Biochemical and functional abnormalities of left and right ventricular function after ultra-endurance exercise
- 1Department of Cardiology, St Vincent’s Hospital, Melbourne, Australia
- 2Department of Medicine, University of Melbourne, Melbourne, Australia
- Dr A La Gerche, Cardiac Investigation Unit, St Vincent’s Hospital, PO Box 2900, Fitzroy 3065, Victoria, Australia;
- Accepted 19 December 2006
- Published Online First 4 May 2007
Background: There is evidence that ultra-endurance exercise causes myocardial injury. The extent and duration of these changes remains unresolved. Recent reports have speculated that structural adaptations to exercise, particularly of the right ventricle, may predispose to tachyarrhythmias and sudden cardiac death.
Objective: To quantify the extent and duration of post-exercise cardiac injury with particular attention to right ventricular (RV) dysfunction.
Methods: 27 athletes (20 male, 7 female) were tested 1 week before, immediately after and 1 week after an ultra-endurance triathlon. Tests included cardiac troponin I (cTnI), B-type natriuretic peptide (BNP) and comprehensive echocardiographic assessment.
Results: 26 athletes completed the race and testing procedures. Post-race, cTnI was raised in 15 athletes (58%) and the mean value for the entire cohort increased (0.17 vs 0.49 μg/l, p<0.01). BNP rose in every athlete and the mean increased significantly (12.2 vs 42.5 ng/l, p<0.001). Left ventricular ejection fraction (LVEF) was unchanged (60.4% vs 57.5%, p = 0.09), but integrated systolic strain decreased (16.9% vs 15.1%, p<0.01). New regional wall motion abnormalities developed in seven athletes (27%) and LVEF was reduced in this subgroup (57.8% vs 45.9%, p<0.001). RV function was reduced in the entire cohort with decreases in fractional area change (0.47 vs 0.39, p<0.01) and tricuspid annular plane systolic excursion (21.8 vs 19.1 mm, p<0.01). At follow-up, all variables returned to baseline except in one athlete where RV dysfunction persisted.
Conclusion: Myocardial damage occurs during intense ultra-endurance exercise and, in particular, there is a significant reduction in RV function. Almost all abnormalities resolve within 1 week.
Competing interests: None.
Funding: This project was primarily funded by the St Vincent’s Hospital Research and Grants Unit (protocol No HREC 004/04). KAC is funded by a National Heart Foundation Australia postgraduate research scholarship. GE Australia assisted in providing transport costs for the echocardiographic equipment.
Ethics approval: Approved by the St Vincent’s Hospital Human Research and Ethics Committee.