Key result
High salt intake abolishes postexercise hypotension, raising 12-hour ambulatory systolic BP by ~6 mm Hg.
Why the study?
High salt intake causes plasma volume expansion that may interfere with postexercise hypotension, but its effects on central and peripheral indices of postexercise hypotension remain unknown.
Does high salt intake attenuate central and peripheral postexercise hypotension in healthy adults?
RCT (n=19)
Double-blind
Randomized crossover
Does high salt intake attenuate central and peripheral postexercise hypotension in healthy adults?
High salt intake blunts the acute blood pressure-lowering effects of aerobic exercise in healthy adults.
Answers are grounded in this paper and cite their sources.
High salt intake blunts acute BP-lowering effects of exercise; extends evidence on dietary modulation of postexercise hypotension.
INTRODUCTION: High 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. METHODS: Nineteen healthy adults (7 female/12 male; age, 25 ± 4 yr; body mass index, 23.3 ± 2.2 kg·m; V[Combining Dot Above]O2peak, 41.6 ± 8.7 mL·min·kg; 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 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 (3900 mg·d) 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. RESULTS: Ten days of high salt intake increased urinary sodium excretion (134 ± 70 (dextrose) vs 284 ± 74 mmol per 24 h (salt), P < 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. CONCLUSION: High salt intake attenuates peripheral and central PEH, potentially reducing the beneficial cardiovascular effects of acute aerobic exercise.
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Babcock et al. (2019) conducted an RCT in Healthy adults (n=19). Table salt vs. Placebo (dextrose) was evaluated on Ambulatory systolic blood pressure change for 12 h after exercise (p=0.01). High salt intake abolished postexercise hypotension and increased ambulatory systolic blood pressure for 12 hours post-exercise compared to placebo (9.9 vs 3.6 mm Hg; P=0.01).
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