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APPETITE, OBESITY, DIGESTION, AND METABOLISM
Human Integrative Physiology Laboratory, Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, Virginia
Submitted 15 December 2006 ; accepted in final form 6 January 2007
We tested the hypothesis that modest, overfeeding-induced weight gain would increase sympathetic neural activity in nonobese humans. Twelve healthy males (23 ± 2 years; body mass index, 23.8 ± 0.7) were overfed
1,000 kcal/day until a 5-kg weight gain was achieved. Muscle sympathetic nerve activity (MSNA, microneurography), blood pressure, body composition (dual energy X-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 wk of weight stability at each individual's elevated body weight. Overfeeding increased body weight (73.5 ± 3.1 vs. 78.4 ± 3.2 kg, P < 0.001) and body fat (14.9 ± 1.2 vs. 18 ± 1.1 kg, P < 0.001) in 42 ± 8 days. Total abdominal fat increased (220 ± 22 vs. 266 ± 22 cm2, P < 0.001) with weight gain, due to increases in both subcutaneous (158 ± 15 vs. 187 ± 12 cm2, P < 0.001) and visceral fat (63 ± 8 vs. 79 ± 12 cm2, P = 0.004). As hypothesized, weight gain elicited increases in MSNA burst frequency (32 ± 2 vs. 38 ± 2 burst/min, P = 0.002) and burst incidence (52 ± 4 vs. 59 ± 3 bursts/100 heart beats, P = 0.026). Systolic, but not diastolic blood pressure increased significantly with weight gain. The change in MSNA burst frequency was correlated with the percent increase in body weight (r = 0.59, P = 0.022), change in body fat (r = 0.52, P = 0.043) and percent change in body fat (r = 0.51, P = 0.045). The results of the current study indicate that modest diet-induced weight gain elicits sympathetic neural activation in nonobese males. These findings may have important implications for understanding the link between obesity and hypertension.
adiposity; autonomic nervous system; overfeeding
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