Human obesity is characterized by profound alterations in the hemodynamic and metabolic states. Whether these alterations involve sympathetic drive is controversial. In 10 young obese subjects (body mass index, 40.5 +/- 1.2 kg/m2, mean +/- SEM) with normal blood pressure and 8 age-matched lean normotensive control subjects, we measured beat-to-beat arterial blood pressure (Finapres technique), heart rate (electrocardiogram), postganglionic muscle sympathetic nerve activity (microneurography at the peroneal nerve), and venous plasma norepinephrine (high-performance liquid chromatography). The measurements were performed in baseline conditions and, with the exception of plasma norepinephrine, during baroreceptor stimulation and deactivation caused by increases and reductions of blood pressure via intravenous infusions of phenylephrine and nitroprusside. Baseline blood pressure and heart rate were similar in obese and control subjects. Plasma norepinephrine was also similar in the two groups. Muscle sympathetic nerve activity, however, was 38.6 +/- 5.1 bursts per minute in obese subjects and less than half that level in control subjects (18.7 +/- 1.3 bursts per minute), the difference being highly statistically significant (P < .02). Muscle sympathetic nerve activity and heart rate were reduced during phenylephrine infusion and increased during nitroprusside infusion, but the changes were about half as great in obese subjects as in control subjects. Thus, even in the absence of any blood pressure alteration, human obesity is characterized by a marked sympathetic activation, possibly because of an impairment of reflex sympathetic restraint. This may be involved in the high rate of hypertension and cardiovascular complications seen in obesity.

OBJECTIVE: Conventional body composition methods may produce biased quanti®cation of fat and fat-free mass in obese subjects, due to possible violation of the assumption of constant (73%) tissue hydration. We used an assumption-free, graphical method for interpreting body weight variation in obesity using bioelectrical measurements. DESIGN: 540 obese subjects with body mass index (BMI) b 31 kgam 2 without apparent edema were compared to 726 healthy subjects with BMI`31 kgam 2 and to 50 renal patients with apparent edema. A subgroup of 48 obese subjects were evaluated again after weight loss (8.6 kg, 3 BMI units) following one-month energy restriction (5 MJad, 1200 kcalad). 32 obese uremic patients were evaluated before and after a dialysis session (3.2 kg¯uid removed). Direct measurements obtained from standard 50 kHz frequency bioelectrical impedance analyzer were used as impedance vectors in the Resistance-Reactance Graph. RESULTS: 1) Impedance vectors of obese subjects could be discriminated from those of edematous patients with 91% correct allocation; 2) A signi®cant lengthening of vectors was observed after¯uid loss of 3 kg in obese subjects; but 3) A body weight loss of about 9 kg after energy restriction was associated with no vector displacement. CONCLUSION: A different impedance vector pattern was associated with body weight loss in obesity due to¯uid removal (vector lengthening) versus an energy-restricted diet (no vector displacement).

This study investigates motor (MNCS) and sensory (SNCS) nerve conduction in a sample of non-diabetic obese people without symptoms suggestive of neuropathy and looks for a possible metabolic alteration. Twenty-one patients and 20 age-matched controls underwent (a) MNCS (median, ulnar, peroneal, and tibial) and SNCS (median, ulnar, and sural); (b) quantitative sensory testing to measure sensory threshold for vibration, warm and cold sensation (WS-CS), heat and cold-induced pain; and (c) blood sample analysis to evaluate glucose and insulin levels and calculate the quantitative insulin-sensitivity check index (QUICKI). The obese group showed significantly decreased compound muscle action potential amplitude of tibial and peroneal nerves and decreased sensory action potential amplitude of all nerves. Most of the sensory thresholds were altered in obese patients. Insulin serum levels were significantly increased while QUICKI decreased in obese patients. WS and CS from the index and little fingers and WS from the big toe significantly correlated with QUICKI. Thermal and pain thresholds from the index and thermal thresholds from the little finger correlated with QUICKI values. The non-diabetic obese patients showed a subclinical involvement of different diameter sensory fibers. Such impairment was related to hyperinsulinemia and insulin sensitivity. The increase in sensory threshold of obese patients might be due to a metabolic alteration, potentially leading to a future clinical neuropathy.