No agreement exists as to the mechanisms responsible for the sympathetic hyperactivity characterizing human
obesity, which has been ascribed recently to a chemoreflex stimulation brought about by
obstructive sleep apnea rather than to an increase in
body weight, per se. In 86 middle-age normotensive subjects classified according to body mass index, waist-to-hip ratio, and
apnea/hypopnea index (overnight polysomnographic evaluation) as lean and obese subjects without or with
obstructive sleep apnea, we assessed via microneurography muscle sympathetic nerve traffic. The 4 groups were matched for age, gender, and blood pressure values, the 2 obese groups with and without
obstructive sleep apnea showing a similar increase in body mass index (32.4 versus 32.0 kg/m2, respectively) and waist-to-hip ratio (0.96 versus 0.95, respectively) compared with the 2 lean groups with or without
obstructive sleep apnea (body mass index 24.3 versus 23.8 kg/m2 and waist-to-hip ratio 0.77 versus 0.76, respectively; P<0.01). Compared with the nonobstructive
sleep apnea lean group, muscle sympathetic nerve activity showed a similar increase in the
obstructive sleep apnea lean group and in the nonobstructive
sleep apnea obese group (60.4+/-2.3 and 59.3+/-2.0 versus 40.9+/-1.8 bs/100 hb, respectively; P<0.01), a further increase being detected in
obstructive sleep apnea subjects (73.1+/-2.5 bursts/100 heart beats; P<0.01). Our data demonstrate that the sympathetic activation of
obesity occurs independently in
obstructive sleep apnea. They also show that this condition exerts sympathostimulating effects independent of
body weight, and that the
obstructive sleep apnea-dependent and -independent sympathostimulation contribute to the overall
adrenergic activation of the obese state.