TY - JOUR
T1 - High salt intake augments blood pressure responses during submaximal aerobic exercise
AU - Babcock, Matthew C.
AU - Robinson, Austin T.
AU - Migdal, Kamila U.
AU - Watso, Joseph C.
AU - Martens, Christopher R.
AU - Edwards, David G.
AU - Pescatello, Linda S.
AU - Farquhar, William B.
N1 - Funding Information:
This research was supported by American College of Sports Medicine Foundation Doctoral Student Research Grant 17-00521 (Babcock), NIH R01HL128388 (Farquhar), and American Heart Association 18POST34060020 (Robinson). This publication was made possible by the Delaware Center of Biomedical Research Excellence in Cardiovascular Health, supported by a grant from the National Institute of General Medical Sciences – NIGMS (5 P20 GM113125) from the NIH.
Publisher Copyright:
© 2020 The Authors.
PY - 2020/5/18
Y1 - 2020/5/18
N2 - BACKGROUND: High sodium (Na+) intake is a widespread cardiovascular disease risk factor. High Na+ intake impairs endothelial function and exaggerates sympathetic reflexes, which may augment exercising blood pressure (BP) responses. Therefore, this study examined the influence of high dietary Na+ on BP responses during submaximal aerobic exercise. METHODS AND RESULTS: Twenty adults (8F/12M, age=24±4 years; body mass index 23.0±0.6 kg·m−2; VO2 peak=39.7± 9.8 mL·min−1·kg−1; systolic BP=111±10 mm Hg; diastolic BP=64±8 mm Hg) participated in this randomized, double-blind, placebo-controlled crossover study. Total Na+ intake was manipulated via ingestion of capsules containing either a placebo (dextrose) or table salt (3900 mg Na+/day) for 10 days each, separated by ≥2 weeks. On day 10 of each intervention, endothelial function was assessed via flow-mediated dilation followed by BP measurement at rest and during 50 minutes of cycling at 60% VO2peak . Throughout exercise, BP was assessed continuously via finger photoplethysmography and every 5 minutes via auscultation. Venous blood samples were collected at rest and during the final 10 minutes of exercise for assessment of norepinephrine. High Na+ intake increased urinary Na+ excretion (placebo=140±68 versus Na+=282±70 mmol·24H−1; P<0.001) and reduced flow-mediated dilation (placebo=7.2±2.4 versus Na+=4.2±1.7%; P<0.001). Average exercising systolic BP was augmented following high Na+ (placebo=Δ30.0±16.3 versus Na+=Δ38.3±16.2 mm Hg; P=0.03) and correlated to the reduction in flow-mediated dilation (R=−0.71, P=0.002). Resting norepinephrine concentration was not different between conditions (P=0.82). Norepinephrine increased during exercise (P=0.002), but there was no Na+ effect (P=0.26). CONCLUSIONS: High dietary Na+ augments BP responses during submaximal aerobic exercise, which may be mediated, in part, by impaired endothelial function.
AB - BACKGROUND: High sodium (Na+) intake is a widespread cardiovascular disease risk factor. High Na+ intake impairs endothelial function and exaggerates sympathetic reflexes, which may augment exercising blood pressure (BP) responses. Therefore, this study examined the influence of high dietary Na+ on BP responses during submaximal aerobic exercise. METHODS AND RESULTS: Twenty adults (8F/12M, age=24±4 years; body mass index 23.0±0.6 kg·m−2; VO2 peak=39.7± 9.8 mL·min−1·kg−1; systolic BP=111±10 mm Hg; diastolic BP=64±8 mm Hg) participated in this randomized, double-blind, placebo-controlled crossover study. Total Na+ intake was manipulated via ingestion of capsules containing either a placebo (dextrose) or table salt (3900 mg Na+/day) for 10 days each, separated by ≥2 weeks. On day 10 of each intervention, endothelial function was assessed via flow-mediated dilation followed by BP measurement at rest and during 50 minutes of cycling at 60% VO2peak . Throughout exercise, BP was assessed continuously via finger photoplethysmography and every 5 minutes via auscultation. Venous blood samples were collected at rest and during the final 10 minutes of exercise for assessment of norepinephrine. High Na+ intake increased urinary Na+ excretion (placebo=140±68 versus Na+=282±70 mmol·24H−1; P<0.001) and reduced flow-mediated dilation (placebo=7.2±2.4 versus Na+=4.2±1.7%; P<0.001). Average exercising systolic BP was augmented following high Na+ (placebo=Δ30.0±16.3 versus Na+=Δ38.3±16.2 mm Hg; P=0.03) and correlated to the reduction in flow-mediated dilation (R=−0.71, P=0.002). Resting norepinephrine concentration was not different between conditions (P=0.82). Norepinephrine increased during exercise (P=0.002), but there was no Na+ effect (P=0.26). CONCLUSIONS: High dietary Na+ augments BP responses during submaximal aerobic exercise, which may be mediated, in part, by impaired endothelial function.
KW - Acute exercise
KW - Blood pressure
KW - Dietary sodium
KW - Exercise pressor reflex
KW - Flow-mediated dilation
UR - http://www.scopus.com/inward/record.url?scp=85084936993&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85084936993&partnerID=8YFLogxK
U2 - 10.1161/JAHA.120.015633
DO - 10.1161/JAHA.120.015633
M3 - Article
C2 - 32406312
AN - SCOPUS:85084936993
SN - 2047-9980
VL - 9
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
IS - 10
M1 - e015633
ER -