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.
Nineteen healthy adults (7 female/12 male; age, 25 ± 4 yr; body mass index, 23.3 ± 2.2 kg·m−2
; V[Combining Dot Above]O2peak
, 41.6 ± 8.7 mL·min−1
; systolic blood pressure (BP), 112 ± 9 mm Hg; diastolic BP, 65 ± 9 mm Hg) participated in this double-blind, randomized, placebo-controlled crossover study. Participants were asked to maintain a 2300 mg·d−1
sodium diet for 10 d on two occasions separated by ≥2 wk. Total salt
intake was manipulated via ingestion of capsules containing either table salt
) or placebo (dextrose) during each diet. On the 10th day, participants completed 50 min of cycling at 60% V[Combining Dot Above]O2peak
. A subset of participants (n
= 8) completed 60 min of seated rest (sham trial). Beat-to-beat BP was measured in-laboratory for 60 min after exercise via finger photoplethysmography. Brachial and central BPs were measured for 24 h after exercise via ambulatory BP monitor.
Ten days of high salt
intake increased urinary sodium excretion (134 ± 70 (dextrose) vs 284 ± 74 mmol per 24 h (salt
< 0.001), expanded plasma volume (7.2% ± 10.8%), and abolished PEH during in-laboratory BP monitoring (main effect of diet, P
< 0.001). Ambulatory systolic BPs were higher for 12 h after exercise during the salt
and sham trials compared with the dextrose trial (average change, 3.6 ± 2.1 mm Hg (dextrose), 9.9 ± 1.4 mm Hg (salt
), 9.8 ± 2.5 mm Hg (sham); P
= 0.01). Ambulatory central systolic BP was also higher during the salt
trial compared with dextrose trial.
intake attenuates peripheral and central PEH, potentially reducing the beneficial cardiovascular effects of acute aerobic exercise