Adrenocortical activation during long-term exercise in dogs: Evidence for a glucostatic mechanism

Summary

Experiments were performed to elucidate the mechanism of changes in plasma 17-OHCS level during prolonged muscular exercise of moderate intensity. Dogs performed 120 min standard treadmill exercise. Plasma level of 17-OHCS increased during exercise. There was no change in the rate of removal of intravenously injected cortisol as compared with resting conditions. Exercise-dependent increase in plasma 17-OHCS level was prevented by continuous intravenous glucose infusion at a rate sufficient to prevent exercise hypoglycaemia. The same result was obtained when systemic hypoglycaemia persisted but glucose supply to the brain or liver was augmented by continuous glucose infusion to the carotid artery or portal vein. The same amount of glucose infused into a peripheral vein failed to abolish the adrenocortical response to exercise. The insulin-evoked hypoglycaemia of the magnitude comparable to that obtained during standard exercise did not significantly affect plasma 17-OHCS in resting animals.

It is concluded that activation of glucocorticoid secretion during exercise is related to the glucostatic mechanism. Exercise hypoglacaemia per se is not responsible for adrenocortical activation. The results suggest that brain and hepatic glucoreceptors are engaged in the activation of the pituitary-adrenocortical system during exercise.