Acute Cardiac Effects of Marathons Systematic Review

Inside the Heart of the Marathon: A Systematic Review Reveals Acute Cardiac Effects

A 2026 systematic review and meta-analysis in BMJ Open Sport & Exercise Medicine provides a comprehensive picture of what happens to a healthy runner’s heart during and immediately after a marathon. Led by researchers from Amsterdam University Medical Center and the University of Amsterdam, the study analyzed data from 3,274 participants across 69 studies. The findings describe a consistent, multifaceted physiological response involving biomarkers of stress, changes in heart chamber volumes, and shifts in function.

Biomarkers Spike, Revealing Myocardial Stress

The meta-analysis quantified clear increases in key proteins released by the heart. After 26.2 miles, levels of troponin T rose by an average of 42 ng/L, troponin I by 77 ng/L, and N-terminal pro B-type natriuretic peptide (NT-proBNP) by 114 ng/L. These proteins are standard clinical tools for diagnosing heart attacks and heart failure. In the context of a marathon, their elevation is generally interpreted as a sign of reversible myocardial stress or strain, not necessarily cell death.

The mechanism is thought to involve the extreme and prolonged demand placed on the heart muscle. Over four to five hours of continuous work, the heart beats over 25,000 times, requiring massive blood flow and oxygen delivery. This stress can cause temporary changes in the permeability of heart cell membranes, allowing these biomarkers to leak into the bloodstream. The review confirmed that these changes are almost universal among marathon finishers but typically normalize within 24 to358 hours.

Echocardiography Shows a Heart Remodeled, For a Time

Imaging data revealed how the heart’s structure adapts under duress. The left ventricle, the chamber that pumps oxygenated blood to the body, showed a decrease in volume and diastolic function—its ability to relax and fill efficiently between beats. More pronounced changes were seen in the right ventricle, which pumps blood to the lungs. Its end-systolic and end-diastolic volumes increased, while its systolic function decreased.

Researchers explain this as a consequence of the marathon’s unique hemodynamic load. The right ventricle works against high pressure in the pulmonary arteries during intense, prolonged exercise. Combined with potential dehydration and high core temperature, this can lead to a transient “fatigue” of the right ventricle, reducing its pumping efficiency and causing it to become slightly stretched. It is a direct observation of the heart operating at its physiological limit.

An Individual’s Response Depends on Demographics and Fitness

A critical insight from the meta-regression analysis is that the cardiac response is not uniform. Factors like age, sex, training status, and marathon finish time significantly influenced the degree of change. For instance, older runners or those less trained might show a larger biomarker release or greater right ventricular strain. This aligns with the principle that well-structured, long-term aerobic base training, such as consistent Zone 2 cycling or running, strengthens the cardiovascular system and likely improves its resilience to extreme events.

The study’s participant pool, over 80% male, is a notable limitation, highlighting a gap in understanding how women’s hearts specifically respond to marathon stress. The authors, including Laily I and Harald T. Jorstad, explicitly call for more research to explore these individual differences and their implications for personalized training advice.

Balancing Adaptation and Risk in Endurance Training

For the endurance athlete, these findings present a nuanced reality. The acute changes are largely physiological—the heart demonstrating its incredible capacity for work and its subsequent need for recovery. The slight improvement in left ventricular ejection fraction seen on MRI suggests an efficient, adaptive response in the immediate aftermath. This reflects the heart’s ability to strengthen over time with endurance training, a process mediated by molecular regulators like PGC-1α, which remodels both muscle and cardiovascular tissues.

However, the consistent biomarker rise and right ventricular changes warrant respect. They underscore why marathon training must be built on a foundation of gradual progression and ample low-intensity volume. Jumping into high-mileage or race-pace workouts without an established aerobic base increases the risk of excessive, perhaps less reversible, strain. Furthermore, allowing for extended recovery after a marathon—far beyond the few days it takes for soreness to fade—is essential for the heart to fully reset. Integrating modalities with different hemodynamic profiles, like swimming, during recovery phases could be beneficial.

The review concludes that while marathon running induces clear acute cardiac changes, their clinical significance is not yet fully established. For most healthy, well-prepared athletes, these changes are likely a normal part of pushing human endurance. The priority for runners and coaches should be intelligent, periodized training that builds resilience, recognizes the need for individualization, and respects the profound physiological challenge a marathon represents.

Sources:
https://pubmed.ncbi.nlm.nih.gov/42299359/
https://pubmed.ncbi.nlm.nih.gov/42272862/
https://pubmed.ncbi.nlm.nih.gov/42138932/