The Effect of Acute High Phosphate Intake on Muscle Metaboreflex Activation and Vascular Function.

Abstract

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 due, in part, to overactivation 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 post-exercise ischemia (PEI) to isolate muscle metaboreflex activation. Resting flow-mediated dilation (FMD) and arterial stiffness were assessed. Measures were made before (pre) and 60 minutes 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.