Thermoregulatory sympathetic nervous system activity and diet‐induced waist‐circumference reduction in obese Japanese women

The present study is designed to investigate how and to what extent sympathovagal behavior in a balanced low-calorie diet relates to favorable changes of body mass, waist circumference, and/or metabolic risk factors. The study involved 28 mildly obese women without clinical complications, who underwent an 8-week calorie restriction program using a 1,200-kcal daily diet with an adequate nutrient content; including two regular meals, and one formula meal replacement. All subjects were examined before and after the dietary intervention. We measured anthropometric parameters, blood pressure, and biochemical blood profiles for lipid metabolism. Autonomic nervous system activity was evaluated by heart rate variability power spectral analysis. The dietary intervention induced moderate, but significant reduction of waist circumference (−5.3% ± 0.8%), body fat percentage (−5.8% ± 0.8%), and body mass (−6.6% ± 0.5%). Linear regression analysis showed that Δvery low frequency (VLF) power reflecting energy metabolic- and thermoregulatory sympathetic function significantly correlated to Δwaist circumference (r = −0.53, P < 0.01), Δbody fat percentage (r = −0.39, P < 0.05), Δbody mass (r = −0.43, P < 0.05), ΔHDL-cholesterol/total cholesterol ratio (HDL-C/TC) (r = 0.62, P < 0.001), and Δnonesterified fatty acids (NEFA) (r = 0.56, P < 0.01). A stepwise multiple regression analysis additionally revealed that Δwaist circumference (P = 0.024), ΔHDL-C/TC (P = 0.013), and ΔNEFA (P = 0.016) were significant and independent factors, which contributing to the variance in ΔVLF power (r2 = 0.61). Although causes and consequences of obesity continue to elude researchers, the present study indicates that thermoregulatory sympathetic activity relates to moderate waist-circumference reduction together with favorable changes of blood lipid profiles after short-term dietary modification in mildly obese women. Am. J. Hum. Biol. 2009. © 2009 Wiley-Liss, Inc.