HDCN Article Review/Hyperlink

Facchini FS, Stoohs RA, Reaven GM

Enhanced sympathetic nervous system activity: the linchpin between insulin resistance, hyperinsulinemia, and heart rate

Am J Hypertens (Oct) 9:1013-1017 1996

Several groups, notably that of Landsberg, have advocated the position that increased sympathetic nervous system (SNS) activity resulting from hyperinsulinemia causes hypertension. However, measures of sympathetic activity are all somewhat flawed: global measures such as plasma and urinary catecholamines often reflect the effects of multiple determinants such as physical activity and emotions, while more direct measures, such as neuronal recordings, may only reflect regional SNS activity. One time-honored clinically available measure, heart rate, has been shown to be a premorbid marker of risk for developing hypertension, and the present study relates nocturnal heart rate to measures of glucose disposal.

The authors subjected 45 normotensive, nondiabetic individuals to nocturnal automated heart rate monitoring (6.9 +/- 0.6 h) and to insulin suppression testing, from which they derived the measure of steady-state plasma glucose (SSPG, a measure of insulin-mediated glucose disposal) as well as an oral GTT, during which they measured the insulin response. They demonstrated that there was a continuous linear relationship between nocturnal heart rate and both insulin response ( r = 0.51) and SSPG (r = 0.61). These relationships remained significant even when potential confounders (age, BMI, gender, family history of hypertension or diabetes, physical activity) were considered. The authors conclude that insulin resistant individuals with compensatory hyperinsulinemia have higher nocturnal heart rates, probably secondary to insulin-induced sympathetic activity.

Comment: This research clearly supports an association of increased SNS activity and insulin resistance but still begs the question of what cause what. Julius has proposed that, in part, insulin resistance in hypertensives results from hemodynamic factors , e.g., vasoconstriction and capillary rarefaction, that impair glucose and insulin delivery to muscle fibers. In this construct, increased SNS activity, by promoting vasoconstriction, is thought to increase insulin resistance. In effect, the "arrow" is drawn in a direction opposite to that proposed by Facchini, et al.

Additionally, while the use of nocturnal heart rate is interesting, in most people, resting heart rate is under a significant degree of vagal inhibition. It would be of interest to apply analytic techniques such as spectral analysis to try to more precisely quantitate the contribution of the SNS to heart rate variablity. (Alan Weder, M.D., University of Michigan)