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Updated: Jun 23, 2026

Magnetic Resonance Derived Myocardial Strain Assessment Using Feature Tracking
Published on: February 12, 2011
Relation of biomarkers and cardiac magnetic resonance imaging after marathon running
Negareh Mousavi1, Andrew Czarnecki, Kanwal Kumar
1Section of Cardiology, Department of Cardiac Sciences, St. Boniface Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada.
Insights
Marathon running causes temporary right ventricular dysfunction, confirmed by cardiac magnetic resonance (CMR) imaging. Elevated cardiac biomarkers after marathons likely stem from cytosolic release, not heart muscle damage.
Area of Science:
- Cardiology
- Sports Medicine
- Biomarkers
Background:
- Previous studies show biochemical and echocardiographic evidence of cardiac injury in endurance athletes.
- Cardiac dysfunction, especially in the right ventricle, has been noted after marathon running.
- A comprehensive study combining biomarkers, echocardiography, and CMR imaging was lacking.
Purpose of the Study:
- To investigate cardiac changes in marathon runners using serial cardiac biomarkers, echocardiography, and CMR imaging.
- To validate right ventricular (RV) systolic dysfunction using CMR imaging.
- To differentiate the cause of elevated cardiac biomarkers post-marathon.
Main Methods:
- 14 participants completed a full marathon.
- Serial measurements of cardiac biomarkers (myoglobin, creatine kinase, troponin T) were taken.
- Echocardiography and cardiac magnetic resonance (CMR) imaging assessed cardiac function before and after the race.
Main Results:
- All athletes showed elevated myoglobin, creatine kinase, and troponin T post-race.
- A strong correlation (r=0.96) was found between echocardiographic RV fractional area change and CMR-assessed RV ejection fraction.
- Transient decrease in RV systolic function (RV fractional area change) and diastolic abnormalities in both ventricles were observed post-race, persisting for a week.
Conclusions:
- Right ventricular systolic dysfunction occurs transiently after marathon running, validated by CMR imaging.
- Elevated cardiac troponin levels post-marathon are likely due to cytosolic release, not myocardial necrosis, as evidenced by the absence of delayed enhancement on CMR.
- Diastolic abnormalities in both ventricles may persist longer than systolic dysfunction.
Abstract:
Although previous studies including endurance athletes after marathon running have demonstrated biochemical evidence of cardiac injury and have correlated these findings with echocardiographic evidence of cardiac dysfunction, particularly of the right ventricle, a study of marathon athletes incorporating biomarkers, echocardiography, and cardiac magnetic resonance (CMR) imaging has not been performed to date. The aim of this study was to demonstrate the cardiac changes associated with participation in a marathon using serial cardiac biomarkers, echocardiography, and CMR imaging. Fourteen participants (mean age 33 +/- 6 years, 8 men) completed the full marathon. Myoglobin, creatine kinase, and troponin T were elevated in all athletes after the race. There was a strong linear correlation between right ventricular (RV) fractional area change as assessed by echocardiography and the RV ejection fraction as assessed by CMR imaging (r = 0.96) after the marathon. RV function, using echocardiography, transiently decreased from before to after the race (RV fractional area change 43 +/- 4% vs 33 +/- 5%, p <0.05). There were also postrace changes in left ventricular and RV diastolic filling. Although RV systolic changes were transient, left ventricular and RV diastolic abnormalities persisted up to 1 week after the marathon. No evidence of delayed enhancement of the left ventricular myocardium was found on CMR imaging, suggesting that the increase in cardiac biomarkers after the marathon may not have be due to myocardial necrosis. In conclusion, RV systolic dysfunction transiently occurs after a marathon and has been validated for the first time by CMR imaging. The increase in cardiac troponin after marathon running is likely due to the cytosolic release of the biomarker, not to the true breakdown of the myocyte, as confirmed by delayed enhancement CMR imaging.
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