Alcohol and postexercise metabolic responses in type 2 diabetes

Abstract

The objective was to investigate the impact of the combination of exercise and alcohol on the metabolic response in nonfasting and fasting type 2 diabetic subjects. In part 1, 12 untrained middle-aged type 2 diabetic subjects participated on 3 test days. On each day, they ingested a light meal (1,824 kJ) containing 48 energy percent (E%) carbohydrate, 38 E% fat, and 14 E% protein. The meal was followed by either (A) rest or (B) 30 minutes of exercise (40% of maximum O 2 consumption [VO 2max]) or (C) taken with alcohol (0.4 g/kg body weight) followed by 30 minutes of exercise (40% of VO 2max). In part 2, 11 untrained middle-aged type 2 diabetic subjects participated on 4 test days without a meal. The subjects were either (A) resting, (B) drinking alcohol (0.4 g/kg body weight), (C) exercising 30 minutes (40% of VO 2max), or (D) drinking alcohol (0.4 g/kg body weight) and exercising 30 minutes (40% of VO 2max). On each test day, regular blood samples were drawn for 4 hours for analysis of glucose, insulin, lactate, triglycerides, nonesterified fatty acid (NEFA), and ethanol. Comparing exercise and rest following a light meal (part 1, no change (7%) occurred in the plasma glucose response area (642 ± 119 v 724 ± 109 mmol · L −1 · 240 min, NS). However, it was significantly reduced (by 27%) in response to exercise and alcohol (509 ± 98 v 724 ± 109 mmol · L −1 × 240 min; P = .03). Similar serum insulin response areas were obtained. After exercise and alcohol, plasma lactate increased compared with the resting state (2.2 ± 0.2 v 1.6 ± 0.1 mmol · L −1, P = .004) and with exercise alone (2.2 ± 0.2 v 1.8 ± 0.2 mmol ± L −1, P = .04). Serum NEFAs were significantly reduced by exercise and alcohol compared with the resting state (0.50 ± 0.04 v 0.65 ± 0.06 mmol · L −1, P = .008) and with exercise alone (0.50 ± 0.04 v 0.61 ± 0.05 mmol · L −1, P = .02). Similar serum triglycerides were found. During the fasting state (part 2), similar plasma glucose response areas were obtained in the four situations. The insulin response area to exercise and alcohol increased significantly compared with the resting state (3,325 ± 744 v 882 ± 295 pmol · L −1 × 240 min, P = .02) and with exercise alone (3,325 ± 744 v 1,328 ± 422 pmol · L −1 × 240 min, P = .007). No difference was found compared with alcohol alone. Plasma lactate was higher after alcohol intake versus the resting state (1.9 ± 0.1 v 1.3 ± 0.1 mmol · L −1, P = .003), as well as after exercise and alcohol (1.9 ± 0.1 v 1.3 ± 0.1 mmol · L −1, P = .01). After exercise and alcohol serum NEFAs were significantly reduced compared with the resting state (0.43 ± 0.02 v 0.64 ± 0.02 mmol · L −1, P < .001), alcohol alone (0.43 ± 0.02 v 0.51 ± 0.02 mmol · L −1, P < .001), and exercise alone (0.43 ± 0.02 v 0.64 ± 0.02 mmol · L −1, P < .001). Serum triglycerides were similar in the four situations. We conclude that moderate exercise with or without moderate alcohol intake does not cause acute hypoglycemia either after a light meal or in the fasting state in untrained overweight type 2 diabetic subjects.