Abstract

Impaired glucose tolerance forms an intermediate stage in the natural history of diabetes mellitus. These individuals with impaired glucose tolerance (IGT) have a significant risk of developing diabetes and thus are an important target group for primary prevention. On the other hand, it is generally accepted that prolonged physical exercise increases insulin sensitivity and might be useful in the prevention of type 2 diabetes. PURPOSE: To determine the effects of chronic exercise and low-calorie diet on plasma NO and ET-1 levels in individuals with impaired glucose tolerance (IGT), and to elucidate the relationship between the oxidant stress markers and NO/ET-1 levels in the plasma before and following exercise episodes. METHODS: Individuals with IGT (n=14) participated in a regular exercise program starting at an intensity corresponding to 35% of the heart rate reserve of the individual and exercised for 40 minutes each day 3 days a week for 12 weeks. Physiological, anthropometric and biochemical measurements were done before, on the 6th week and at the end of the program. RESULTS: There was a significant reduction in BMI, body fat content, systolic and diastolic blood pressures as well as NO and ET-1 concentrations following 12 weeks of exercise and diet program. Exercise training significantly elevated subjects' maximum oxygen consumption whereas resting metabolic rates of the individuals did not change. Formation of TBARS in the plasma, which is an indicator of lipid peroxidation, was significantly reduced, while sulfhydryl (RSH) groups were significantly increased on the 6th weeks (p<0.05) and at the end of program (p<0.01). CONCLUSION: Our results demonstrate that exercise along with low-calorie diet, induced reductions in the plasma of both ET-1 and NO. Furthermore, upon completion of the program, beneficial effects were observed on anthropometrical measurements and plasma oxidant stress markers, indicating weight loss associated with exercise training and calorie restriction may effectively improve endothelial dysfunction in individuals with impaired glucose tolerance.

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