ADENYLYL-CYCLASE SYSTEM IS AFFECTED DIFFERENTLY BY ENDURANCE PHYSICAL-TRAINING IN HEART AND ADIPOSE-TISSUE

Adaptive changes in the beta-adrenergic adenylyl cyclase (AC) system i n response to endurance training were studied in heart and adipose tis sue. Training was performed by making male Wistar rats run on a motor- driven treadmill. The changes following exercise training were opposit e in the two tissues studied. The density of beta-adrenergic receptors in left ventricular membranes of trained rats showed a marked decreas e. Comparison of AC activities in cardiac membranes prepared from trai ned and sedentary rats revealed a depress ing effect of endurance trai ning on: 1. the beta-adrenergic stimulatory pathway and the inhibition of AC via receptor; 2. the G(s) component and the G(s)-adenylyl cycla se coupling, as shown by the response of adenylyl cyclase to GppNHp an d NaF; and 3. the enzyme catalytic activity in the presence of Mn2+ or forskolin. The levels of G(s alpha) subunits in the left ventricle, a s measured in terms of ADP-ribosyrated and immunologically reactive pr oteins, were decreased by endurance exercise, whereas immunodetectable levels of G(i alpha 2) increased in the membranes of trained myocardi um. In contrast to the diminished sensitivity that characterizes the b ehavior of the cardiac beta-adrenergic-AC system, endurance physical t raining increased sensitivity ofthis signal transduction system in adi pose tissue. Thus, the density of beta-ARs as well as AC activity and the beta-adrenergic stimulatory pathway were increased in adipose memb ranes of trained rats compared with the corresponding sedentary contro ls. In addition, the levels of G(s alpha) subunits were higher in the adipose plasma membranes of trained rats. However, immunodetectable le vels of G(il alpha) and G(i3 alpha) increased with training, whereas t he amount of G(i2 alpha), decreased in membranes of trained rats. In c onclusion, the present study shows that chronic exercise is associated with a tissue specific adaptation of the beta-adrenergic AC system.