Ultra-endurance exercise provokes RV dysfunction
MedWire News: Intense exercise induces transient and reversible dysfunction of the right ventricle (RV) but not the left ventricle (LV), study findings indicate.
The findings raise the possibility that people who regularly engage in endurance exercise could be at risk for developing arrhythmogenic RV cardiomyopathy, say André La Gerche (University of Melbourne, Fitzroy, Australia) and fellow researchers.
Their study involved 40 athletes planning to compete in one of four events - a marathon, an endurance triathlon, an alpine cycling race, and an ultra-triathlon. The events lasted between 3 and 11 hours, and athletes were assessed before the race, immediately upon completion (post-race), and 1 week later.
Results reported in the European Heart Journal show that all measures of systolic RV volume increased and all RV functional measures decreased immediately post-race compared with baseline.
Specifically, RV ejection fraction (EF) fell from 51.0% to 46.4%, RV fractional area change fell from 51.5% to 44.3%, tricuspid annular plane systolic excursions fell from 24.9 mm to 24.0 mm, RV peak global strain rose from -27.2% to -23.7%, and RV peak systolic strain rate rose from -1.42 s-1 to -1.26 s-1.
By 1 week post-race, all RV measures had normalized, with the exception of RV peak systolic strain rate, which remained significantly elevated versus baseline.
By contrast, no measure of LV function or volume changed following endurance exercise, either immediately or 1 week later.
Biochemistry results showed that levels of B-type natriuretic peptide and cardiac troponin I - indicators for myocardial necrosis - rose significantly post-race and correlated with reductions in RVEF but not with LVEF.
Interestingly, race duration showed a significant interaction with changes in several measures of RV function (ejection fraction, fractional area change, and peak systolic strain rate). For each of these measures, the greatest reduction in post-race values occurred in athletes who competed in the ultra-triathlon, the longest event lasting on average 10 hours 52 minutes.
Finally, focal delayed gadolinium enhancement (DGE) and increased RV remodeling - indicative of cardiac fibrosis - were seen in five athletes (13%). In each case this was confined to the interventricular septum, frequently at the site of the RV attachment.
Athletes with DGE had been competing in endurance sports for longer and had greater fitness levels than those without DGE, note the researchers. They also had significantly greater RV end-diastolic and end-systolic volumes and significantly lower RVEFs than DGE-free athletes.
Taken together, these results suggest that repetitive ultra-endurance exercise may lead to extensive RV changes and possible myocardial fibrosis, write La Gerche et al.
They conclude: "This adds further weight to the proposition that RV abnormalities may be acquired through cumulative bouts of intense exercise and provides direction for prospective investigations aimed at elucidating whether extreme exercise may promote arrhythmias in some athletes."
In an accompanying editorial, Sanjay Sharma and Abbas Zaidi, both from St George's University of London, UK, say the study raises "burgeoning speculations that regular participation in intensive endurance exercise may induce arrhythmogenic substrates in some athletes.
"The long-term conclusions of the authors may appear preposterous to some, but could prove to be the retrospective 'elephant in the room,' " they write.
By Joanna Lyford