Exercise and Diabetes Mellitus

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Abstract
A well controlled exercise state is generally believed to be beneficial; it increases glucose utilization and decreases insulin requirements. Caution in training programs is recommended because in less controlled states, control of glycemia can deteriorate, and glucose utilization is, at best, only poorly enhanced. Even in well controlled subjects, gluconeogenesis was more accelerated than in controls. In juvenile diabetics [human] with normal work capacity, muscle capillarization was deficient, muscle type distribution was abnormal, and some enzymes were lower than normal. It was encouraging to learn that a training program in middle-aged nonobese chemical diabetics may normalize oxidative capacity of their muscle and improve glucose tolerance. Glycemic response of the diabetic to exercise may depend on insulin levels in blood under given conditions. Insulin injected diabetics have elevated plasma IRI [immunoreactive insulin] levels and, in addition, exercise can accelerate mobilization of insulin from its s.c. depot, so that, due to hyperinsulinemia, glucose production is inhibited while glucose utilization continues at a normal rate. This can, at least in part, explain the mechanism of exercise-induced hypoglycemia. Glycemia does not change when diabetics receive constant infusions of insulin. Exercise deteriorates hyperglycemia, when absolute or relative insulin deficiency causes inadequate glucose uptake by the muscle. The enhanced mobilization of the fasted state is undesirable because it is accompanied with the hazard of hypoglycemia. It would be worthwhile to explore, whether enhanced insulin mobilization, or hyperinsulinemia in general, soon after food ingestion could improve disposal of nutrients and whether, under such conditions, exercise would represent a valuable adjunct to the treatment regimen of the diabetics.