Studies from a number of laboratories demonstrate a biphasic change in
beta adrenergic regulation of hepatic glycogenolysis over the life sp
an of the male rat. The beta adrenergic response is prominent in immat
ure animals, declines rapidly during subsequent development to a minim
um by the time of young adulthood, and then reemerges during postmatur
ational development. Age changes in beta adrenergic-responsive adenyla
te cyclase activity follow a ''U''-shaped curve similar to that descri
bed by changes in liver glycogenolytic responsiveness during aging. De
velopmental and postmaturational changes in beta adrenergic-sensitive
adenylate cyclase activation are related to parallel alterations in th
e density of beta adrenergic receptors and also to functional changes
in nonreceptor components of the enzyme. The prevailing view that cate
cholamines stimulate hepatic glycogenolysis by an alpha adrenergic rec
eptor-mediated, cyclic AMP-independent mechanism is based almost entir
ely on evidence from young adult male rats. We propose that current co
ncepts of alpha adrenergic-responsive liver glycogenolysis underestima
te a physiological role for beta adrenergic responsiveness over the ma
jority of the life span.