Guy E. Alvarez

Sympathetic neural activation in visceral obesity

Background—Muscle sympathetic nerve activity (MSNA) is elevated in obese humans. However, the potential role of abdominal visceral fat as an important adipose tissue depot linking obesity to elevated MSNA has not been explored. Accordingly, we tested the hypothesis that MSNA would be increased in men (age=18 to 40 years, body mass index ≤35 kg/m2) with higher abdominal visceral fat (HAVF; n=13, abdominal visceral fat=118.1±15.8 cm2) compared with their age- (28.7±2.4 versus 25.5±2.0 years, P >0.05), total fat mass-matched (20.6±2.1 versus 20.8±2.4 kg, P >0.05) and abdominal subcutaneous fat-matched (230.6±24.9 versus 261.4±34.8 cm2, P >0.05) peers with lower abdominal visceral fat levels (LAVF; n=13, visceral fat= 73.0±6.0 cm2). Methods and Results—MSNA (microneurography), body composition (dual energy x-ray absorptiometry), and abdominal visceral and subcutaneous fat (computed tomography) were measured in 37 sedentary men across a wide range of adiposity. MSNA was ≈55% higher in men with HAVF compared with men with LAVF (33±4 versus 21±2 bursts/min, P <0.05). Furthermore, MSNA was more closely associated with the level of abdominal visceral fat (r =0.65, P <0.05) than total fat mass (r =0.323, P <0.05) or abdominal subcutaneous fat (r =0.27, P =0.05). The relation between MSNA and abdominal visceral fat was independent of total body fat (r =0.61, P <0.05). Conclusions—The results of our study indicate that MSNA is elevated in men with visceral obesity. Our observations are consistent with the idea that abdominal visceral fat is an important adipose tissue depot linking obesity with sympathetic neural activation in humans. Furthermore, these findings may have important implications for understanding the increased risk of developing cardiovascular diseases in individuals with visceral obesity.