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Updated: May 27, 2026

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
Published on: October 22, 2014
Insights
Marathon running may lead to cardiac and vascular changes that increase sudden death risk. These adaptations, including arterial stiffness and altered blood flow, may promote dangerous heart rhythms.
Area of Science:
- Cardiovascular Physiology
- Exercise Science
- Sports Medicine
Background:
- Subacute and chronic cardiac adaptations from marathon running may elevate sudden cardiac death risk.
- Prolonged strenuous exertion can induce cardiac arrhythmogenic remodeling with potential systemic vascular involvement.
Discussion:
- Marathon running can decrease coronary perfusion pressure and cause endothelial damage, potentially by altering angiogenic growth factors.
- Increased arterial stiffness, augmented wave reflections, and widened pulse pressure are observed in marathon runners.
- These vascular maladaptations are linked to atrial fibrillation and may create a substrate for lethal arrhythmias.
Key Insights:
- Marathon running induces vascular changes like arterial stiffness and altered hemodynamics.
- These vascular changes are associated with increased risk of cardiac arrhythmias, including atrial fibrillation.
- The systemic vascular component of cardiac remodeling in marathon runners warrants further investigation.
Outlook:
- Further research should explore the precise mechanisms linking vascular maladaptations to arrhythmogenesis in endurance athletes.
- Developing targeted interventions to mitigate vascular risks in marathon runners is crucial.
- Long-term studies are needed to fully understand the chronic cardiovascular consequences of marathon running.
Abstract:
Subacute and chronic cardiac adaptations to marathon running may increase risk for sudden death. Herein, it is proposed that cardiac arrhythmogenic remodeling resulting from prolonged strenuous exertion may also have a systemic vascular component. Marathon running reduces coronary perfusion pressure and causes acute endothelial damage, possibly via altering concentrations of circulating angiogenic growth factors with novel vasoregulatory properties. Marathon runners have increased arterial stiffness and augmented pressure from wave reflections contributing to a widening of pulse pressure. Pulsatile hemodynamics may contribute to target organ damage. Moreover, each of these vascular maladaptations (increased arterial stiffness, augmented pressure from wave reflections, and widened pulse pressure) has been associated with atrial fibrillation and may provide a substrate for lethal arrhythmogenesis in the marathon runner.
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