Inflammatory biomarkers are unrelated to endothelial-mediated vasodilation in physically active young men

Abstract

Endothelial dysfunction has an important role in genesis of atherosclerosis and is depicted by a series of inflammatory and endothelial biomarkers. Shear stress arising from repeated episodes of increased blood flow with physical activity (PA) is a possible mechanism that improves vascular endothelial function. Our purpose was to examine whether inflammatory markers mediate the association between PA and endothelial function. Subjects were young, healthy men 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 over 6 months, while sedentary subjects reported no recreational physical activity. Fasting serum samples were analyzed for C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Endothelial function was determined using flow-mediated dilation of the brachial artery induced by post ischemic reactive hyperemia. Hyperemia response was greater in the high-active than in sedentary men (30.2±8.2 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 IL-6. Concentrations of these inflammatory biomarkers were unrelated to reactive hyperemia differences attributable to PA. Improved hyperemic response seen in young physically active subjects may be influenced by factors beyond the inflammatory factors, e.g., enhanced nitric oxide production. Physical activity was associated with an increased vascular function in young adults, although a diminished inflammatory state was no revealed. Additional research is needed to clarify the role of PA on cytokine indicators of inflammation and how this relates to endothelial function.