72-h kinetics of high-sensitive troponin T and inflammatory markers after marathon
Johannes Scherr1, Siegmund Braun, Tibor Schuster
1Department of Prevention and Sports Medicine, Klinikum rechts der Isar, Technische Universitaet Muenchen, Munich, Germany. scherr@sport.med.tum.de
Insights
Marathon running temporarily increases cardiac biomarkers like high-sensitive cardiac troponin T (hs-cTnT). These levels normalize within 72 hours, suggesting altered myocyte metabolism rather than cardiomyocyte necrosis.
Area of Science:
- Exercise Physiology
- Cardiovascular Research
- Biomarker Analysis
Background:
- Strenuous exercise, such as marathon running, elevates cardiac biomarkers.
- The underlying cause of this elevation (e.g., cardiomyocyte necrosis vs. secondary mechanisms) remains unclear.
Purpose of the Study:
- To investigate the kinetics of cardiac biomarkers, inflammation markers, and renal function following a marathon.
- To determine if marathon-induced cardiac biomarker increases are indicative of cardiomyocyte necrosis.
Main Methods:
- Measured high-sensitive cardiac troponin T (hs-cTnT), NT-proBNP, h-FABP, hs-CRP, IL-6, and cystatin C in 102 men before and after a marathon.
- Assessed biomarker levels at 0, 24, and 72 hours post-race.
Main Results:
- Cardiac biomarkers (hs-cTnT, NT-proBNP, h-FABP) peaked immediately post-marathon and returned to baseline within 72 hours.
- Proinflammatory markers (IL-6, hs-CRP) and renal dysfunction (cystatin C) also increased post-race but were not correlated with hs-cTnT elevation.
- Exercise intensity and training history did not correlate with hs-cTnT changes.
Conclusions:
- The rapid normalization of cardiac biomarkers after marathon running suggests that cardiomyocyte necrosis is unlikely.
- The observed biomarker kinetics may be explained by altered myocyte metabolism during strenuous exercise.
- Further research into metabolic changes could elucidate the mechanisms behind exercise-induced cardiac biomarker elevations.
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.
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