title: Exercise training restores abnormal myocardial glucose utilization and cardiac function in diabetes.
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.
authors.affiliation: Department of Physiology, Midwestern University, 19555 59th Avenue, Glendale, AZ 85308, USA. tbrode@midwestern.edu
authors.forename: Tom L
authors.initials: TL
authors.lastname: Broderick
authors.forename: Paul
authors.initials: P
authors.lastname: Poirier
authors.forename: Melissa
authors.initials: M
authors.lastname: Gillis
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000517:prevention & control*; D004195:Disease Models, Animal; D005947:Glucose / Q000378:metabolism*; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D001786:Blood Glucose; D005947:Glucose