Belcastro A N, Maybank P, Rossiter M, Secord D
Can J Physiol Pharmacol. 1985 Sep;63(9):1202-5. doi: 10.1139/y85-198.
Diabetes is characterized by depressed cardiac functional properties attributed to Ca2+-activated ATPase activity. In contrast, endurance swimming enhances the cardiac functional properties and Ca2+-activated myofibril ATPase. Thus, the purpose of this study was to observe if the changes associated with experimental diabetes can be ameliorated with training. Diabetes was induced with a single i.v. injection of streptozotocin (60 mg/kg). Blood and urine glucose concentrations were 802 +/- 44 and 6965 +/- 617 mg/dL, respectively. The training control and training diabetic animals were made to swim (+/- 2% body weight) 4 days/week for 8 weeks. Cardiac myofibril, at 10 microM free Ca2+ concentration was reduced by 54% in the sedentary diabetics compared with sedentary control animals (p less than 0.05). Swim training enhanced the Ca2+-activated myofibril ATPase activities for the normal animals. The diabetic animals, which swam for 8 weeks, had further reduced their Ca2+-activated myofibril ATPase activity when compared with sedentary diabetics (p less than 0.05). Similarly, the Mg2+-stimulated myofibril ATPase activity was depressed by 31% in diabetics following endurance swimming. It is concluded that the depressed Ca2+-activated myofibril ATPase activity of diabetic hearts is not reversible with endurance swimming.
糖尿病的特征是心脏功能特性降低,这归因于钙激活的ATP酶活性。相比之下,耐力游泳可增强心脏功能特性和钙激活的肌原纤维ATP酶。因此,本研究的目的是观察与实验性糖尿病相关的变化是否可以通过训练得到改善。通过单次静脉注射链脲佐菌素(60mg/kg)诱导糖尿病。血糖和尿糖浓度分别为802±44和6965±617mg/dL。训练对照组和训练糖尿病组动物每周游泳4天(±2%体重),共8周。与久坐不动的对照动物相比,久坐不动的糖尿病动物在游离钙浓度为10μM时,心肌原纤维减少了54%(p<0.05)。游泳训练增强了正常动物钙激活的肌原纤维ATP酶活性。与久坐不动的糖尿病动物相比,游泳8周的糖尿病动物其钙激活的肌原纤维ATP酶活性进一步降低(p<0.05)。同样,耐力游泳后,糖尿病动物中镁刺激的肌原纤维ATP酶活性降低了31%。得出的结论是,糖尿病心脏中钙激活的肌原纤维ATP酶活性降低不能通过耐力游泳逆转。