Introduction: Obesity can be associated with hypertension (HTN), which is a major risk factor for cardiovascular disease. Impaired autonomic function: an attenuated baroreflex sensitivity (BRS), which leads to a diminished ability to modulate blood pressure [i.e., augmented blood pressure (BP) variability (BPV)] and elevated muscle sympathetic nerve activity (MSNA), has been demonstrated in adults with HTN, but whether normotensive adults with obesity exhibit impaired autonomic function, is equivocal. We tested the hypothesis that BPV, MSNA and BRS will be impaired in normotensive adults with obesity (Ob) compared with adults without obesity (NOb). Methods: Thirty-five participants (Ob: n=5f/11m; NOb: n=13f/6m) underwent assessments of resting beat-to-beat BP, heart rate (HR), and microneurography of the fibular or radial nerve to measure MSNA for 5-10 min in the supine position. Females were assessed in the early follicular phase or placebo phase with oral contraceptives (n=5) of their menstrual cycle. Average real variability (ARV) as a novel index of short-term BPV was calculated for BP variables. MSNA was quantified as burst frequency (BF; bursts/min) and burst incidence (BI; bursts/100 heartbeats, Hb). Cardiac BRS (cBRS; Ob; n=15, NOb; n=19) was quantified to determine the slope of the relationship between systolic BP and R-R intervals. Sympathetic BRS (sBRS; Ob; n=13, NOb; n=15) was quantified as the slope of the relationship between diastolic BP and MSNA. Results: The Ob group had an elevated body mass index (Ob: 31.7±1.9 vs. NOb: 23.2±1.5 kg/m2, p <0.001), but was similar in age (Ob: 29±6 vs. NOb: 33±9 yrs, p =0.21) to the NOb group. Both groups had similar levels of systolic BP (Ob: 115±11 vs. NOb: 111±9 mmHg, p =0.23), diastolic BP (Ob: 71±5 vs. NOb: 71±8 mmHg, p =0.82) and HR (Ob: 60±8 vs. NOb: 61±9 b/min, p =0.28). ARV was similar between groups for systolic BP (Ob: 1.7±0.4 vs. NOb: 1.6±0.4 mmHg, p =0.42) and diastolic BP (Ob: 1.5±0.8 vs. NOb: 1.2±1.1 mmHg, p =0.45). MSNA BF (Ob: 17±7 vs. NOb: 18±6 bursts/min, p=0.59), MSNA BI (Ob: 29±15 vs. NOb: 29±7 bursts/100Hb, p =0.96) and cBRS (Ob: 18.7±17.3 vs. NOb: 17.1±18.6 ms/mmHg, p =0.65) were similar between groups. However, sBRS was attenuated in the Ob compared with the NOb group (Ob: -1.5±0.9 vs. NOb: -2.6±2.0 bursts/100Hb/mmHg, p <0.001). An association was observed between sBRS and ARV of diastolic BP in the whole cohort ( r =0.46, p =0.01), but not when stratified by group. Conclusion: Our results indicate an altered sBRS, but not MSNA and ARV, in normotensive adults with obesity. Further, independent of obesity, we observed that adults who had the lowest sBRS had the greatest diastolic ARV. These findings are important because reduced sBRS may lead to augmented BPV and subsequently, obesity-related hypertension, which may further our understanding of cardiovascular dysregulation in normotensive adults with obesity. NIH (R01HL118313, D.W.W.; K01AG064038 & R21AG080503, M.L.K.R.) and the U.S. Department of Veterans Affairs (I01RX001311, D.W.W.; IK2RX003670, to K.B.). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
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