CONTRIBUTION OF LIVER NERVES, GLUCAGON, AND ADRENALINE TO THE GLYCEMIC RESPONSE TO EXERCISE IN RATS

The contribution of hepatic sympathetic innervation, glucagon and adre naline to the glycaemic response to exercise was investigated in rats. Hepatically denervated (LDX) or sham operated (SHAM) rats with perman ent catheters were therefore submitted to swimming with or without inf usion of somatostatin in combination with adrenodemedullation. Blood s amples were taken for measurements of blood glucose, plasma free fatty acids (FFA), adrenaline (A), noradrenaline (NA), insulin and glucagon . Liver denervation by itself did not influence glucose levels during exercise. Infusion of somatostatin in SHAM animals, which inhibited th e exercise-induced glucagon response, led to enhanced sympathoadrenal outflow (measured as plasma A and NA) and a reduced blood glucose duri ng exercise, suggesting that glucagon serves as a powerful mediator of the glycaemic response during swimming. Infusion os somatostatin in L DX animals failed to enhance plasma NA levels and led to a more pronou nced reduction in blood glucose levels. This indicates that liver nerv es do contribute to the glycaemic response to exercise when glucagon s ecretion is suppressed. Reduced blood glucose levels after adrenodemed ullation revealed that adrenal A is another important mediator of the glucose response to exercise. Infusion of somatostatin in adrenodemedu llated SHAM or LDX animals was not accompanied with increased NA outfl ow, suggesting that adrenal A is necessary to allow the compensatory i ncreased outflow of NA from sympathetic nerves. In conclusion, the stu dy shows that pancreatic glucagon and adrenal A are the predominant fa ctors influencing the glycaemic response to exercise, whereas a role o f the sympathetic liver nerves becomes evident when glucagon secretion is suppressed.