Autonomic and Hemodynamic Responses to Insulin in Lean and Obese Humans

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Abstract
To study the acute effects of insulin on autonomic control of cardiac function, we performed spectral analysis of heart rate variability and measured cardiac dynamics (by two-dimensional echocardiography) in 18 obese (BMI = 35 ± 1 kg · m-2) and 14 lean (BMI = 24 ± 1 kg · m-2) subjects in the basal state and in response to physiological hyperinsulinemia (1 mU · min-1 · kg-1 insulin clamp). In the lean group, insulin promptly (within 20 min) and consistently depressed spectral powers, both in the low-frequency and high-frequency range. These changes were twice as large as accounted for by the concomitant changes in heart rate (68 ± 2 to 70 ± 2 beats/min). At the end of the 2-h clamp, stroke volume (67 ± 4 to 76 ± 9 ml · min-1) and cardiac output (4.45 ± 0.21 to 5.06 ± 0.55 l·min-1) rose, whereas peripheral vascular resistance fell. The low-to-high frequency ratio increased from 1.7 ± 0.2 to 2.3 ± 0.3 (P < 0.01), indicating sympathetic shift of autonomic balance. In the obese group, all basal spectral powers were significantly lower (by 40% on average) than in the lean group, and were further reduced by insulin administration. The low-to-high frequency ratio was higher than in controls at baseline (2.4 ± 0.4, P < 0.03), and failed to increase after insulin (2.2 ± 0.3, P = ns). Furthermore, obesity was associated with higher resting stroke volume (89 ± 5 vs. 67 ± 4 ml · min- 1, P < 0.01) and cardiac output (6.01 ± 0.31 vs. 4.45 ± 0.21 l · min- 1, P = 0.001) but lower peripheral vascular resistance (15.1 ± 0.8 vs. 19.2 ± 1.1 mmHg · min · L-1, P = 0.002), whereas mean arterial blood pressure was similar to control (90 ± 2 vs. 86 ± 2 mmHg, P = not significant). We conclude that physiological hyperinsulinemia causes acute desensitization of sinus node activity to both sympathetic and parasympathetic stimuli, sympathetic shift of autonomic balance, and a high-output, low-resistance hemodynamic state. In the obese, these changes are already present in the basal state, and may therefore be linked with chronic hyperinsulinemia

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