Insulin Sensitivity Regulates Autonomic Control of Heart Rate Variation Independent of Body Weight in Normal Subjects1

• Published in: The journal of clinical endocrinology and metabolism Vol. 86; no. 3; pp. 1403 - 1409
• Main Authors: Bergholm, R., Westerbacka, J., Vehkavaara, S., Seppälä-Lindroos, A., Goto, T., Yki-Järvinen, H.
• Format: Journal Article
• Language: English
• Published: Endocrine Society 01-03-2001
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jcem.86.3.7307

It is unclear whether insulin sensitivity independent of body
weight regulates control of heart rate variation (HRV) by the autonomic
nervous system.
Insulin action on whole-body glucose uptake (M-value) and heart rate
variability were measured in 21 normal men. The subjects were divided
into 2 groups [normally insulin sensitive (IS, 8.0 ± 0.4
mg/kg·min) and less insulin sensitive (IR, 5.1 ± 0.3
mg/kg·min)] based on their median M-value (6.2 mg/kg·min).
Spectral power analysis of heart rate variability was performed in the
basal state and every 30 min during the insulin infusion.
The IS and IR groups were comparable, with respect to age (27 ± 2
vs. 26 ± 2 yr), body mass index (22 ±
1 vs. 23 ± 1 kg/m2), body fat (13±
1 vs. 13 ± 1%), systolic (121 ± 16
vs. 117 ± 14 mm Hg) and diastolic (74 ± 11
vs. 73 ± 11 mm Hg) blood pressures, and fasting
plasma glucose (5.4 ± 0.1 vs. 5.5 ± 0.1
mmol/L) concentrations. Fasting plasma insulin was significantly higher
in the IR (30 ± 4 pmol/L) than in the IS (17 ± 3 pmol/L,
P < 0.05) group. In the IS group, insulin
significantly increased the normalized low-frequency (LFn) component, a
measure of predominantly sympathetic nervous system activity, from
36 ± 5 to 48 ± 4 normalized units (nu; 0 vs.
30–120 min, P < 0.001); whereas the normalized
high-frequency (HFn) component, a measure of vagal control of HRV,
decreased from 66 ± 9 to 48 ± 5 nu (P< 0.001). No changes were observed in either the normalized LF
component [35 ± 5 vs. 36 ± 2 nu, not
significant (NS)] or the normalized HF component (52 ± 6
vs. 51 ± 4 nu, NS) in the IR group. The ratio
LF/HF, a measure of sympathovagal balance, increased significantly in
the IS group (0.92 ± 0.04 vs. 1.01 ± 0.04,
P < 0.01) but remained unchanged in the IR group
(0.91 ± 0.04 vs. 0.92 ± 0.03, NS). Heart
rate and systolic and diastolic blood pressures remained unchanged
during the insulin infusion in both groups.
We conclude that insulin acutely shifts sympathovagal control of HRV
toward sympathetic dominance in insulin-sensitive, but not in
resistant, subjects. These data suggest that sympathetic overactivity
is not a consequence of hyperinsulinemia.