department of Physiology, Radboud University Medical Centre, Nijmegen, The Netherlands; Henry Low Heart Center, Department of Cardiology, Hartford Hospital, Hartford, CT, USA. Electronic address: Thijs.Eijsvogels@Radboudumc.nl. 2. Department of Physiology, Radboud University Medical Centre, Nijmegen, The Netherlands. 3. Department of Physiology, Radboud University Medical Centre, Nijmegen, The Netherlands; Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom. 4. Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom.
Abstract
OBJECTIVES: Exercise leads to an increase in cardiac troponin I in healthy, asymptomatic athletes after a marathon. Previous studies revealed single factors to relate to post-race cardiac troponin I levels. Integrating these factors into our study, we aimed to identify independent predictors for the exercise-induced cardiac troponin I release. DESIGN: Observational study. METHODS: Ninety-two participants participated in a marathon at a self-selected speed. Demographic data, health status, physical activity levels and marathon experience were obtained. Before and immediately after the marathon fluid intake was recorded, body mass changes were measured to determine fluid balance and venous blood was drawn for analysis of high-sensitive cardiac troponin I. Exercise intensity was examined by recording heart rate. We included age, participation in previous marathons, exercise duration, exercise intensity and hydration status (relative weight change) in our model as potential determinants to predict post-exercise cardiac troponin I level. RESULTS: Cardiac troponin I increased significantly from 14±12 ng/L at baseline to 94±102 ng/L post-race, with 69% of the participants demonstrating cardiac troponin I levels above the clinical cut-off value (40 ng/L) for an acute myocardial infarction. Linear backward regression analysis identified younger age (β=-0.27) and longer exercise duration (β=0.23) as significant predictors of higher post-race cardiac troponin I levels (total r=0.31, p<0.05), but not participation in previous marathons, relative weight change and exercise intensity. CONCLUSIONS: We found that cardiac troponin I levels significantly increased in a large heterogeneous group of athletes after completing a marathon. The magnitude of this response could only be partially explained, with a lower age and longer exercise duration being related to higher post-race cardiac troponin I levels.
OBJECTIVES: Exercise leads to an increase in cardiac troponin I in healthy, asymptomatic athletes after a marathon. Previous studies revealed single factors to relate to post-race cardiac troponin I levels. Integrating these factors into our study, we aimed to identify independent predictors for the exercise-induced cardiac troponin I release. DESIGN: Observational study. METHODS: Ninety-two participants participated in a marathon at a self-selected speed. Demographic data, health status, physical activity levels and marathon experience were obtained. Before and immediately after the marathon fluid intake was recorded, body mass changes were measured to determine fluid balance and venous blood was drawn for analysis of high-sensitive cardiac troponin I. Exercise intensity was examined by recording heart rate. We included age, participation in previous marathons, exercise duration, exercise intensity and hydration status (relative weight change) in our model as potential determinants to predict post-exercise cardiac troponin I level. RESULTS: Cardiac troponin I increased significantly from 14±12 ng/L at baseline to 94±102 ng/L post-race, with 69% of the participants demonstrating cardiac troponin I levels above the clinical cut-off value (40 ng/L) for an acute myocardial infarction. Linear backward regression analysis identified younger age (β=-0.27) and longer exercise duration (β=0.23) as significant predictors of higher post-race cardiac troponin I levels (total r=0.31, p<0.05), but not participation in previous marathons, relative weight change and exercise intensity. CONCLUSIONS: We found that cardiac troponin I levels significantly increased in a large heterogeneous group of athletes after completing a marathon. The magnitude of this response could only be partially explained, with a lower age and longer exercise duration being related to higher post-race cardiac troponin I levels.
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