Canadian Journal of Cardiology

Transient Myocardial Tissue and Function Changes During a Marathon in Less Fit Marathon Runners

Published:August 01, 2013DOI:



      Although regular physical activity improves health, strenuous exercise might transiently increase cardiac risk. Training and fitness might provide protection.


      We prospectively studied 20 recreational marathon runners without known cardiovascular disease or symptoms: at peak training before, immediately after, and 3 months after a 42.2-km marathon. Changes in global/segmental myocardial function, edema, resting perfusion, and fibrosis were measured.


      At peak training, runners exercised 8.1 ± 2.3 hours and 62 ± 18 km per week with mean maximal oxygen consumption (VO2max) of 53.2 ± 8.3 mL/kg/min. In response to the marathon, global left ventricular and right ventricular ejection fraction decreased in half of the runners; these runners had poorer peak training distance, training time, and fitness level. Change in global left ventricular ejection fraction was associated with VO2max. Overall, 36% of segments developed edema, 53% decreased function, and 59% decreased perfusion. Significant agreement was observed between segment decreasing function, decreasing perfusion, and developing edema. Myocardial changes were reversible at 3 months.


      Completing a marathon leads to localized myocardial edema, diminished perfusion, and decreased function occurring more extensively in less trained and fit runners. Although reversible, these changes might contribute to the transient increase in cardiac risk reported during sustained vigorous exercise.



      Bien que l’activité physique régulière améliore la santé, l’exercice intense pourrait augmenter de façon passagère le risque de maladies du cœur. L’entraînement et la bonne forme physique pourraient apporter une protection contre ce risque.


      Nous avons étudié de façon prospective les coureurs récréatifs de marathon n’ayant pas de maladies ou de symptômes cardiovasculaires connus : au sommet de leur entraînement, avant, immédiatement après et 3 mois après un marathon de 42,2 km. Les changements dans le fonctionnement myocardique global et segmentaire, l’œdème, la perfusion au repos et la fibrose ont été mesurés.


      Au sommet de leur entraînement, les coureurs ont accompli 8,1 ± 2,3 heures et 62 ± 18 km par semaine selon une consommation d'oxygène maximal (VO2 max) moyenne de 53,2 ± 8,3ml/kg/min. En réponse au marathon, la fraction d’éjection globale du ventricule gauche et du ventricule droit a diminué chez la moitié des coureurs; ces coureurs ont obtenu au sommet de leur entraînement une distance, une durée et un niveau de forme physique médiocres. La modification de la fraction d’éjection globale du ventricule gauche a été associée à la VO2 max. Dans l’ensemble, 36 % des segments ont développé un œdème, 53 % ont diminué le fonctionnement et 59 % ont diminué la perfusion. Une concordance significative a été observée entre le segment diminuant le fonctionnement, le segment diminuant la perfusion et le segment développant l’œdème. Les modifications du myocarde ont été réversibles à 3 mois.


      La réalisation d’un marathon mène à un œdème localisé du myocarde, à une perfusion réduite et à un fonctionnement diminué apparaissant davantage chez les coureurs moins entraînés et moins en forme. Bien que ces modifications soient réversibles, ils pourraient contribuer à l’augmentation passagère du risque de problèmes cardiaques signalés durant l’exercice intense soutenu.
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