The Effect of Propranolol on Glycogen Tabolism During Exercise

Abstract

It is well known that adrenalin (epinephrine) will cause activation of glycogen phosphorylase (EC 2.4.1.1.) through an increased conversion of phosphorylase b to a (1, 2, 3). This reaction has been shown to occur in skeletal muscle (4, 6, 7) and to be the result of an activation of phosphorylase kinase (EC 2.7.1.38.) mediated through increased levels of 3′5′ AMP (5). In a series of unpublished experiments performed in this laboratory it was shown that infusion of adrenlin resulted in decreased levels of glycogen in the quadriceps femoris muscle and an increase in lactate production. In an attempt to investigate whether or not adrenalin released during moderate or heavy bicycle exercise was of importance in regulating glycogen breakdown, experiments were performed in which the beta-receptor sites in the working muscles were blocked. The blocking agent used was propranolol. The results obtained did not show any direct effects of beta-blocking upon glycogen utilization but did point to possible changes at the level of phosphofructo-kinase (EC 2.7.1.11.).