| Literature DB >> 12422437 |
H Dorchy1.
Abstract
Energy for muscular exercise is derived initially from the breakdown of muscle glycogen, and later from circulating glucose released by the liver and from non-esterified fatty acids. Muscle glucose uptake may increase 20-fold. In normal subjects, insulin secretion declines and release of counter-regulatory hormones increases. In type 1 diabetes, glycaemic changes during exercise depend largely on blood insulin levels. In the young diabetic, during insulin deficiency, and therefore in a poor degree of metabolic control, i.e. hyperglycaemic and ketotic, exercise accentuates hyperglycaemia and ketosis, leading to extreme fatigue. If the insulin dosage is too high, the increase in muscular assimilation, combined with the shutdown of liver glucose production, may result in a severe hypoglycaemia. During the recovery period, the repletion of muscular and hepatic glycogen stores may also provoke an hypoglycaemia during hours after the cessation of muscular work. The recommendations for physical activity in type 1 diabetes include: 1) obtain good metabolic control; 2) in the few hours preceding the exercise, ingest complex carbohydrates; 3) in the case of unforeseen physical activity, increase glucose consumption immediately before, during, and after the activity; 4) in the case of foreseen activity, decrease the insulin dose (from 10 to 50%) acting during and even after intense muscular work; 5) do not inject the insulin at a site that will be heavily involved in the muscular activity.Entities:
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Year: 2002 PMID: 12422437
Source DB: PubMed Journal: Rev Med Brux ISSN: 0035-3639