Fell R D, Terblanche S E, Winder W W, Holloszy J O
Am J Physiol. 1981 Jul;241(1):C55-8. doi: 10.1152/ajpcell.1981.241.1.C55.
Rats were given a daily injection of L-epinephrine, 100 micrograms/100 g body wt, for 6 wk. The hearts of the epinephrine-treated animals were heavier (11.5%), and blood glucose and plasma insulin concentrations were lower than those of control rats. Acute responses to epinephrine were compared in the two groups. An increase in blood glucose and decreases in plasma insulin, liver glycogen, and muscle glycogen occurred in both groups. The magnitude of these responses were similar in the two groups except for the decrease in muscle glycogen, which was smaller in the chronic epinephrine-treatment group. There were no changes in respiratory capacity, citrate synthase or succinate dehydrogenase activities, or in cytochrome c concentration in skeletal muscle in response to 6 wk of epinephrine treatment. These results are compatible with the suggestion that catecholamines may play a role in some of the metabolic and cardiac adaptations to exercise training. However, they argue strongly against the hypothesis that catecholamines are responsible for inducing the increase in muscle mitochondria that occurs in response to exercise training.
给大鼠每日注射100微克/100克体重的L-肾上腺素，持续6周。接受肾上腺素治疗的动物心脏更重（重11.5%），且血糖和血浆胰岛素浓度低于对照大鼠。比较了两组对肾上腺素的急性反应。两组均出现血糖升高以及血浆胰岛素、肝糖原和肌糖原降低。除了慢性肾上腺素治疗组的肌糖原降低幅度较小外，两组这些反应的程度相似。接受6周肾上腺素治疗后，骨骼肌的呼吸能力、柠檬酸合酶或琥珀酸脱氢酶活性以及细胞色素c浓度均无变化。这些结果与儿茶酚胺可能在运动训练的某些代谢和心脏适应性变化中起作用的观点相符。然而，它们有力地反驳了儿茶酚胺是导致运动训练引起肌肉线粒体增加的原因这一假说。
