The Effects Of Prolonged Endurance Exercise On Markers Of Myocardial Damage

Abstract

Exercise induced cardiac fatigue can be identified by a multitude of symptoms including transitory elevation of cardiac markers indicative of myocardial damage that have been recorded following prolonged endurance exercise (PEE). To date, the study of exercise-induced cardiac fatigue has focused primarily on elite athletes during long duration events such as marathons and Ironman triathlons. PURPOSE The present study was designed to examine cardiac function during three consecutive bouts of PEE in healthy, non-competitive males for the determination of cardiac myocyte damage indicative of cardiac fatigue. METHODS Nine fit college-age males (VO2 max 50.7 ± 3.8 ml/kg/min) performed exhaustive cardiovascular exercise on three successive days. The exercise protocol consisted of a 3-stage treadmill run (Stage 1: 10% above ventilatory threshold; Stage 2: a 5% reduction in work rate; Stage 3: an additional 5% reduction in work rate performed until volitional exhaustion). Fasting venous blood samples were taken immediately before (resting) and after each exercise bout. Creatine kinase (CK), creatine kinase-MB (CK-MB), and cardiac troponin-T (cTnT) were analyzed and adjusted for shifts in plasma volume. Data were analyzed using repeated measures ANOVA with a Tukey post hoc test. RESULTS The individual times for exercise bouts 1, 2, and 3 were 70.6 ± 31.4, 70.0 ± 25.4, and 63.90 ± 24.0 minutes, respectively. The average exercise intensity was 81.9 ± 4.4% of estimated VO2 max. Although significant CK increases of 208% (73.9 ± 77.5 U/L, pre-bout1; 227.7 ± 135.5 U/L, post-bout3) were found, evaluation of cardiac markers (CK-MB, cTnT) revealed no signs of cardiac fatigue. CK-MB activity values increased but were within the normal reference range (0–24 U/L). In addition, no elevation in cTnT was detected. CONCLUSIONS Data from the present study suggests that PEE does not induce myocardial damage in healthy, fit male subjects. Considering alternate protocols that have caused cardiac fatigue, the exercise intensity in the present study may have inhibited a duration sufficient to induce a similar response.