AIMS/HYPOTHESIS: Acute insulinaemia activates the sympathetic drive in a nonuniform manner. The extent and nature of such activation in type 2 diabetic patients who do not have neuropathy have not yet been addressed despite evidence relating sympathetic activation to cardiovascular risk. We planned to determine the magnitude and extent of the sympathetic drive and its reflex responses in patients with type 2 diabetes and fasting hyperinsulinaemia. METHODS: We measured resting muscle sympathetic nerve activity (MSNA) as the mean frequency of multi-unit bursts and single unit muscle sympathetic nerve activity (s-MSNA) in 17 overweight patients with type 2 diabetes and two matched normal control groups comprising 17 overweight and 16 normal-weight subjects. We also tested the MSNA and s-MSNA responses to cold pressor and isometric hand-grip tests, along with the effect of sympatho-vagal balance on heart period variability. RESULTS: Both MSNA and s-MSNA in the group with type 2 diabetes (66+/-3.5 bursts/100 beats and 78+/-4.5 impulses/100 beats) were greater (at least p<0.0001) than in the overweight control group (42+/-2.6 bursts/100 beats and 48+/-3.4 impulses/100 beats) and normal-weight control group (43+/-6.2 bursts/100 beats and 51+/-7.1 impulses/100 beats), though the three groups had similar reflex responses, baroreflex sensitivity and sympatho-vagal balance controlling the heart period. CONCLUSIONS/ INTERPRETATION: The patients with type 2 diabetes had no evidence of impaired reflex or autonomic control of heart period variability at a time when there was central sympathetic activation to the periphery. Furthermore, being overweight itself was not associated with sympathetic activation.
AIMS/HYPOTHESIS: Acute insulinaemia activates the sympathetic drive in a nonuniform manner. The extent and nature of such activation in type 2 diabeticpatients who do not have neuropathy have not yet been addressed despite evidence relating sympathetic activation to cardiovascular risk. We planned to determine the magnitude and extent of the sympathetic drive and its reflex responses in patients with type 2 diabetes and fasting hyperinsulinaemia. METHODS: We measured resting muscle sympathetic nerve activity (MSNA) as the mean frequency of multi-unit bursts and single unit muscle sympathetic nerve activity (s-MSNA) in 17 overweight patients with type 2 diabetes and two matched normal control groups comprising 17 overweight and 16 normal-weight subjects. We also tested the MSNA and s-MSNA responses to cold pressor and isometric hand-grip tests, along with the effect of sympatho-vagal balance on heart period variability. RESULTS: Both MSNA and s-MSNA in the group with type 2 diabetes (66+/-3.5 bursts/100 beats and 78+/-4.5 impulses/100 beats) were greater (at least p<0.0001) than in the overweight control group (42+/-2.6 bursts/100 beats and 48+/-3.4 impulses/100 beats) and normal-weight control group (43+/-6.2 bursts/100 beats and 51+/-7.1 impulses/100 beats), though the three groups had similar reflex responses, baroreflex sensitivity and sympatho-vagal balance controlling the heart period. CONCLUSIONS/ INTERPRETATION: The patients with type 2 diabetes had no evidence of impaired reflex or autonomic control of heart period variability at a time when there was central sympathetic activation to the periphery. Furthermore, being overweight itself was not associated with sympathetic activation.
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