The Acute Effect of Hyperglycemia on the Exercise Pressor Reflex

Abstract

Previous work has shown that the exercise pressor reflex is exaggerated in type 2 diabetic rats that present with hyperglycemia. Although it is likely that chronic hyperglycemia plays a role, no studies have isolated the acute effects of high blood glucose levels on this reflex. Therefore, the purpose of the current study was to determine the acute effects of hyperglycemia on the exercise pressor reflex. We first determined the glucose concentration needed to increase local blood glucose level in the hindlimb vasculature to a similar level seen in our type 2 diabetic rats that had an exaggerated exercise pressor reflex. To do this, healthy Sprague‐Dawley rats were infused over 20 min with one of two different concentrations of glucose (125 mg/ml, male n=3 or 250 mg/ml, male n=3) into the arterial supply of the left hindlimb with blood flow to and from the hindlimb restricted. At the same time somatostatin (3.9 ug/100 ul) was infused systemically in order to prevent an endogenous insulin response. Blood glucose was measured every two minutes from both hindlimbs to determine how long it would take to bring blood glucose concentration up to the desired level. We then determined the acute effect of glucose on the pressor and cardioaccelerator responses during static contraction of the hindlimb. The exercise pressor reflex was evoked in healthy, unanesthetized, decerebrated Sprague‐Dawley rats by statically contracting the hindlimb muscle for 30 seconds before and after 15 minutes of either glucose (250 mg/ml) or saline infusion, while mean arterial pressure and heart rate were recorded. We found that infusing 250 mg/ml of glucose significantly raised blood glucose levels to 486 ± 84 mg/dl by the 3rd minute compare to the control leg. However, infusing 125 mg/ml of glucose did not raise blood glucose concentration to 546 ± 33 mg/dl until the 11th minute compare to the control leg (p<0.05). Therefore, we decided to use 250 mg/ml glucose for the exercise pressor experiment. We then found that acutely infusing 250 mg/ml of glucose into the arterial supply of the hindlimb did not significantly affect the pressor (ΔMAP before glucose: 13 ± 0.4 mmHg; after glucose: 12 ± 0.8 mmHg, n=4; before saline: 11 ± 2 mmHg; after saline: 10 ± 2 mmHg, n=3; p>0.05) or cardioaccelerator (ΔHR before glucose: 14 ± 1 bpm; after glucose: 12 ± 2 bpm, n=4; before saline: 14 ± 3 bpm; after saline: 12 ± 4 bpm, n=3; p>0.05) responses to static contraction. We conclude that the acute presence of glucose in the circulation of the hindlimb muscles plays no role in exaggerating the exercise pressor reflex.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.