MENTAL STRESS INCREASES GLUCOSE-UPTAKE DURING HYPERINSULINEMIA - ASSOCIATIONS WITH SYMPATHETIC AND CARDIOVASCULAR RESPONSIVENESS

Infusion of epinephrine and norepinephrine reduces insulin-mediated glucose disposal, ie, induces insulin resistance. Mental stress increases concentrations of both plasma catecholamines. However, the effect of acute mental stress on insulin-mediated glucose uptake has not been examined. We observed in pilot studies that a mental stress test (MST) during a euglycemic glucose clamp decreased blood glucose concentration. In a prospective study, euglycemic hyperinsulinemia was established during 120 minutes of glucose clamping; the subjects (N = 74) then underwent 5 minutes of intense mental arithmetics with infusion rates of glucose and insulin kept constant. During MST. plasma epinephrine and norepinephrine increased (by 0.23 +/- 0.02 and 0.50 +/- 0.05 nmol/L) together with blood pressure ([BP] by 18 +/- 8/9 +/- 1 mm Hg) and heart rate ([HR] by 21 +/- 1 beats per minute), with P less than .0001 for all changes. During mental stress, blood glucose concentration decreased by 0.4 +/- 0.1 mmmol/L (P<0.0001), followed by full recovery after another 10 minutes. Serum insulin was unchanged. indicating an acute hut transient increase in glucose uptake. This finding was unrelated to age, sex, body mass, and BP status. Fifty-nine subjects with a decrease in glucose concentrations during MST were characterized by accentuated epinephrine response to MST (a change of 0.25 +/- 0.03 v 0.12 + 0.02 nmol/L, P=.001), increase in systolic BP (by 20 +/- 2 v 10 +/- 3 mm Hg, P=.008), and increase in HR (by 23 +/- 2 v 15 +/- 2 beats per minute, P=.008) as compared with 15 subjects with unchanged/increased glucose concentration. Thus, when mental stress is applied while insulin-mediated glucose uptake is already stimulated, sympathetic overactivity is initially accompanied by increased glucose uptake. This finding is unexpected and cannot be fully explained. The increase in skeletal muscle blood flow during mental stress, with increased substrate delivery to the metabolically active muscle cells, or other unknown interactions between insulin and the sympathetic nervous system (SNS) may explain the observation. Copyright (C) 1995 by W.B. Saunders Company