The effect of intense exercise on postprandial glucose homeostasis in TypeII diabetic patients

Aims/hypothesis. The influence of postprandial high intensity exercise on g lycaemia was studied in patients with Type II diabetes mellitus. Methods. Patients who were treated by diet only (n = 8) ate a standardised breakfast and 4 h later a standardised lunch. They were studied in the rest ing state (control day) and on another day (exercise day) when they did int ermittent exercised at high intensity after breakfast) (4 bouts including 3 min at 56.5 +/- 3.9% (V) over dot (O2 max) (means +/- SEM), 4 min at 98.3 +/- 5.1% (V) over dot (O2 max) and 6 min of rest). Responses were calculate d as areas under the plasma concentration curve (AUC) during 4 h after eith er breakfast or lunch. Results. Breakfast-AUCs for glucose, insulin and C peptide were lower (p < 0.05) on the exercise day compared with the control day (glucose: 538 +/- 9 4 vs 733 +/- 64 mmol . l(-1) . 240 min; insulin: 16 +/- 4 vs 22 +/- 3 pmol . ml(-1) . 240 min; C peptide: 143 +/- 22 vs 203 +/- 29 pmol . ml(-1) . 240 min). After breakfast glucose appearance was unaffected by exercise, where as disappearance and clearance increased (p < 0.05). Muscle glycogen was di minished by exercise (p < 0.05). After lunch no differences were observed b etween experiments. Exercise-induced reductions in glucose, insulin and C p eptide responses were similar (p > 0.05) in this study of intermittent, hig h intensity exercise and in a previous study of isocaloric but prolonged mo derate (45 min at 53 +/- 2% (V) over dot (O2 max)) postprandial exercise. Conclusion/interpretation. Postprandial high intensity exercise does not de teriorate glucose homeostasis but reduces both glucose concentrations and i nsulin secretion. The effect of exercise is related to energy expenditure r ather than to peak exercise intensity. Finally, postprandial exercise does not: influence glucose homeostasis during a subsequent main meal.