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J Appl Physiol (April 12, 2007). doi:10.1152/japplphysiol.01462.2006
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Submitted on December 31, 2006
Accepted on April 10, 2007

Substrate source utilisation during moderate exercise with 13C-glucose ingestion in type 1 diabetic patients

Mathieu Robitaille1, Marie-Christine Dubé2, S. J. Weisnagel2, Denis Prud'homme3, Denis Massicotte4, Francois Peronnet5, and Carole Lavoie1*

1 Sc activité physique, Université du Québec à Trois-Rivières, Trois-Rivières, Canada
2 2Département de Médecine sociale et préventive, Division de kinésiologie, Université Laval, Québec, Canada
3 School of Human Kinetics, Faculty of Health Sciences, University of Ottawa, Ottawa, Canada
4 Department of Kinanthropologie, UQAM, Montreal, Canada
5 Departement de kinesiologie, Universite de Montreal, Montreal P.Q. H3C 3J7, Canada

* To whom correspondence should be addressed. E-mail: Carole.Lavoie{at}uqtr.ca.

Substrate oxidation and the respective contributions of exogenous glucose, glucose released from the liver and muscle glycogen oxidation were measured using indirect respiratory calorimetry combined with tracer technique in eight control subjects and eight diabetic patients (5 men and 3 women in both groups) of similar age, height, body mass, and VO 2 max, over a 60-min exercise period on cycle ergometer at 50.8 (4.0) % VO 2 max (mean [SD]) (131.0 [38.2] W). Both the subjects and patients ingested a breakfast (containing ~80 g of carbohydrates) 3 hours before and 30 g of glucose labeled with 13C, 15 min before the beginning of exercise. The diabetic patients also received their usual insulin dose (Humalog® = 9.1 [0.9] U; Humulin N® = 13.9 [4.4] U) immediately before the breakfast. Over the last 30 min of exercise the oxidation of carbohydrate (1.32 [0.48] and 1.42 [0.63] g/min) and fat (0.33 [0.10] and 0.30 [0.10] g/min) and their contribution to the energy yield were not significantly different in the control subjects and diabetic patients. Exogenous glucose oxidation was also not significantly different in the control subjects and diabetic patients (6.3 [1.3] and 5.2 [1.6] g/30 min, respectively). In contrast, the oxidation of plasma glucose and of glucose released from the liver was significantly lower in the diabetic patients than in control subjects (14.5 [4.3]; 9.3 [2.8] vs 27.9 [13.3]; 21.6 [12.8] g/30 min, respectively) while that of muscle glycogen was significantly higher (28.1 [15.5] vs 11.6 [8.1] g/30 min). These data indicate that when compared to control subjects, in diabetic patients fed glucose before exercise, overall substrate oxidation and exogenous glucose oxidation are similar but plasma glucose oxidation is lower and this is associated with a compensatory higher utilisation of muscle glycogen.







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