Sympathetic vasoconstrictor response to lower body negative pressure in young obese adults: the preliminary finding
Results: No differences in age (39+/-9 v 39+/-9 years P 0.87) or BMI (24.85+/-3.29 v 25.75+/-3.68 kg.m 2 P 0.24) were observed. No differences in IVSd (0.86+/-0.15 v 0.85+/-0.18 cm P 0.64), LVIDd (4.98+/-0.55 v 4.96+/-0.42 cm P 0.95), LVPWd (0.81+/-0.17 v 0.90+/-0.21 cm P 0.05) or LV Mass (168.86+/-56.85 v 182.61+/-61.70 g P 0.43) were observed. However, MV E/A (1.85+/-0.51 v 1.48+/-0.51 P 0.0004), but not LV IVRT (0.09+/-0.02 v 0.09+/-0.01 P 0.25), was different. Conclusions: Changes in
... : Changes in cardiac function are observed before alterations in cardiac structure in healthy subjects with premature vascular stiffening. References 1. Mansour AS, YannoutsosA, MajahalmeN, AgnolettiD, Safar ME, OuerdaneS, BlacherJ. Aortic stiffness and cardiovascular risk in type 2 diabetes. Background: Elevations in muscle sympathetic nerve activity (MSNA) and sympathetic vasoconstrictor responsiveness to sympathoexcitation are associated with increased cardiovascular risks, which affect hemodynamics, and have been reported in obese adults with metabolic syndrome (1-3). It remains unclear whether this observation may also be present in young metabolically healthy obese adults. Purpose: To compare sympathetic vasoconstrictor and hemodynamic responsiveness to lower body negative pressure (LBNP, -20 mmHg) in young normal-weight (NW) vs. obese (OB) adults. Method: Eleven NW (femaleZ6; 25AE2 yrs; 22.4AE0.6 kg/m2) and 13 OB adults (femaleZ6; 27AE1 yrs; 32.7AE0.6 kg/m2) underwent 2-min of LBNP in the supine position. Ultrasonography [brachial diameter, forearm blood flow (FBF), forearm vascular conductance (FVC)], MSNA [burst frequency, total MSNA, sympathetic vascular transduction], and beat-to-beat hemodynamics [heart rate (HR), mean arterial pressure (MAP), total peripheral resistance (TPR), cardiac output (CO), stroke volume (SV), systemic compliance (SC)] were reported. FBF and FVC were normalized to lean forearm mass, and TPR, CO, SV, and SC to body surface area. Results: Baseline MAP was lower in OB (P<0.05). In response to LBNP, normalized FBF, FVC, SV, CO, and SC decreased whereas TPR increased similarly in both groups (P<0.05). Brachial diameter and HR did not change in both groups. MAP decreased similarly by w2-4 mmHg, but the values were lower in the OB group (P<0.05). Burst frequency, total MSNA, and sympathetic vascular transduction increased similarly in both groups (P<0.05). Conclusion: Young metabolically healthy obese adults did not exhibit altered sympathetic vasoconstrictor responsiveness under resting condition. References 1. Straznicky NE, Grima MT, Sari CI, Eikelis N, Lambert EA, Nestel PJ, et al. Neuroadrenergic dysfunction along the diabetes continuum: a comparative study in obese metabolic syndrome subjects. Diabetes. 2012; 61(10): 2506-16. 2. Huggett RJ, Burns J, Mackintosh AF, Mary DA. Sympathetic neural activation in nondiabetic metabolic syndrome and its further augmentation by hypertension. Hypertension. 2004; 44(6):847-52. 3. Kuniyoshi FH, Trombetta IC, Batalha LT, Rondon MU, Laterza MC, Gowdak MM, et al. Abnormal neurovascular control during sympathoexcitation in obesity. Obesity research. 2003; 11(11):1411-9.