Effect of acute high-phosphate intake on muscle metaboreflex activation and Vascular function

Brandi Y. Stephens, Jasdeep Kaur, Jennifer R. Vranish, Thales C. Barbosa, Jeanette K. Blankenship, Scott A Smith, Paul J. Fadel

Research output: Contribution to journalArticle

Abstract

Effect of acute high-phosphate intake on muscle metaboreflex activation and vascular function. Am J Physiol Heart Circ Physiol 317: H308 –H314, 2019. First published May 17, 2019; doi:10.1152/ajpheart.00082.2019.—Increased consumption of inorganic phosphate (Pi), an abundant ingredient in processed foods, has been associated with elevated cardiovascular disease risk; however, studies investigating underlying mechanisms are limited. Recently, high dietary Pi was shown to exaggerate the pressor response to static muscle contraction in rodents in part because of overactiva-tion of metabolically sensitive skeletal muscle afferents. Whether acute high Pi consumption affects muscle metaboreflex activation in humans remains unknown. Furthermore, although acute high Pi consumption has been shown to impair vascular function in young healthy men, equivocal results have been reported. Therefore, we hypothesized that acute high Pi consumption augments mean arterial pressure (MAP) responses during muscle metaboreflex activation, impairs endothelial function, and increases arterial stiffness in young healthy men. Subjects performed 35% maximal voluntary contraction static handgrip (HG), followed by postexercise ischemia (PEI) to isolate muscle metaboreflex activation. Resting flow-mediated dilation (FMD) and arterial stiffness were assessed. Measures were made before (pre) and 60 min after (post) subjects consumed either a high-phosphate drink (2,000 mg phosphorus and 1,520 mg sodium) or a sodium drink (1,520 mg sodium; control). MAP responses during HG (pre = +23 ± 3 mmHg; post = +21 ± 2 mmHg; P = 0.101) and PEI (pre = +21 ± 4 mmHg; post = +18 ± 3 mmHg; P = 0.184) were similar before and after Pi consumption. In contrast, FMD was significantly attenuated following Pi (pre = 5.1 ± 0.5%; post = 3.5 ± 0.5%; P = 0.010), whereas arterial stiffness remained unchanged. There were no changes in any measured variable after control drink consumption. In summary, although the muscle metaboreflex remains unaffected following acute high Pi consumption in young healthy men, endothelial function is impaired. NEW & NOTEWORTHY This study was the first to investigate the influence of acute high-phosphate consumption on the pressor response during isometric handgrip and isolated muscle metaboreflex activation during postexercise ischemia in young healthy humans. We demonstrated that a single high dose of phosphate (2,000 mg) did not augment blood pressure in response to exercise or isolated muscle metaboreflex activation, but endothelial function was blunted in young healthy men.

Original languageEnglish (US)
Pages (from-to)H308-H314
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume317
Issue number2
DOIs
StatePublished - Aug 1 2019

Fingerprint

Blood Vessels
Phosphates
Muscles
Vascular Stiffness
Ischemia
Sodium
Dilatation
Arterial Pressure
Muscle Contraction
Phosphorus
Rodentia
Skeletal Muscle
Cardiovascular Diseases
Exercise
Blood Pressure
Food

Keywords

  • Blood pressure
  • Brachial artery
  • Flow-mediated dilation
  • Handgrip exercise
  • Postexercise ischemia

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Effect of acute high-phosphate intake on muscle metaboreflex activation and Vascular function. / Stephens, Brandi Y.; Kaur, Jasdeep; Vranish, Jennifer R.; Barbosa, Thales C.; Blankenship, Jeanette K.; Smith, Scott A; Fadel, Paul J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 317, No. 2, 01.08.2019, p. H308-H314.

Research output: Contribution to journalArticle

Stephens, Brandi Y. ; Kaur, Jasdeep ; Vranish, Jennifer R. ; Barbosa, Thales C. ; Blankenship, Jeanette K. ; Smith, Scott A ; Fadel, Paul J. / Effect of acute high-phosphate intake on muscle metaboreflex activation and Vascular function. In: American Journal of Physiology - Heart and Circulatory Physiology. 2019 ; Vol. 317, No. 2. pp. H308-H314.
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abstract = "Effect of acute high-phosphate intake on muscle metaboreflex activation and vascular function. Am J Physiol Heart Circ Physiol 317: H308 –H314, 2019. First published May 17, 2019; doi:10.1152/ajpheart.00082.2019.—Increased consumption of inorganic phosphate (Pi), an abundant ingredient in processed foods, has been associated with elevated cardiovascular disease risk; however, studies investigating underlying mechanisms are limited. Recently, high dietary Pi was shown to exaggerate the pressor response to static muscle contraction in rodents in part because of overactiva-tion of metabolically sensitive skeletal muscle afferents. Whether acute high Pi consumption affects muscle metaboreflex activation in humans remains unknown. Furthermore, although acute high Pi consumption has been shown to impair vascular function in young healthy men, equivocal results have been reported. Therefore, we hypothesized that acute high Pi consumption augments mean arterial pressure (MAP) responses during muscle metaboreflex activation, impairs endothelial function, and increases arterial stiffness in young healthy men. Subjects performed 35{\%} maximal voluntary contraction static handgrip (HG), followed by postexercise ischemia (PEI) to isolate muscle metaboreflex activation. Resting flow-mediated dilation (FMD) and arterial stiffness were assessed. Measures were made before (pre) and 60 min after (post) subjects consumed either a high-phosphate drink (2,000 mg phosphorus and 1,520 mg sodium) or a sodium drink (1,520 mg sodium; control). MAP responses during HG (pre = +23 ± 3 mmHg; post = +21 ± 2 mmHg; P = 0.101) and PEI (pre = +21 ± 4 mmHg; post = +18 ± 3 mmHg; P = 0.184) were similar before and after Pi consumption. In contrast, FMD was significantly attenuated following Pi (pre = 5.1 ± 0.5{\%}; post = 3.5 ± 0.5{\%}; P = 0.010), whereas arterial stiffness remained unchanged. There were no changes in any measured variable after control drink consumption. In summary, although the muscle metaboreflex remains unaffected following acute high Pi consumption in young healthy men, endothelial function is impaired. NEW & NOTEWORTHY This study was the first to investigate the influence of acute high-phosphate consumption on the pressor response during isometric handgrip and isolated muscle metaboreflex activation during postexercise ischemia in young healthy humans. We demonstrated that a single high dose of phosphate (2,000 mg) did not augment blood pressure in response to exercise or isolated muscle metaboreflex activation, but endothelial function was blunted in young healthy men.",
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