In mammals, the roles of liver and skeletal muscle glycogen in adrenaline-induced hyperglycaemia are well known. However, in amphibians, there is limited information on the relative contribution of liver and skeletal muscle glycogen in adrenaline-induced hyperglycaemia. This study investigated the effects of adrenaline on blood glucose, plasma lactate, liverand skeletal muscle glycogen and the role of adrenergic receptors in the common African toad, bufo regularis. One hundred and twenty-five adult common African toads (70-100g) of both sexes were randomly collected and used in the study.Blood samples were collected from truncus arteriosus to estimate glucose and lactate levels. Blood glucose was determined immediately by modified glucose oxidase method. Plasma lactate was determined by modification of the Barker-Summerson method. Liver and gastrocnemius muscle glycogen were determined using anthrone reagents method. Adrenaline caused significant increase in blood glucose, lactate levels and significant reduction in liver and muscle glycogen. When toads were pre-treated with propranolol or prazosin, adrenalines reduction in liver and muscle glycogen was significantly reduced while the increase in blood glucose and lactate levels was prevented. Combination of both blockers abolished the increase in blood glucose, lactate levels and blocked reduction in liver and muscle glycogen produced by adrenaline. The results of this study showed that adrenalinecaused liver and skeletal muscle glycogen breakdown, increase in plasma lactate levels which resulted in hyperglycaemia in the common African toad bufo regularis. The study also showed that both alpha- and beta-adrenergic receptors are involved in mediating the effects of adrenaline on blood glucose, plasma lactate, liver, and muscle glycogenolysis and gluconeogenesis.