Resistance exercise timing and metabolic risk factors in type 2 diabetics
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Abnormally elevated postprandial glucose and triacylglycerol (TAG) concentrations are risk factors for cardiovascular disease in patients with type-2 diabetes. The most effective time to exercise to lower postprandial glucose and TAG concentrations is unknown. Thus, the aim of this study was to determine what time is more effective, either pre- or post-dinner resistance exercise (RE), at improving postprandial risk factors in patients with type-2 diabetes. Methods: Thirteen obese patients with type 2 diabetes completed three trials in a random order in which they consumed a standardized dinner meal with 1) no RE (NoRE), 2) pre-dinner RE (RE?��M), and 3) post-dinner RE beginning 45 min after dinner (M?��RE). During each trial blood samples were taken to measure glucose, TAG, acetaminophen (gastric emptying), endocrine responses, and mathematical modeling was used to assess beta-cell function. Indirect calorimetry was used to measure energy expenditure and substrate oxidation. A continuous glucose monitor was used to assess nocturnal and morning glycemic control the next day. A fasting blood sample was taken the following morning and the quantitative insulin sensitivity check index (QUICKI) was used to estimate whole body insulin sensitivity and the homeostatic model assessment of insulin resistance (HOMA-IR) was used as an estimate of hepatic insulin resistance. Results: The postprandial glucose iAUC was reduced (P < 0.05) by ?�18% and 30% during the RE?��M and M?��RE trials, respectfully, compared to NoRE, with no difference between RE trials. The postprandial total TAG iAUC was ?�92% lower (P < 0.05) during M?��RE compared to NoRE and RE?��M, an effect due to lower VLDL-1 TAG concentrations. RE?��M and M?��RE reduced the insulin iAUC by 35% and 48%, respectfully, compared to NoRE (P < 0.05), but via different mechanisms as RE?��M enhanced insulin clearance, whereas M?��RE reduced pancreatic insulin secretion and enhanced insulin clearance. The postprandial GLP-1
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