In this study, it has been investigated whether chronic isoproterenol treatments can reproduce the effect of exercise-training on rat epididymal adipose tissue (WAT) .
1. Exercise-training (treadmill running 5 days/week for 8 weeks) reduced the weight-gain, the amount of WAT and the mean daily food intake compared with control. Exercise-training caused hypertrophy of heart and submandibular glands.
2. Chronic isoproterenol-treatments (2.5 mg/100 g body weight/day sc for 6 days) reduced the body weight and the amount of WAT and caused hypertrophy of heart and submandibular glands compared with saline (0.9%) treated rats.
3. Exercise-training markedly increased lipolysis induced by adrenaline (5.5 μM) in WAT segments, and slightly increased lipolysis induced by noradrenaline (5.5 μM) and caffeine (3 mM) . However, lipolysis induced by ACTH (0.5 μM) was markedly decreased.
4. Chronic isoproterenol-treatments markedly increased lipolysis induced by each lipolytic agent.
5. Chronic isoproterenol-treatments mimicked the effect of exercise-training on the weight of various organs, but not on lipolysis induced by ACTH.
6. Chronic isoproterenol-treatments could not reproduce all effects of exercisetraining on rat WAT. Therefore, these results suggest that the response of rat WAT to exercise-training is mediated not only by the beta effect of catacholamine but also by various hormonal factors, and further suggest that it is difficult to reproduce the effect of physiological nerve stimulation only by chronic injections of a neurotransmitter.

The present study was designed to provide more extensive information on the effects of chronic in vivo β-adrenergic stimulation as produced in two different fashions, one through exercise training and the other through the chronic administration of isoproterenol, on the characteristics of β-adrenergic receptors (β-AR) in rat adipocyte membranes.
1. The chronic administration of isoproterenol (2.5 mg/kg BW sc, daily for 21 days; IPR-treatment) significantly reduced lipolysis induced by noradrenaline in isolated adipocytes. However, exercise training (8 weeks of treadmill running) significantly increased the lipolytic response of adipocytes to noradrenaline.
2. IPR-treatment significantly decreased the percentage of the high affinity state (%R_H) and increased the dissociation constants of the high affinity state (K_H) of β-AR in computer modeling of (-) -noradrenaline competition curves. However, exercise training significantly increased %R_H.
In conclusion, IPR-treatment reduced the lipolytic response of adipocytes to noradrenaline, at least partially, which resulted in the decreased formation of the high affinity state of β-AR. Exercise training may enhance the lipolytic ability of adipocytes to catecholamines through facilitating the formation of the high affinity state of β-AR.

The present study was designed to provide more extensive information on the effects of chronic in vivo β-adrenergic stimulation as produced in two different fashions, one through exercise training and the other through the chronic administration of isoproterenol, on the characteristics of β-adrenergic receptors (β-AR) in rat adipocyte membranes.
1. The chronic administration of isoproterenol (2.5 mg/kg BW sc, daily for 21 days; IPR-treatment) significantly reduced lipolysis induced by noradrenaline in isolated adipocytes. However, exercise training (8 weeks of treadmill running) significantly increased the lipolytic response of adipocytes to noradrenaline.
2. IPR-treatment significantly decreased the percentage of the high affinity state (%R_H) and increased the dissociation constants of the high affinity state (K_H) of β-AR in computer modeling of (-) -noradrenaline competition curves. However, exercise training significantly increased %R_H.
In conclusion, IPR-treatment reduced the lipolytic response of adipocytes to noradrenaline, at least partially, which resulted in the decreased formation of the high affinity state of β-AR. Exercise training may enhance the lipolytic ability of adipocytes to catecholamines through facilitating the formation of the high affinity state of β-AR.