HYPOGLYCEMIA INCREASES MUSCLE SYMPATHETIC-NERVE ACTIVITY IN IDDM AND CONTROL SUBJECTS

OBJECTIVE - The relationship between the increase in adrenomedullary c atecholamine secretion and the sympathetic response to hypoglycemia is not well understood in humans. To explore this relationship more clos ely, we directly recorded muscle sympathetic nerve activity (MSNA) in control subjects and in insulin-dependent diabetes mellitus (IDDM) sub jects without clinically evident diabetic complications. RESEARCH DESI GN AND METHODS - Twelve IDDM subjects (22.5 +/- 3.9 years of age, diab etes duration of 9.8 +/- 8.3 years) and 12 age-matched control subject s were studied. MSNA was measured during insulin infusion (720 pM.m(-2 ).min(-1)) with 30-min periods of 1) euglycemia, 2) hypoglycemia (targ et plasma glucose, 2.8 mM), and 3) recovery. The effect of increased i nsulin dose (1,440 pM.m(-2).min(-1)) was studied in six subjects in ea ch group, and the effect of prolonged hypoglycemia (1 h) was studied i n five IDDM subjects and four control subjects. RESULTS - MSNA levels increased in IDDM and control subjects, 31 +/- 8 and 29 +/- 6%, respec tively, above euglycemia during hypoglycemia and returned to euglycemi c levels during recovery. MSNA levels during hypoglycemia were lower i n IDDM subjects than in control subjects (26 +/- 3 vs. 35 +/- 2 bursts /min, P < 0.01). Importantly, no relationships were found between the MSNA and epinephrine responses to hypoglycemia in either group. Increa sing the insulin infusion rate did not alter the MSNA response to hypo glycemia. During prolonged hypoglycemia, MSNA remained elevated above euglycemic levels throughout hypoglycemia.CONCLUSIONS - These results demonstrate that insulin-induced hypoglycemia increases muscle sympath etic neural-outflow in IDDM and control subjects. The lack of correlat ion between the MSNA and epinephrine responses to hypoglycemia indicat es that the adrenomedullary and peripheral sympathetic responses to hy poglycemia are independently mediated.