Hyperglycemia and type 2 diabetes : impact on neural cardiovascular control

Abstract

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Type 2 diabetes (T2D) is often characterized by chronic hypertension and exaggerated increases in arterial blood pressure (BP) during exercise. However, investigations of the neural mechanisms that are known to be critically involved in BP regulation at rest and during exercise in T2D have been lacking. Also, hyperglycemia decreases arterial baroreflex (ABR) control of heart rate (HR) in conditions of reduced insulin sensitivity, but whether hyperglycemia reduces ABR control of HR in healthy subjects has not been investigated. In study #1, findings demonstrated that ABR control of HR is reduced following acute hyperglycemia in healthy subjects independent of insulin sensitivity, and also during hyperinsulinemia. Study #2 focused on ABR control of HR and muscle sympathetic nerve activity (MSNA) in T2D patients, which are chronically hyperglycemic and hyperinsulinemic. No differences in ABR control of MSNA were observed; however, ABR control of HR was significantly reduced in T2D patients compared to lean controls, but not weight-matched (i.e., obese) controls. These findings suggest a potential selective impairment in ABR control of HR in T2D that may be a consequence of obesity. Finally, given the exaggerated BP responses to exercise in T2D patients, and the vital contribution of skeletal muscle neural feedback to the BP responses to exercise, study #3 focused on BP and MSNA responses to activation of skeletal muscle neural afferents in T2D patients. The findings demonstrated that BP and MSNA responses to activation of skeletal muscle afferents sensitive to muscle metabolites was augmented in T2D patients.