Salt Loading Blunts Central and Peripheral Postexercise Hypotension

Abstract

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.

Figure 1.

Changes in (A) systolic, (B) mean, and (C) diastolic BP from baseline during recovery from submaximal aerobic exercise. Following 10 days of habitual salt intake plus dextrose capsules (open circles), systolic BP is reduced compared to pre-exercising levels. However, after 10 days of high dietary salt intake (closed squares), this effect of exercise is abolished. Data are presented as mean±SD. *indicates p<0.05 between diets

Figure 2.

Changes in Modelflow-derived estimates of (A) CO and (B) TPR from baseline during recovery from submaximal aerobic exercise. CO remains elevated following submaximal aerobic exercise, however, CO after exercise is modestly, but significantly, higher following 10 days of salt capsules (filled squares) compared to dextrose (open circles). Changes in TPR were similar regardless of dietary condition. Data are presented as mean±SD.

Figure 3.

Hourly (A) and average (B) changes in systolic BP over 12 hours after a bout of submaximal aerobic exercise or one hour of quiet rest. Following quiet rest (sham, gray triangles and bars), ambulatory systolic BP increased over the following 12 hours. One hour of submaximal aerobic exercise following habitual salt intake (dextrose, open circles and bars) attenuated the rise in systolic BP, however 10 days of high dietary salt intake (salt, filled squares and bars) prevented the BP lowering effects of exercise. Hourly (C) and average (D) changes in diastolic BP were not different between conditions. Data are presented as mean±SD. *indicates significantly different than sham.

Figure 4.

Average ambulatory central (A) systolic BP is reduced over 12 hours following a bout of submaximal aerobic exercise compared to sham exercise (gray bars) on a habitual salt diet (Dextrose, open bars), however 10 days of high dietary salt intake (salt, black bars) attenuates the BP-lowering effects of central systolic BP. High dietary salt intake did not significantly affect central (B) diastolic BP. Data are presented as mean±SD. *indicates significantly different than sham.