72-h Kinetics of High-Sensitive Troponin T and Inflammatory Markers after Marathon


Medicine & Science in Sports & Exercise:
doi: 10.1249/MSS.0b013e31821b12eb
Clinical Sciences

Introduction: Strenuous exercise induces significant increases in cardiac biomarkers. However, it is still unclear whether this is caused by cardiomyocyte necrosis or secondary mechanisms such as ischemia, cardiac energy deficiency, increased inflammation, or renal dysfunction.

Methods: Therefore, we investigated cardiac biomarkers (high-sensitive cardiac troponin T (hs-cTnT), N-terminal pro-brain natriuretic peptide (NT-proBNP), heart-type fatty acid-binding protein (h-FABP)), inflammation markers (high-sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), interleukin-10, tumor necrosis factor-α), and renal function (cystatin C) in 102 healthy men age 42 ± 9 yr before and 0, 24, and 72 h after a marathon.

Results: Kinetics of hs-cTnT revealed a peak immediately after the race (V3) that decreased rapidly to pretest values within 72 h (V5) (median (interquartile range) = 31.07 (19.25-46.86) ng·L−1 at V3 and 3.61 (3.20-6.70) ng·L−1 at V5, P < 0.001). NT-proBNP and h-FABP kinetics showed a similar pattern (NT-proBNP = 92.6 (56.9-149.7) ng·L−1 at V3 and 34.9 (21.7-54.5) ng·L−1 at V5; h-FABP = 44.99 (32.19-64.42) μg·L−1 at V3 and 7.66 (5.64-10.60) μg·L−1 at V5; always P < 0.001). Proinflammatory markers, such as IL-6 and hs-CRP, and renal dysfunction were significantly augmented immediately after the race (before the race compared with maximum after the race: IL-6 = 15.5-fold, hs-CRP = 28-fold, cystatin C = 1.22-fold, all P < 0.001). These increases were not related to the increase of hs-cTnT. Similarly, training history, finishing time, and exercise intensity were not associated with changes of hs-cTnT.

Conclusions: Cardiac biomarkers were increased immediately after a marathon race. Interestingly, values returned to normal levels within 72 h. These kinetics with a sharp peak indicate that cardiac necrosis during marathon running seems very unlikely but may be explained by altered myocyte metabolism.

Author Information

1Department of Prevention and Sports Medicine, Klinikum rechts der Isar, Technische Universitaet Muenchen, Munich, GERMANY; 2Institute for Laboratory Medicine, Deutsches Herzzentrum Muenchen der Technischen Universitaet Muenchen, Munich, GERMANY; 3Department for Medical Statistics and Epidemiology, Klinikum rechts der Isar, Technische Universitaet Muenchen, Munich, GERMANY; and 4Department of Cardiology, University Hospital, Essen, GERMANY

Address for correspondence: Johannes Scherr, M.D., Department of Prevention and Sports Medicine, Klinikum rechts der Isar, Technische Universitaet Muenchen, Connollystr. 32, D-80809 Munich, Germany; E-mail: scherr@sport.med.tum.de.

Submitted for publication November 2010.

Accepted for publication March 2011.

©2011The American College of Sports Medicine