The Effect of Acute High Phosphate Intake on Muscle Metaboreflex Activation in Young, Healthy Men
Authors: Stephens Brandi Y. , Kaur Jasdeep , Vranish Jennifer R. , Barbosa Thales C. , Johnson Auburn L. , Blankenship Jeanette K. , Vongpatanasin Wanpen , Smith Scott A. , Fadel Paul J. 
Published: June 2021

Emerging evidence suggests that long term high consumption of inorganic phosphate (Pi) is associated with an increased risk of cardiovascular disease. Importantly, over the last 20 years, with the growing abundance of processed foods, dietary intake of Pi in the United States has doubled the daily‐recommended amount. Recently, Mizuno et al. demonstrated that chronic high dietary Pi consumption results in significantly exaggerated increases in mean arterial pressure (MAP) and renal sympathetic nerve activity in response to muscle metaboreflex activation in Sprague‐Dawley rats. Whether acute high Pi consumption can affect the muscle metaboreflex in humans remains unknown. Notably, acute high Pi intake has been shown to impair endothelial function in otherwise healthy subjects, but a recent study does not support this finding. Therefore, the goal of this research was to investigate whether acute high Pi consumption affects muscle metaboreflex activation and endothelial function in humans. We hypothesized that acute high Pi consumption augments the pressor response during muscle metaboreflex activation and attenuates endothelial function in young, healthy men. To investigate, subjects participated in two protocols performed on separate days: 1) Monosodium Phosphate (NaPi) containing 2,000 mg of phosphorus and 1,520 mg of sodium (N= 13; 23 ± 1 yrs; mean ± SEM) and 2) Sodium Chloride (NaCl) control containing 1,520 mg of sodium (N=5; 23 ± 2 yrs). On each study day, endothelial function was assessed via brachial artery flow‐mediated dilation (FMD), and blood was drawn to measure baseline serum phosphate. Subjects then performed static handgrip at 35% maximal voluntary contraction for 2 minutes, followed by post‐exercise ischemia (PEI), to isolate muscle metaboreflex activation. The subjects then ingested either NaPi or NaCl. After 60 minutes, FMD and PEI were repeated and blood was drawn at 60 and 120 min post‐ NaPi and NaCl ingestion. Serum phosphate was significantly elevated at 60 min (baseline, 3.2 ± 0.2 mg/dL; 60 min, 4.5 ± 0.2 mg/dL; p<0.01) and 120 min (4.9 ± 0.3 mg/dL; p<0.01) post‐ NaPi consumption, but did not change with NaCl consumption (p=0.51). Resting blood pressure was unaffected by NaPi (p=0.88), and NaCl (p=0.40). Likewise, metaboreflex‐induced increases in MAP were not different following NaPi (pre, Δ 20.9 ± 4.1; post, Δ 17.9 ± 2.9; p=0.84) or NaCl (pre, Δ 20.9± 3.7; post Δ 18.5 ± 1.9; p=0.94). In contrast, FMD was significantly attenuated after NaPi ingestion, (pre, 5.4± 0.6%; post, 3.1 ± 0.5%; p<0.01) but did not change following NaCl ingestion (p=0.97). In summary, acute high NaPi consumption did not affect muscle metaboreflex responses in young, healthy men, whereas endothelial function was impaired. These data suggest that the peripheral vasculature is vulnerable to acute NaPi consumption in young healthy men.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.