Studies were carried out to define the possible role of insulin in the increased assimilation of glucose caused by exercise. First, plasma immunoreactive insulin (IRI) response in conventional intravenous glucose tolerance tests was measured in normal subjects at rest and during or immediately after ergometer exercise. In all cases the glucose disappearance rate (K value) was increased by exercise but the plasma IRI level assayed at two minutes after glucose showed no constant change from corresponding values at rest. Secondly, the insulin secretion rate was assessed by giving I-131-labeled insulin as a constant-rate infusion and measuring the plasma IRI specific activity. In the fasting state the insulin secretion rate varied from 0.7 to 6.0 mU. per min., and was highest in obese subjects. Increase of blood glucose level to 130-150 mg. per 100 ml. with a constant-rate glucose infusion doubled the insulin secretion rate. In subjects with a normal working capacity moderate exercise of thirteen to twenty minutes' duration did not significantly change the secretion rate whether the muscular work occurred in the fasting state or with glucose infusion. On the contrary, in all subjects with a reduced performance due to coronary heart disease the insulin secretion rate was strikingly increased by exercise and the plasma IRI level rose.
It is concluded that immunoreactive insulin is not the mediator of accelerated glucose metabolism caused by muscular work but that hypoxia of islet tissue may be a stimulus to insulin release.