Vascular And Inflammatory Biomarkers Are Unrelated To Endothelial-mediated Vasodilation In Physically Active Young Men

Abstract

Endothelial dysfunction has an important role in atherosclerosis and is depicted by a series of inflammatory and endothelial biomarkers. Assessment of endothelial-dependent vasodilation by venous occlusion plethysmography (VOP) is an established technique for endothelial function testing. Shear stress arising from repeated episodes of increased blood flow with physical activity (PA) is a possible mechanism that improves vascular endothelial function. PURPOSE: To examine the relationship of hyperemia response to flow occlusion vs. vascular and inflammatory cytokines as a result of high PA. METHODS: Subjects were men (Mean ± SD: age = 20.8 ± 2.2 yr; BMI = 22.4 ± 1.6 kg/m2) recruited according to recreational PA habits: high-active (n = 21) vs. sedentary (n = 17). Active subjects reported > 45 min/day of moderate-vigorous physical activities, > 4 days/week, for the last 6 months, while sedentary subjects reported no recreational physical activity for the same period. Flow-mediated vasodilation was determined following 5 minutes of cuff occlusion using VOP. Fasting serum samples were analyzed for C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α) and vascular endothelial growth factor (VEGF), using single and multiplex ELISA assays. RESULTS: Hyperemia response to flow occlusion with VOP was greater in the high-active than in sedentary men (30.2 ± 8.2 mL/min/100mL vs. 24.3 ± 5.2 mL/ min/100mL; p<0.001). There were no differences between the groups with respect to CRP, TNF-α, or VEGF. In these healthy young men, the vascular and inflammatory biomarkers evaluated were unrelated to observed VOP differences attributable to PA. This lack of association may suggest that these biomarkers report different functional properties and mechanisms within the vascular wall. Moreover, the high hyperemia response seen in physically active subjects does not exclude the possibility of explanations other than endothelial function (e.g., increased muscle capillarization, changes in neuroendocrine balance and/or myogenic factors). CONCLUSION: Additional research is needed to clarify the underlying relations between functional indicators of arterial stiffness and cytokine indicators of endothelial status.