R. Bergholm et al., Insulin sensitivity regulates autonomic control of heart rate variation independent of body weight in normal subjects, J CLIN END, 86(3), 2001, pp. 1403-1409
It is unclear whether insulin sensitivity independent of body weight regula
tes control of heart rate variation (HRV) by the autonomic nervous system.
Insulin action on whole-body glucose uptake (M-value) and heart rate variab
ility were measured in 21 normal men. The subjects were divided into 2 grou
ps [normally insulin sensitive (IS, 8.0+/-0.4 mg/kg min) and less insulin s
ensitive (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/m(2)), body fat (13+/-1 vs. 13
+/-1%), systolic (121+/-16 vs. 117+/-14 mm Hg) and diastolic (74+/-11vs. 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 hig
her 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-frequ
ency (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 us. 36
+/-2 nu, not significant (NS)I or the normalized HF component (52+/-6 vs. 5
1+/-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 LR 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.