Impact of different endurance races on the heart: the point of view of the biologist

Abstract

peer reviewedObjective The aim of this study was to investigate the impact of intense exercise, represented by different endurance races, in relationship with oxidative stress and cardiac markers. In a second time, we tried to demonstrate if oxidative stress induced by physical activity is a physiological or pathological process, and to establish some issues to diagnose the risk of sudden death in athletes. Methods Four populations were compared, a control group of 16 participants “sedentary” (37 ± 4,39 years old), a group of 24 semi-marathon runners (41 years ± 8,76 years old), a group of 28 marathon runners (44,1 ± 8,37 years old) and a group of 33 ultra-trail runners (45,8 ± 8,7 years old). Three blood tests were drowned, one just before, one just after, and the last three hours after the end of the race.Different oxidative and stress and cardiac biomarkers were measured. The ultra-trail runners will be subject to an echocardiography and an ECG pre- and post-race. For statistical analysis, STATISTICA 10 software was used. We performed a non-parametric test of Kruskal-Wallis for independent sample and a Friedman ANOVA for paired samples. Results Myeloperoxydase increased during exercise, but the release is less important according to the level of training of the runners. GSH/GSSG ratio seems to remain stable during the race but it could increase during the 24 hours post-race. There is a decrease in lipidic peroxidation during exercise. But, we note an increase of creatine kinase, isoform MB, myoglobin and C-reactive protein during the race. We observe an increase of troponin T and natriuretic peptide but with a different kinetic than the kinetic obtained for a myocardial infarction. Medical imaging in ultra-trail runners present cardiac adaptations to endurance training, as left ventricular hypertrophy (LVH) and incomplete right bundle branch block (IRBBB). A decrease of systolic and diastolic volumes of the left ventricle and a decrease of longitudinal strain were observed by echocardiography at the end of the race. Conclusion Endurance races induce the income of oxidative stress objectified by different biomarkers increase, but a cell necrosis is not specially observed. In fact, the increase of the cardiac markers during endurance races but may be explained by a transient modification of myocyte permeability, with a release of pool cytosolic. These races may induce micro-muscle damages causing the appearance of an inflammatory process explaining our observations of markers of inflammation. For the medical imaging, it was observed a myocardial adaptation to training and a transient impairment of ventricular function due to dehydration