Cardiac Damage in Recreational London Marathon Runners

Abstract

2285 PURPOSE: Recent studies have demonstrated sub-myocardial infarction elevations in cardiac troponin T and evidence of reduced cardiac function following prolonged exercise in a limited number of highly trained athletes. Limited work has been completed examining the impact of prolonged exercise on cardiac damage and function in less trained recreational athletes. METHODS: Thirty-nine recreational runners (mean ± SD; age 36 ± 10 years) in the 2003 London marathon volunteered to take part in the study. Venous blood samples and echocardiographs were taken the day prior to the race, and immediately following race completion. Echocardiographic indices of left ventricular (LV) contractility (systolc blood pressure/end systolic volume ratio [sBP:ESV]) and filling (early to late ventricular filling ratio [E:A]) were calculated. Blood samples were analyzed for cardiac troponin T (cTnT) utilizing the 3rd generation rd cTnT immunoassay. Differences between baseline and post race variables were assessed using students T-tests. The relationship between positive cTnT values, age, completion time, left ventricular contractility and filling were statistically analyzed using Pearson product moment correlation. Alpha was set at 0.05. RESULTS: All subjects completed the marathon (mean ± SD; 234 ± 45 minutes). LV contractility was not significantly different following completion of the marathon whilst E:A was significantly depressed (1.7 ± 0.5 vs. 1.1 ± 0.3) P<0.05. Cardiac troponin T was significantly elevated immediately post exercise P<0.05 (0.1 ± 0.16μg/L vs. <0.01μg/L). No significant correlation was observed between elevated cTnT and either completion time (r = 0.06), age (r = 0.24), sBP:ESV (r = 0.27) or E:A (r = 0.08). Thirty-two subjects presented elevated cTnT following completion of the marathon (range 0.012- 0.733 μg/L), of these subjects eight presented values above the 0.1μg/L cut off limit for acute myocardial infarction (AMI). CONCLUSIONS: Cardiac troponin T release following prolonged exercise may be more widespread than previously suggested; further some individuals may present cTnT values indicative of AMI following such exercise. Exercise induced cardiac damage is not associated with changes in cardiac function following prolonged exercise. The mechanisms and long-term ramifications of such cardiac troponin release and decreased diastolic filling subsequent to prolonged exercise are yet to be elucidated.