Myocardial fatigue in recreational marathon runners: A speckle-tracking echocardiography study

Abstract

BackgroundProlonged aerobic exercise such as marathon running produces supraphysiological hemodynamic stress that can potentially affect the athlete's cardiac homeostasis. While cardiac structural and functional adaptations in professional athletes are well characterized, only a limited information is available for recreational runners undergoing this supraphysiological stress. MethodsPremarathon and post-marathon echocardiography was performed in 50 recreational marathon runners [age 40.8 ± 7.5 years, 44 (88%) males; running distance 42.195 km]. All the runners received 4-month training for the marathon. The baseline echocardiogram and N-terminal B-type natriuretic peptide (NT-proBNP) were obtained before training, whereas the post-marathon study was performed within 10 days (7.27 ± 0.92 days) of completion of marathon. Two-dimensional speckle-tracking echocardiography was used for characterizing the changes in myocardial mechanics. ResultsThere was a significant reduction in heart rate post-marathon, whereas the levels of NT-proBNP increased significantly (86.0 ± 9.5 pg/ml vs 106.5 ± 24.2 pg/ml, p = 0.001). The left ventricular (LV) end-diastolic volume (61.8 ± 16.5 ml vs 72.8 ± 5.1 ml, p < 0.001), LV mass (120.2 ± 30.0 gm vs 160.3 ± 43.0 gm, p < 0.001), and LV ejection fraction (64.9 ± 5.6% vs 72.0 ± 5.7%, p < 0.001) also increased significantly. However, there was a significant attenuation in LV global longitudinal (−19.3 ± 2.71% vs −16.5 ± 4.6%, p = 0.003) and circumferential strain (−17.2 ± 2.41% vs −15.2 ± 2.6%, p = 0.001) post-marathon. The LV global radial strain showed a nonsignificant reduction. ConclusionRecreational marathon runners have reduced longitudinal and circumferential shortening of the left ventricle with elevation of NT-proBNP. However, the LV ejection performance remains maintained because of an increase in the LV end-diastolic volume and mass. These changes suggest the possibility of “myocardial fatigue” occurring in response to supraphysiological hemodynamic stress of marathon running.