Responses of N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP) and Cardiac Troponin I (cTnI) to Competitive Endurance Exercise in Recreational Athletes

Abstract

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.

Serum levels of ischemia-modified albumin in healthy volunteers after exercise-induced calf-muscle ischemia

“…Measurement of NT-proBNP before and immediately after strenuous exercise can help to distinguish individuals with and without myocardial ischemia with a high degree of accuracy (18). Previous studies have shown that NT-proBNP levels may also increase significantly in healthy male athletes after strenuous exercise as a response to ventricular volume expansion (19)(20)(21). However, owing to the moderate workload applied in our study, no significant increases in this marker were observed.…”

The Effect of Prolonged Physical Activity Performed during Extreme Caloric Deprivation on Cardiac Function

“…Several recent reports have demonstrated myocardial dysfunction after endurance physical activity [2], [3], [5], [7], [8], [21], [22], [23], [24]. Most of these studies demonstrated transient cardiac dysfunction manifested as left ventricular systolic and diastolic abnormalities as well as right ventricular dysfunction.…”

“…Several studies have demonstrated transient left and right ventricular systolic and diastolic dysfunction [1], [2], pulmonary hypertension, and abnormally elevated levels of cardiac biomarkers such as brain natriuretic peptide (BNP) and troponin following endurance exercise [3], [4], [5], [6], [7], [8]. There was a positive correlation between the intensity of the endurance activity and the level of cardiac abnormalities developed.…”

Changes of Cardiac Biomarkers after High-intensity Exercise in Male and Female Elite Athletes of Dragon Boating

“…These parameters are assumed to indicate cardiac injury or dysfunction [5,18] since troponin T and troponin I are highly specific markers of myocardial cell damage, even in the presence of simultaneous skeletal muscle damage [16]. Furthermore significant cardiac stress leads to an elevation of these biomarkers even in absence of obstructive coronary disease [1].…”

“… Prolonged strenuous exercise leads to an elevation of cardiac specific biomarkers such as troponin T (TnT), troponin I (TnI), MB-creatine kinase (CKMB) and N-terminal pro brain natriuretic peptide (NT-pro BNP) in apparently healthy endurance athletes [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. These parameters are assumed to indicate cardiac injury or dysfunction [5,18] since troponin T and troponin I are highly specific markers of myocardial cell damage, even in the presence of simultaneous skeletal muscle damage [16].…”