Salt Loading Blunts Central and Peripheral Postexercise Hypotension.

Abstract

INTRODUCTION\nHigh salt intake is a widespread cardiovascular risk factor with systemic effects. These effects include an expansion of plasma volume, which may interfere with postexercise hypotension (PEH). However, the effects of high salt intake on central and peripheral indices of PEH remain unknown. We tested the hypothesis that high salt intake would attenuate central and peripheral PEH.\n\n\nMETHODS\nNineteen healthy adults (7F/12M, age=25±4 yrs; BMI=23.3±2.2 kg•m; VO2peak=41.6±8.7 mL•min•kg; SBP=112±9 mmHg; DBP=65±9 mmHg) participated in this double-blind, randomized, placebo-controlled crossover study. Participants were asked to maintain a 2300 mg/d sodium diet for 10 days on two occasions separated by ≥two weeks. Total salt intake was manipulated via ingestion of capsules containing either table salt (3900 mg/d) or placebo (dextrose) during each diet. On the 10 day, participants completed 50 minutes of cycling at 60% VO2peak. A subset of participants (n=8) completed 60 minutes of seated rest (sham trial). Beat-to-beat blood pressure (BP) was measured in-lab for 60 minutes post-exercise via finger photoplethysmography. Brachial and central BP were measured for 24 hours post-exercise via ambulatory BP monitor.\n\n\nRESULTS\nTen days of high salt intake increased urinary sodium excretion (dextrose=134±70 vs. salt=284±74 mmol•24H, p<0.001), expanded plasma volume (7.2±10.8%), and abolished PEH during in-lab BP monitoring (main effect of diet: p<0.001). Ambulatory systolic BPs were higher for 12 hours following exercise during the salt and sham trials compared to the dextrose trial (average change, dextrose=3.6±2.1, salt=9.9±1.4, sham=9.8±2.5 mmHg; p=0.01). Ambulatory central systolic BP was also higher during the salt trial compared to dextrose trial.\n\n\nCONCLUSION\nHigh salt intake attenuates peripheral and central PEH, potentially reducing the beneficial cardiovascular effects of acute aerobic exercise.