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/m ² , 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.

Four hundred million adults are obese. Such a pandemic involves people of working age. Excess weight imposes abnormal mechanics on body movements, which could account for the high incidence of musculoskeletal disorders in these subjects. This article reviews the physiological and biomechanical causes of the reduced work capacity in obese workers and speculates on the relationships between occupational exposure and obesity. The reduction in work capacity appears to be due to the following factors: reduced spine flexibility, decay in endurance, limited range of movement of the major joints, reduced muscle strength and capacity to hold prolonged fixed postures, impaired respiratory capacity and visual control. Work capacity in morbidly obese workers should always be evaluated to match specific job demands. Due to the relationship between obesity, musculoskeletal disorders, disability and health costs, prevention of obesity and ergonomic interventions on-site are a priority in the work place.