This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator. Post exercise hypotension is described as a 5-10 mmHg drop in BP after a single bout of dynamic exercise at 50-60% VO2max elicited after 30-60 min or 75% VO2max for 15- 30 minutes in normotensive men and women. This is due to a persistent rise in vascular conductance and drop in vascular resistance without being offset by a matched increase in Q. PEH is currently attributed to an 'unknown vasodilator.' Additionally, physiological hyperinsulinemia is known to have a vasodilatory effect. This proposal seeks to identify the effects of insulin on post exercise hypotension by using physiological stimulation of insulin secretion, exercise, and pharmacological inhibition of insulin secretion. We postulate that high intensity exercise inhibits insulin secretion leading to a post exercise insulin surge contributing to post exercise hypotension. Accordingly, we will determine achieved hypotension post exercise in a group of normally fit young men and women and relate it to blood insulin concentration. We will then manipulate insulin concentration by infusing a somatostatin analogue, Octreotide, inhibiting insulin secretion, and measure changes in blood pressure. Regression analysis will be used to determine the relationship between blood pressure and insulin concentration. Analysis of variables will be used to determine shifts in blood pressure due to experimental manipulation (octreotide or sham). The Bland-Altman approach will be used to determine repeatability of measurements.
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