TY - JOUR
T1 - Salt Loading Blunts Central and Peripheral Postexercise Hypotension
AU - Babcock, Matthew C.
AU - Robinson, Austin T.
AU - Watso, Joseph C.
AU - Migdal, Kamila U.
AU - Martens, Christopher R.
AU - Edwards, David G.
AU - Pescatello, Linda S.
AU - Farquhar, William B.
N1 - Funding Information:
This research was supported by the American College of Sports Medicine Foundation Doctoral Student Research Grant 17-00521 (M. C. B.), National Institutes of Health R01HL128388 (W. B. F.), and American Heart Association 18POST34060020 (A. T. R.). This publication was made possible by the Delaware COBRE in Cardiovascular Health, supported by a grant from the National Institute of General Medical Sciences (5 P20 GM113125) from the National Institutes of Health. The authors have no conflicts of interest to declare. The results of this study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. The results of the present study do not constitute endorsement by the American College of Sports Medicine.
Publisher Copyright:
© 2019 Lippincott Williams & Wilkins.
PY - 2020/4/1
Y1 - 2020/4/1
N2 - 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-2; VO2peak, 41.6 ± 8.7 mL·min-1·kg-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 (3900 mg·d-1) or placebo (dextrose) during each diet. On the 10th day, participants completed 50 min of cycling at 60% VO2peak. 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.
AB - 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-2; VO2peak, 41.6 ± 8.7 mL·min-1·kg-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 (3900 mg·d-1) or placebo (dextrose) during each diet. On the 10th day, participants completed 50 min of cycling at 60% VO2peak. 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.
KW - AEROBIC EXERCISE
KW - BRACHIAL BLOOD PRESSURE
KW - CENTRAL BLOOD PRESSURE
KW - POSTEXERCISE HYPOTENSION
KW - SALT
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U2 - 10.1249/MSS.0000000000002187
DO - 10.1249/MSS.0000000000002187
M3 - Article
C2 - 31609296
AN - SCOPUS:85081964657
SN - 0195-9131
VL - 52
SP - 935
EP - 943
JO - Medicine and Science in Sports and Exercise
JF - Medicine and Science in Sports and Exercise
IS - 4
ER -