Key result
Post-triathlon cardiac troponin and NT-proBNP rises are not associated with inflammation or oxidative stress.
Why the study?
The pathophysiological mechanisms behind increased myocardial stress biomarkers after strenuous endurance exercise are not fully elucidated, with unclear roles of inflammation and oxidative stress.
Are post-race increases in cardiac troponin T and NT-proBNP associated with markers of exercise-induced inflammation, oxidative stress, or antioxidant vitamins in triathletes following an Ironman triathlon?
Cohort
Are post-race increases in cardiac troponin T and NT-proBNP associated with markers of exercise-induced inflammation, oxidative stress, or antioxidant vitamins in triathletes following an Ironman triathlon?
Exercise-induced increases in myocardial stress markers (troponin T, NT-proBNP) do not appear to be driven by the specific inflammatory or oxidative stress pathways measured in this study.
No association with measured pathways does not support targeted interventions; leaves open alternative mechanisms for post-exercise biomarker rises in endurance athletes.
Increased concentrations of biomarkers reflecting myocardial stress such as cardiac troponin I and T and brain natriuretic peptide (BNP) have been observed following strenuous, long-lasting endurance exercise. The pathophysiological mechanisms are still not fully elucidated and the interpretations of increased post-exercise concentrations range from (i) evidence for exercise-induced myocardial damage to (ii) non-relevant spurious troponin elevations, presumably caused by assay imprecision or heterophilic antibodies. Several lines of evidence suggest that inflammatory processes or oxidative stress could be involved in the rise of NT-proBNP and Troponin observed in critically ill patients with sepsis or burn injury. We tested the hypothesis that inflammatory or oxidative stress is also responsible for exercise-induced cardiomyocyte strain in a large cohort of triathletes following an Ironman triathlon. However the post-race increase in cardiac troponin T and NT-proBNP was not associated with several markers of exercise-induced inflammation, oxidative stress or antioxidant vitamins. Therefore, we clearly need more studies with other inflammatory markers and different designs to elucidate the scientific background for increases in myocardial stress markers following strenuous endurance events.
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Bissé et al. (2026) conducted a cohort in Exercise-induced myocardial stress. Ironman triathlon (strenuous endurance exercise) was evaluated on Association between post-race increase in cardiac troponin T and NT-proBNP and markers of inflammation or oxidative stress. Post-race increases in cardiac troponin T and NT-proBNP following an Ironman triathlon were not associated with markers of exercise-induced inflammation, oxidative stress, or antioxidant vitamins.
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