Sympathetic Activation in Obese Normotensive Subjects

TLDR

Human obesity involves significant hemodynamic and metabolic changes, yet the contribution of sympathetic activation remains debated. The authors compared 10 obese normotensive subjects with 8 lean controls by measuring beat‑to‑beat blood pressure, heart rate, muscle sympathetic nerve activity, and plasma norepinephrine at baseline and during baroreceptor manipulation with phenylephrine and nitroprusside. Obese subjects exhibited markedly higher muscle sympathetic nerve activity than controls despite similar blood pressure, heart rate, and plasma norepinephrine, and their sympathetic responses to baroreceptor manipulation were blunted, indicating obesity‑associated sympathetic over‑activation that may underlie hypertension risk.

Abstract

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.