Tom L Broderick1, Paul Poirier, Melissa Gillis. 1. Department of Physiology, Midwestern University, 19555 59th Avenue, Glendale, AZ 85308, USA. tbrode@midwestern.edu
Abstract
BACKGROUND: Clinical and experimental studies have shown that a reduction in myocardial glucose utilization is a factor contributing to diabetic cardiomyopathy. This study determined whether exercise training could prevent the depression in glucose utilization observed in the diabetic rat heart. METHODS: Diabetes was induced in Sprague-Dawley rats by an intravenous injection of streptozotocin (60 mg/kg). After 10 weeks of treadmill running, exogenous myocardial glucose utilization and cardiac function were determined in isolated working hearts perfused under aerobic conditions and then subjected to a 60-min period of low-flow ischemia followed by reperfusion. RESULTS: Compared to aerobically perfused sedentary control hearts, rates of myocardial glucose oxidation and glycolysis were lower in diabetic hearts. Diabetes was also characterized by a pronounced decrease in cardiac function. Following exercise training, rates of myocardial glucose oxidation and glycolysis were restored and cardiac performance was improved compared to sedentary diabetic hearts. During low-flow ischemia, the decrease in glycolysis observed in hearts of sedentary diabetic rats was attenuated following exercise training. Following ischemia, glucose oxidation and glycolysis returned to preischemic levels in all groups. However, hearts from trained diabetic animals had higher rates of glucose oxidation compared to their respective sedentary group. This was accompanied by an enhanced recovery of heart function following ischemia. CONCLUSIONS: Our results indicate that exercise training is effective in preventing the depression in myocardial glucose metabolism observed in the diabetic rat. This may explain the benefits of exercise in preventing cardiac dysfunction in diabetes. Copyright (c) 2004 John Wiley & Sons, Ltd.
BACKGROUND: Clinical and experimental studies have shown that a reduction in myocardial glucose utilization is a factor contributing to diabetic cardiomyopathy. This study determined whether exercise training could prevent the depression in glucose utilization observed in the diabeticrat heart. METHODS:Diabetes was induced in Sprague-Dawley rats by an intravenous injection of streptozotocin (60 mg/kg). After 10 weeks of treadmill running, exogenous myocardial glucose utilization and cardiac function were determined in isolated working hearts perfused under aerobic conditions and then subjected to a 60-min period of low-flow ischemia followed by reperfusion. RESULTS: Compared to aerobically perfused sedentary control hearts, rates of myocardial glucose oxidation and glycolysis were lower in diabetic hearts. Diabetes was also characterized by a pronounced decrease in cardiac function. Following exercise training, rates of myocardial glucose oxidation and glycolysis were restored and cardiac performance was improved compared to sedentary diabetic hearts. During low-flow ischemia, the decrease in glycolysis observed in hearts of sedentary diabeticrats was attenuated following exercise training. Following ischemia, glucose oxidation and glycolysis returned to preischemic levels in all groups. However, hearts from trained diabetic animals had higher rates of glucose oxidation compared to their respective sedentary group. This was accompanied by an enhanced recovery of heart function following ischemia. CONCLUSIONS: Our results indicate that exercise training is effective in preventing the depression in myocardial glucose metabolism observed in the diabeticrat. This may explain the benefits of exercise in preventing cardiac dysfunction in diabetes. Copyright (c) 2004 John Wiley & Sons, Ltd.
Authors: Frank Christopher Howarth; F A Almugaddum; M A Qureshi; M Ljubisavljevic; M Ljubisavijevic Journal: Mol Cell Biochem Date: 2008-06-16 Impact factor: 3.396