Department of Physiology.
Department of Family Medicine, Adana Numune Hospital , Adana, Turkey.
J Sports Sci Med. 2005 Dec 1;4(4):472-81. eCollection 2005 Dec.
The effects of aerobic exercise training on skeletal muscle endurance capacity were examined in diabetic rats in situ. Moderate diabetes was induced by iv injection of streptozotocin and an exercise training program on a treadmill was carried out for 8 weeks. The animals randomly assigned to one of the four experimental groups: control-sedentary (CS), control-exercise (CE), diabetic-sedentary (DS) or diabetic-exercise (DE). The changes in the muscle endurance capacity were evaluated through the square wave impulses (supramaximal) of 0.2-ms duration at 1 Hz in the in situ gastrocnemius-soleus muscle complex. Muscle was stimulated continuously until tension development reduced to the half of this maximal value. Time interval between the beginning and the end of stimulation period is defined as contraction duration. Following the training period, blood glucose level reduced significantly in the DE group compared to DS group (p < 0.05). The soles muscle citrate synthase activity was increased significantly in both of the trained groups compared to sedentary animals (p < 0.05). Fatigued muscle lactate values were not significantly different from each other. Ultrastractural abnormality of the skeletal muscle in DS group disappeared with training. Presence of increased lipid droplets, mitochondria clusters and glycogen accumulation was observed in the skeletal muscle of DE group. The contraction duration was longer in the DE group than others (p < 0.001). Fatigue resistance of exercised diabetic animals may be explained by increased intramyocellular lipid droplets, high blood glucose level and muscle citrate synthase activity. Key PointsAerobic training of diabetic animals increased the endurance capacity.Presence of abnormal ultrastructural alterations with diabetes disaapered with regular training.Increased intramyocelluler lipid droplets, high blood glucose level with citrate synthase activity may explain this finding.
研究人员采用在体实验观察了有氧运动训练对糖尿病大鼠骨骼肌耐力的影响。通过静脉注射链脲佐菌素诱导中度糖尿病,然后让动物在跑步机上进行 8 周的运动训练。动物随机分为四组:对照组安静(CS)、对照组运动(CE)、糖尿病组安静(DS)或糖尿病组运动(DE)。通过在体比目鱼肌-跟腱复合体上 0.2-ms 持续时间、1Hz 的方波脉冲(超最大刺激)评估肌肉耐力的变化。肌肉持续受到刺激,直到张力发展降低到最大张力的一半。刺激期开始和结束之间的时间间隔定义为收缩持续时间。经过训练期后,DE 组的血糖水平明显低于 DS 组(p < 0.05)。与安静组相比,两组训练组的跖肌柠檬酸合酶活性均显著升高(p < 0.05)。疲劳肌肉的乳酸值彼此之间没有显著差异。DS 组骨骼肌的超微结构异常在训练后消失。DE 组骨骼肌中观察到增加的脂质滴、线粒体簇和糖原积累。与其他组相比,DE 组的收缩持续时间更长(p < 0.001)。运动糖尿病动物的抗疲劳能力可能归因于细胞内脂质滴增加、高血糖水平和肌肉柠檬酸合酶活性。关键点糖尿病动物的有氧运动训练增加了耐力。糖尿病时存在的异常超微结构改变在定期训练后消失。细胞内脂质滴增加、高血糖水平和柠檬酸合酶活性可能解释了这一发现。