Elevated heart muscle damage biomarkers have been reported in runners after completion of a marathon. Treponin has become the major biomarker used in the clinical assessment of a patient with acute chest pain and elevated levels have been reported in subjects immediately after completing a 26.2 mile marathon and other endurance athletic events.
Does the increase represent myocardial cell necrosis or could the increase be due to "leaky muscle membranes" also known as "cytosolic release". The authors of this recent article suggest the second mechanism may be responsible. I hope they are right as I have not given up running marathons just yet. See here for an abstract of that research.
A 2009 paper by Knebel et al investigated biomarkers and echocardiographic changes in 28 older marathon runners ( aged 60-72) and found no changes suggestive of systolic dysfunction but confirmed the finding previously reported of transient right ventricular diastolic dysfunction.These changes were no different from a group of younger marathoners. See here for abstract. So at least here the older runners were no worse off.
A 2002 paper by Shave,RE et al reported left ventricular systolic and diastolic dysfunction in 11 bikers after a 2 day mountain bike marathon.See here for abstract.
Twenty-seven athletes were studied with echocardiography after what was described as a ultra-endurance triathlon. In all, right ventricular dysfunction was demonstrated and while LV ejection fraction was normal and unchanged in most . However,in the 7 who demonstrated post exercise LV wall motion abnormalities there was a decrease in average LVEF from 57.8% to 45.9%. The authors described also that the "integrated systolic strain decreased from 16.9 to 15.1." I have no idea of the significance of that index nor if that degree of decrease mean anything.See here for abstract.
More elaborate cardiac echo testing was carried out on twenty 2003 Boston marathon finishers pre and post race and one month later. They used regular TTE (trans thoracic echo) but in addition used a technique called "spectal and tissue doppler (TD"). While systolic ejection fractions were unchanged, TD derived indices of LV and RV systolic function were said to be abnormal with at least some of the diastolic dysfunction indicators remaining abnormal one month later.See here for abstract.
Neilan and co workers published detailed results from extensive echo and biomarker studies on 60 finishers of the 2004 and 2005 Boston marathon. See here for full text. They reported elevations in cTnT and NT-ProBNP and similar echo findings to those reported in the previous article from the 2003 Boston marathoners.They noted more marked changes in biomarkers and echo changes in the group who trained less ( less than 35 miles per week in preparation for the race .) So maybe the better trained runners were less susceptible to whatever it is that long events bring about with heart function which is also suggested by the following reference.
A slightly optimistic note is sounded in this paper which describes echo findings of dysynchrony only in first time participants in a long distance event and not in more experienced distance runners and that a predictor of the echo changes was the type of ACE gene polymorphism.
More recently, a review also expressed an optimistic,reassuring note while a rebuttal letter to the editor offered the opposite view proposing the term " exercise induced right ventricular dysplasia" suggesting that the elevation in troponin post endurance events actually reflects tissue death and not just leakage. Both views lack the support on longitudinal follow up data. See here for the two letters.If troponin elevation does signal cell death would we see some type of clinically apparent cardiomyopathy in older endurance event participants after years of beating up their hearts or perhaps myocardial fibrosis noted on autopsy. I wonder if anyone has investigated cardiac function or reported autopsy data on the prolific running Tarahumara Indians.
At least so far there do not seem to be cases of what might represent endurance exercise induced cardiomyopathy.