Running a marathon triggers measurable heart changes

By Dr. Sanchari Sinha Dutta, Ph.D.Reviewed by Lauren HardakerJun 11 2026

A review of 69 studies reveals that marathon runners frequently show post-race spikes in cardiac biomarkers and subtle cardiac changes, but researchers say the evidence does not yet show that these responses translate into lasting heart damage. 

Study: Acute effects of marathon running on the heart: a systematic review and meta-analysis. Image credit: Pavel1964/Shutterstocl.com

Marathon running can increase circulating biomarkers of myocardial injury and alter cardiac structure and function in healthy adults, according to a new study published in BMJ Open Sport & Exercise Medicine.

Marathon popularity raises questions about cardiac safety

Regular endurance running is associated with a range of health benefits, including improvement in cardiac health and physical fitness. However, evidence indicates that high levels of running throughout the lifetime may increase the risk of cardiovascular disease and mortality.

Previous studies investigating the cardiovascular effects of long-term endurance running events, such as marathons, have found increased blood levels of cardiac injury biomarkers, including troponins. In clinical settings, elevated levels of these biomarkers have been linked to an increased risk of myocardial damage, hemodynamic stress, or cardiac inflammation in patients. However, the clinical significance of these biomarkers in endurance athletes remains largely unknown.

Given the increasing popularity of endurance running events worldwide, this systematic review and meta-analysis aimed to characterize the acute cardiac effects of marathon running in healthy adults.

A total of 69 studies were included in the systematic review after screening 7,377 records identified from electronic databases. Of these studies, 49 were included in the meta-analysis on myocardial biomarkers, structure, and function.

Marathon running elevates cardiac biomarkers beyond thresholds

The meta-analysis of myocardial biomarkers revealed significantly elevated blood levels of troponin T, troponin I, and N-terminal pro-B-type natriuretic peptide following marathon running. The reported levels of these biomarkers exceeded the commonly used clinical thresholds for myocardial injury or ischemia and for heart failure, although the significance of these elevations in healthy endurance athletes remains uncertain.

Regarding structural and functional changes in the heart, the meta-analysis showed marathon-induced reduction in left ventricular dimensions and increases in right ventricular volume and diameter. However, the magnitude of these structural changes was modest and did not reflect significant clinical relevance.

Modest changes in systolic functions were also observed in the meta-analysis. These changes included a 3% increase in left ventricular fractional shortening and 3.5% reduction in right ventricular ejection fraction. These changes fell outside the ranges commonly accepted as indicating clinically relevant ventricular function impairment in healthy individuals.

Regarding diastolic functions, the meta-analysis revealed a 16% reduction in early ventricular filling velocity and a 26% increase in late ventricular filling velocity. These changes were also within physiological ranges.

Biomarker spikes may reflect physiological exercise responses

This systematic review and meta-analysis indicate that marathon running can trigger acute cardiovascular changes in healthy adults. However, the clinical significance of these responses remains uncertain and requires further investigation. The findings also suggest that the magnitude of these changes varies according to age, sex, training status, marathon performance, and overall exercise load, highlighting substantial differences in how individuals respond to endurance exercise.

Troponin 

One of the most consistent findings was a significant rise in circulating cardiac biomarkers following marathon completion. Blood troponin levels, regulatory proteins involved in cardiac muscle contraction, increased markedly after racing. Although elevated troponin concentrations are commonly used in clinical medicine as markers of myocardial injury, exercise-induced increases may occur through several physiological mechanisms and do not necessarily indicate permanent cardiac damage.

Existing evidence suggests that prolonged endurance exercise can increase cardiac cell membrane permeability, allowing troponins to enter the bloodstream.

N-terminal pro B-type natriuretic peptide

Marathon runners also showed elevated levels of N-terminal pro B-type natriuretic peptide (NT-proBNP), with several studies reporting concentrations above thresholds commonly used in heart failure assessment. NT-proBNP is released by cardiac cells in response to myocardial stretch caused by pressure overload or expansion of the left ventricle.

The prolonged cardiovascular demands of marathon running may promote cardiac cell stretching, endocrine activation, and myocardial hypoxia, all of which could contribute to increased NT-proBNP release. However, whether repeated elevations in this biomarker are associated with adverse long-term cardiac outcomes remains unknown.

Structural cardiac changes

To assess structural and functional cardiac changes, most studies used echocardiography. These analyses revealed modest reductions in left ventricular dimensions alongside increases in right ventricular volume and diameter. Such changes are generally not considered clinically meaningful structural abnormalities, but the researchers note that long-term follow-up studies are needed to determine whether repeated exposure to extreme endurance exercise could contribute to chronic cardiac remodeling or arrhythmias in susceptible individuals.

The analysis also identified a 3% increase in left ventricular fractional shortening. Combined with the observed reduction in left ventricular dimensions, this finding may reflect enhanced contractility or temporary alterations in cardiac loading conditions during and immediately after marathon running.

Fewer studies used cardiac Magnetic Resonance Imaging (MRI), and these findings did not replicate the structural changes observed with echocardiography. The discrepancy may be explained by differences in assessment timing.

MRI scans were typically performed around seven hours after marathon completion, whereas echocardiographic measurements were obtained immediately after the race. Transient factors such as hydration status and pulmonary pressure may therefore have influenced the echocardiographic findings and contributed to the differences between imaging modalities.

Marathon running causes measurable but modest cardiac changes

Overall, the meta-analysis findings highlight the need for age-, sex-, and exercise load-stratified longitudinal studies to determine whether these acute changes translate to long-term cardiac malfunctioning.

Importantly, the researchers note that the observed biomarker elevations and cardiac changes are likely to represent predominantly physiological responses to the intense cardiovascular demands of marathon running, although the possibility of adverse effects in susceptible individuals cannot yet be excluded.

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