High Salt Intake Augments Blood Pressure Responses During Submaximal Aerobic Exercise

Background High sodium (Na⁺) intake is a widespread cardiovascular disease risk factor. High Na⁺ intake impairs endothelial function and exaggerates sympathetic reflexes, which may augment exercising blood pressure (BP) responses. Therefore, this study examined the influence of high dietary Na⁺ on BP responses during submaximal aerobic exercise. Methods and Results Twenty adults (8F/12M, age=24±4 years; body mass index 23.0±0.6 kg·m^-2; VO₂peak=39.7±9.8 mL·min^-1·kg^-1; systolic BP=111±10 mm Hg; diastolic BP=64±8 mm Hg) participated in this randomized, double-blind, placebo-controlled crossover study. Total Na⁺ intake was manipulated via ingestion of capsules containing either a placebo (dextrose) or table salt (3900 mg Na⁺/day) for 10 days each, separated by ≥2 weeks. On day 10 of each intervention, endothelial function was assessed via flow-mediated dilation followed by BP measurement at rest and during 50 minutes of cycling at 60% VO_2peak. Throughout exercise, BP was assessed continuously via finger photoplethysmography and every 5 minutes via auscultation. Venous blood samples were collected at rest and during the final 10 minutes of exercise for assessment of norepinephrine. High Na⁺ intake increased urinary Na⁺ excretion (placebo=140±68 versus Na⁺=282±70 mmol·24H^-1; P<0.001) and reduced flow-mediated dilation (placebo=7.2±2.4 versus Na⁺=4.2±1.7%; P<0.001). Average exercising systolic BP was augmented following high Na⁺ (placebo=Δ30.0±16.3 versus Na⁺=Δ38.3±16.2 mm Hg; P=0.03) and correlated to the reduction in flow-mediated dilation (R=-0.71, P=0.002). Resting norepinephrine concentration was not different between conditions (P=0.82). Norepinephrine increased during exercise (P=0.002), but there was no Na⁺ effect (P=0.26). Conclusions High dietary Na⁺ augments BP responses during submaximal aerobic exercise, which may be mediated, in part, by impaired endothelial function.