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.

The influence of excess total and abdominal adiposity on cardiovagal baroreflex gain remains unclear. We tested the hypotheses that cardiovagal baroreflex gain would be reduced in men with 1) higher [higher fat (HF), mass >20 kg, n = 11] compared with lower [lower fat (LF), mass <20 kg, n = 10] levels of total body and abdominal fat and 2) higher abdominal visceral fat (HAVF; n = 10) compared with total body weight- and subcutaneous fat-matched peers with lower abdominal visceral fat (LAVF; n = 7) levels. To accomplish this, we measured cardiovagal baroreflex gain (modified Oxford technique), body composition (dual energy X-ray absorptiometry), and abdominal visceral and subcutaneous fat (computed tomography) in sedentary men (age, 18–40 yr; body mass index, <34.9 kg/m2) across a wide range of adiposity. Cardiovagal baroreflex gain was significantly lower in HF compared with LF (14.3 ± 2.8 vs. 21.4 ± 2.8 ms/mmHg, respectively). In addition, cardiovagal baroreflex gain was lower in HAVF compared with LAVF (13.0 ± 2.0 vs. 21.4 ± 3.6 ms/mmHg, P< 0.05). Therefore, the results of the present study indicate that cardiovagal baroreflex gain is reduced in men with elevated total body and abdominal fat mass. The reduced cardiovagal baroreflex gain in these individuals appears to be linked to their higher level of abdominal visceral fat. Importantly, reduced cardiovagal baroreflex gain may contribute to the increased risk of cardiovascular disease observed in men with the metabolic syndrome.

We tested the hypothesis that muscle sympathetic nerve activity (MSNA) would not differ in subcutaneously obese (SUBOB) and nonobese (NO) men with similar levels of abdominal visceral fat despite higher plasma leptin concentrations in the former. We further hypothesized that abdominal visceral fat would be the strongest body composition- or regional fat distribution-related correlate of MSNA among these individuals. To accomplish this, we measured MSNA (via microneurography), body composition (via dual-energy X-ray absorptiometry), and abdominal fat distribution (via computed tomography) in 15 NO (body mass index 0.05, respectively) despite approximately 2.6-fold higher (P < 0.05) plasma leptin concentration in the SUBOB men. Furthermore, abdominal visceral fat was the only body composition- or regional fat distribution-related correlate (r = 0.45; P < 0.05) of MSNA in the pooled sample. In addition, abdominal visceral fat was related to MSNA in NO (r = 0.58; P = 0.0239) but not SUBOB (r = 0.39; P = 0.3027) men. Taken together with our previous observations, our findings suggest that the relation between obesity and MSNA is phenotype dependent. The relation between abdominal visceral fat and MSNA was evident in NO but not in SUBOB men and at levels of abdominal visceral fat below the level typically associated with elevated cardiovascular and metabolic disease risk. Our observations do not support an obvious role for leptin in contributing to sympathetic neural activation in human obesity and, in turn, are inconsistent with the concept of selective leptin resistance.

We tested the hypothesis that women would demonstrate lower cardiovagal baroreflex gain compared with men. If so, we further hypothesized that the lower cardiovagal baroreflex gain in women would be associated with their lower aerobic fitness and higher body fat percentage compared with men. To accomplish this, we measured cardiovagal baroreflex gain (modified Oxford technique) in sedentary, nonobese (body mass index < 25 kg/m2) men (age = 26.0 +/- 2.1 yr, n = 11) and women (age = 26.9 +/- 1.6 yr, n = 14). Resting R-R interval and diastolic blood pressure were similar in the two groups, but systolic blood pressure was lower (P < 0.05) in the women. Cardiovagal baroreflex gain was significantly lower in the women compared with the men (13.3 +/- 1.5 vs. 20.0 +/- 2.8 ms/mmHg, P < 0.05). The lower cardiovagal baroreflex gain in the women was not related (P > 0.05) to their lower aerobic fitness and was only marginally related to their higher body fat percentage (r = -0.34, P < 0.05). There were no gender differences in the threshold and saturation, operating range, or operating point (all P > 0.05), although the operating point fell significantly to left (i.e., at a lower systolic blood pressure) compared with men. Therefore, the findings of this study suggest that the gain of the cardiovagal baroreflex is reduced whereas other parameters were similar in women compared with men. The mechanisms responsible for the reduced cardiovagal baroreflex gain remain unclear.

The results from this study indicate that ADP is a valid measure of body composition in female athletes and nonathletes when compared with DXA.