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OBJECTIVE: Low sodium intake may trigger sympathetic nervous system (SNS) activation and endothelial dysfunction. Studies have not explored these associations along the glucose continuum. Accordingly, we compared endothelial function and SNS activity in individuals with low sodium intake and differing categories of metabolic risk along the glucose continuum. We hypothesized that low sodium intake is associated with (1) impairment of endothelial function and (2) higher SNS activity in individuals with higher metabolic risk. RESEARCH DESIGN AND METHODS: In this prospective observational study, participants (n=54) with low sodium intake (single 24 hours urine sodium excretion <150 mmol/24 hours) were categorized based on oral glucose tolerance testing as: normal glucose tolerance (NGT, n=10), impaired glucose tolerance (IGT, n=15), treatment naive type 2 diabetes (T2D-) (n=12) or treated type 2 diabetes (T2D+) (n=17). We assessed endothelial function using pulse amplitude tonometry (PAT) derived reactive hyperemic index and PAT ratio; arterial stiffness via augmentation index; muscle sympathetic nerve activity (MSNA) using microneurography; cardiac baroreflex; heart rate; blood pressure; glycosylated hemoglobin A1c (HbA1c) and lipid profile. RESULTS: Mean (SD) sodium excretion was 110.6 (26) mmol/24 hours. Compared with NGT, IGT and T2D-, the T2D+ group had lower MSNA (p=0.005), PAT ratio (p=0.04) and baroreflex sensitivity (p=0.0002) and an augmented heart rate (p=0.02). The T2D+ group had appropriate mean (SD) glycemic (HbA1c 7.2 (1.72)%), total cholesterol (4.2 (1.0) mmol/L), low-density lipoprotein (2.2 (1.0) mmol/L) and blood pressure (systolic 136 (13), diastolic 78 (12)) (mm Hg) control. CONCLUSIONS: Individuals with T2D+ have impaired endothelial and baroreflex function, despite low sodium intake, appropriately managed cardiometabolic risk factors and lower SNS activity, compared with others along the glucose continuum. Whether low sodium intake is associated w

Acute slow breathing may have beneficial effects on cardiovascular regulation by affecting hemodynamics and the autonomic nervous system. Whether breathing at the resonance frequency (RF), a breathing rate that maximizes heart rate oscillations, induces differential effects to that of slow breathing is unknown. We compared the acute effects of breathing at either RF and RF + 1 breaths per minute on muscle sympathetic nervous activity (MSNA) and baroreflex function. Ten healthy men underwent MSNA, blood pressure (BP), and heart rate (HR) recordings while breathing for 10 min at their spontaneous breathing (SB) rate followed by 10 min at both RF and RF + 1 randomly assigned and separated by a 10‐min recovery. Breathing at either RF or RF + 1 induced similar changes in HR and HR variability, with increased low frequency and decreased high frequency oscillations (p < .001 for both). Both respiration rates decreased MSNA (−5.6 and −7.3 bursts per min for RF and RF + 1 p < .05), with the sympathetic bursts occurring more often during mid‐inspiration to early expiration (+57% and + 80%) and longer periods of silence between bursts were seen (p < .05 for RF + 1). Systolic BP was decreased only during RF (−4.6 mmHg, p < .05) but the decrease did not differ to that seen during RF + 1 (−3.1 mmHg). The sympathetic baroreflex function remained unchanged at either breathing rates. The slope of the cardiac baroreflex function was unaltered but the cardiac baroreflex efficiency was improved during both RF and RF + 1. Acute breathing at either RF or RF + 1 has similar hemodynamic and sympatho‐inhibitory effects in healthy men.

OBJECTIVE: Excess adiposity increases the risk of type-2 diabetes and cardiovascular disease development. Beyond the simple level of adiposity, the pattern of fat distribution may influence these risks. We sought to examine if higher android fat distribution was associated with different hemodynamic, metabolic or vascular profile compared to a lower accumulation of android fat deposits in young overweight males. METHODS: Forty-six participants underwent dual-energy X-ray absorptiometry and were stratified into two groups. Group 1: low level of android fat (<9.5%) and group 2: high level of android fat (>9.5%). Assessments comprised measures of plasma lipid and glucose profile, blood pressure, endothelial function [reactive hyperemia index (RHI)] and muscle sympathetic nerve activity (MSNA). RESULTS: There were no differences in weight, BMI, total body fat and lean mass between the two groups. Glucose tolerance and insulin resistance (fasting plasma insulin) were impaired in group 2 (p < 0.05). Levels of plasma triglycerides and 5 lipid species were higher in group 2 (p < 0.05). Endothelial function was less in group 2 (RHI: 1.64 vs. 2.26, p = 0.003) and heart rate was higher (76 vs. 67 bpm, p = 0.004). No difference occurred in MSNA nor blood pressure between the 2 groups. CONCLUSION: Preferential fat accumulation in the android compartment is associated with increased cardiovascular and metabolic risk via alteration of endothelial function.