A diet that is high in salt is known to increase the risk of stroke and cardiovascular disease, which are leading causes of mortality worldwide (WHO 2024). Additionally, endothelial dysfunction is a common predictor of cardiovascular disease and an indicator of vascular impairment. While acute exercise is known to cause transient endothelial dysfunction, the combined effects of high salt intake and exercise remain unclear. The activation of the immune system from exercise or alterations in immune functions after high salt intake may contribute to endothelial dysfunction. In this study, participants underwent standardized acute exercise bouts during periods of salt and placebo supplementation. Ultrasound measurements of the brachial and
popliteal arteries were taken to assess flow mediated dilation responses, effectively measuring endothelial function before and after exercise, and before and after high salt intake. Blood samples were also collected to analyze any changes in immune cell populations. Results indicate that exercise induced local endothelial dysfunction in the popliteal artery, suggesting that locally produced reactive oxygen species and glycocalyx damage due to increased shear stress were more significant factors than immune system activation and sodium related dysfunction in reducing flow-mediated dilation responses. Additionally, no significant changes were observed in leukocyte populations before and after exercise or salt supplementation, likely due to insufficient exercise stimulus, high variation in a small sample size, or the greater importance of alterations in immune cell functions, such as increases in pro-inflammatory phenotypes, rather than absolute counts.
