ArticleScientific reports2026
Concurrent inflammatory, hemorheological and macrovascular responses to a 230-km ultramarathon: an exploratory study.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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7 authors.
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Abstract
To investigate the concurrent physiological response to extreme endurance exercise by examining inflammatory, hemorheological, endothelial, and vascular adaptations following an ultramarathon. Twelve runners (9 men/3 women; 48 ± 7 years) participating in a 230-km non-stop ultramarathon were assessed before and immediately after the race. Systemic inflammatory and oxidative stress markers, indices of red blood cell (RBC) aggregation and fibrinogen, plasma nitrite as a marker of nitric oxide (NO) bioavailability, and macrovascular hemodynamic parameters were measured. White blood cell count (WBC) (p < 0.001), interleukin (IL)-6 (p = 0.0002), IL-10 (p = 0.0002) and C-reactive protein (CRP) (p < 0.001) increased, while plasma free reactive oxygen species (ROS) (p = 0.0043) and total antioxidant capacity (p = 0.0041) decreased post-race. RBC aggregation increased (p = 0.0003) in concert with elevated fibrinogen (p < 0.0001). Plasma nitrite increased post-race (p = 0.0013). Macrovascular hemodynamics exhibited increased heart rate (p < 0.0001) with preserved pulse wave velocity (PWV; p = 0.257) and central pressures. Wave reflection indices were altered, with reduced augmentation index (AIx; p = 0.034), whereas heart rate-standardized AIx75 remained unchanged (p = 0.104), alongside an increase in diastolic reflection area (DRA; p = 0.020) and divergent peripheral pressure responses. The 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. Together, these findings suggest that acute responses to extreme endurance exercise involve parallel inflammatory, hemorheological, endothelial, and macrovascular alterations, with cardiovascular adjustments primarily reflecting functional changes in peripheral vascular regulation rather than substantial changes in central arterial mechanical properties.
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