| Literature DB >> 8787548 |
J L Nieto1, I D Laviada, A Guillén, A Haro.
Abstract
Adaptive changes in the beta-adrenergic adenylyl cyclase (AC) system in response to endurance training were studied in heart and adipose tissue. Training was performed by making male Wistar rats run on a motor-driven treadmill. The changes following exercise training were opposite in the two tissue studied. The density of beta-adrenergic receptors in left ventricular membranes of trained rats showed a marked decrease. Comparison of AC activities in cardiac membranes prepared from trained and sedentary rats revealed a depressing effect of endurance training on: 1. the beta-adrenergic stimulatory pathway and the inhibition of AC via receptor; 2. the Gs component and the Gs-adenylyl cyclase coupling, as shown by the response of adenylyl cyclase to GppNHp and NaF; and 3. the enzyme catalytic activity in the presence of Mn2+ or forskolin. The levels of Gsalpha subunits in the left ventricle, as measured in terms of ADP-ribosylated and immunologically reactive proteins, were decreased by endurance exercise, whereas immunodetectable levels of Gialpha2 increased in the membranes of trained myocardium. In contrast to the diminished sensitivity that characterizes the behavior of the cardiac beta-adrenergic-AC system, endurance physical training increased sensitivity of this signal transduction system in adipose tissue. Thus, the density of beta-ARs as well as AC activity and the beta-adrenergic stimulatory pathway were increased in adipose membranes of trained rats compared with the corresponding sedentary controls. In addition, the levels of Gsalpha subunits were higher in the adipose plasma membranes of trained rats. However, immunodetectable levels of Gi1alpha and Gi3alpha increased with training, whereas the amount of Gi2alpha decreased in membranes of trained rats. In conclusion, the present study shows that chronic exercise is associated with a tissue-specific adaptation of the beta-adrenergic AC system.Entities:
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Year: 1996 PMID: 8787548 DOI: 10.1016/0006-2952(96)00040-8
Source DB: PubMed Journal: Biochem Pharmacol ISSN: 0006-2952 Impact factor: 5.858