An ultramarathon was associated with pronounced inflammatory responses accompanied by increased fibrinogen-related RBC aggregation and elevated plasma nitrite concentrations, while macrovascular properties remained largely preserved, suggesting cardiovascular adjustments primarily reflect functional changes in peripheral vascular regulation rather than substantial changes in central arterial mechanical properties.
Systemic inflammatory markers were significantly elevated immediately after the 230-km ultramarathon.
Both plasma free reactive oxygen species and total antioxidant capacity decreased post-race, indicating oxidative stress-related changes.
Red blood cell aggregation increased post-race in concert with elevated fibrinogen levels.
Plasma nitrite, a marker of nitric oxide (NO) bioavailability, increased following the ultramarathon.
Macrovascular hemodynamic properties were largely preserved after the ultramarathon, with no significant change in pulse wave velocity or central pressures.
Wave reflection indices were altered post-race, with changes in augmentation index and diastolic reflection area but not heart rate-standardized augmentation index.
The concurrent physiological responses to the ultramarathon involved parallel inflammatory, hemorheological, endothelial, and macrovascular alterations.
This research examined what happens to the body's blood, blood vessels, and immune system during and after an extreme 230-kilometer non-stop ultramarathon race. Twelve experienced runners had their blood and vascular function measured before and immediately after the race. The study looked at inflammation markers, red blood cell behavior, nitric oxide levels, and the stiffness and pressure dynamics of major blood vessels. The researchers found that the race triggered a significant inflammatory response — with markers like IL-6, IL-10, CRP, and white blood cells all rising substantially. Interestingly, a protein called fibrinogen also rose sharply, and this was linked to increased clumping (aggregation) of red blood cells, which could affect how easily blood flows through small vessels. At the same time, a molecule called nitric oxide — which helps blood vessels relax and widen — became more available, possibly as a compensatory mechanism. Despite all these changes, the large central arteries (like the aorta) showed no significant increase in stiffness, and blood pressure in central vessels remained stable, suggesting the heart and main arteries coped well with the extreme stress. This research suggests that completing an extreme ultramarathon causes intense but largely functional — rather than structural — changes to the cardiovascular system. The body appears to adjust primarily through changes in peripheral blood vessel regulation and blood composition rather than through lasting damage to large artery walls. However, the simultaneous increase in red blood cell clumping and inflammation raises questions about short-term blood flow risks that may be worth examining in future larger studies, particularly in older endurance athletes.
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Upload Your LabsGrau M, Bruns J, John L, Munk M, Siebers M, Bloch W, et al.. (2026). Concurrent inflammatory, hemorheological and macrovascular responses to a 230-km ultramarathon: an exploratory study.. Scientific reports. https://doi.org/10.1038/s41598-026-55821-1