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Given these divergent actions, the \u201cnet effect\u201d of insulin on the transduction of muscle sympathetic nerve activity (MSNA) into vasoconstriction and thus, blood pressure (BP) remains unclear. We hypothesized that sympathetic transduction to BP would be attenuated during hyperinsulinemia compared with baseline. In 22 young healthy adults, MSNA (microneurography), and beat-to-beat BP (Finometer or arterial catheter) were continuously recorded, and signal-averaging was performed to quantify the mean arterial pressure (MAP) and total vascular conductance (TVC; Modelflow) responses following spontaneous bursts of MSNA at baseline and during a euglycemic-hyperinsulinemic clamp. Hyperinsulinemia significantly increased MSNA burst frequency and mean burst amplitude (baseline: 46\u2009\u00b1\u20096 au; insulin: 65\u2009\u00b1\u200916 au, P &lt; 0.001) but did not alter MAP. The peak MAP (baseline: 3.2\u2009\u00b1\u20091.5 mmHg; insulin: 3.0\u2009\u00b1\u20091.9 mmHg, P = 0.67) and nadir TVC ( P = 0.45) responses following all MSNA bursts were not different between conditions indicating preserved sympathetic transduction. However, when MSNA bursts were segregated into quartiles based on their amplitudes at baseline and compared with similar amplitude bursts during hyperinsulinemia, the peak MAP and TVC responses were blunted (e.g., largest burst quartile: MAP, baseline: \u03944.4\u2009\u00b1\u20091.7 mmHg; hyperinsulinemia: \u03943.0\u2009\u00b1\u20090.8 mmHg, P = 0.02). Notably, \u223c15% of bursts during hyperinsulinemia exceeded the size of any burst at baseline, yet the MAP\/TVC responses to these larger bursts (MAP, \u03944.9\u2009\u00b1\u20091.4 mmHg) did not differ from the largest baseline bursts ( P = 0.47). These findings indicate that increases in MSNA burst amplitude contribute to the overall maintenance of sympathetic transduction during hyperinsulinemia. <\/jats:p>","DOI":"10.1152\/ajpregu.00162.2022","type":"journal-article","created":{"date-parts":[[2023,2,20]],"date-time":"2023-02-20T13:05:52Z","timestamp":1676898352000},"page":"R536-R546","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":5,"title":["Sympathetic transduction to blood pressure during euglycemic-hyperinsulinemia in young healthy adults: role of burst amplitude"],"prefix":"10.1152","volume":"324","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0239-005X","authenticated-orcid":false,"given":"Benjamin E.","family":"Young","sequence":"first","affiliation":[{"name":"Department of Kinesiology, University of Texas at Arlington, Arlington, Texas, United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7944-4936","authenticated-orcid":false,"given":"Jaume","family":"Padilla","sequence":"additional","affiliation":[{"name":"Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri, United States"},{"name":"Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6794-5979","authenticated-orcid":false,"given":"J. 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