Impaired response of cardiac autonomic nervous system to glucose load in severe obesity

Abstract

Objective This study was undertaken to further analyze the response of the cardiovascular autonomic nervous system (ANS) to changes in plasma insulin concentration induced by an oral glucose load. We hypothesized that, as a consequence of insulin resistance, an inability of insulin to increase the sympathetic modulation of heart rate (HR) and blood pressure (BP) would be observed in normotensive obese patients. Methods We used spectral analysis to measure simultaneously the short-term variability of HR and BP in 23 never-obese subjects and in 70 normotensive overweight or obese patients subdivided into 3 subgroups: (1) overweight group (body mass index [BMI], 25-29.9 kg/m 2), n = 23; (2) class I-II obese group (BMI, 30-39.9 kg/m 2), n = 23; (3) class III obese group (BMI, ≥40 kg/m 2), n = 23. Results Oral glucose ingestion and the related increased insulinemia caused significant changes in the indices of sympathetic modulation (low-frequency [LF] power and LF/high-frequency ratio) of both HR and BP in normal weight, overweight, and obese subjects. However, the LF increments gradually decreased with the BMI classes, suggesting that sympathetic nervous system modulation in these subjects may be insulin-resistant. Conclusion Obesity could develop resistance to the sympatho-excitatory effects of insulin that might play a role in the etiology of obesity. Spectral analysis of BP and HR can be used in research to evaluate the reactivity of the sympathetic nervous system in a manner that represents another feature of the obesity/insulin-resistance syndrome.