Responses of N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP) and Cardiac Troponin I (cTnI) to Competitive Endurance Exercise in Recreational Athletes
C. Vidotto1
, H. Tschan2
, J. Atamaniuk1
, R. Pokan2
, N. Bachl2
, M. M. Müller1
1Ludwig Boltzman Institute for Cardiothoracic Research at the Institute of Laboratory Diagnostics, Kaiser Franz Josef Hospital, Vienna, Austria
2Institute of Sports Science, Department of Sports and Exercise Physiology, University of Vienna, Austria
The present study was designed to investigate whether the stress of a half-marathon race can induce myocardial cell injury or left ventricular dysfunction in moderately trained runners of both gender, as assessed by post-race plasma concentrations of biochemical cardiac-specific markers and by quantitative echocardiographic measurements. We examined 12 male (mean ± SD); age: 42.8 ± 7.3 yr; height: 177.6 ± 7.4 cm; body mass: 75.6 ± 9.4 kg; BMI: 24.1 ± 1.8 and 13 female (mean ± SD); age: 39.0 ± 6.5 yr; height: 164.6 ± 6.2 cm; body mass: 58.4 ± 9.8 kg; BMI: 21.5 ± 3.4 recreational runners, who completed a half-marathon race. Blood samples were collected from each subject before the half-marathon race as well as 20 min and 2 h post-race and cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured. Quantitative echocardiographic analyses of wall dimensions and ejection fraction were also obtained from 14 of 25 subjects within 1 wk after the race. Both blood markers showed significant changes (p < 0.05 - 0.001) over the time course of the three blood draws. A significant percentage of laboratory analytes analyzed in this study were outside the reference ranges and fulfilled conventional criteria for cardiac muscle damage. However, echocardiography within one week following the competition did not show any evidence that running a half-marathon competition damages the myocardium. Strenuous endurance exercise in middle-aged recreational runners induces a significant elevation of biochemical cardiac-specific markers, which may reflect transient subclinical myocardial damage, but can also reflect a physiological reparative or adaptive process.
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