Wardlaw G M, Kaplan M L, Lanza-Jacoby S
J Nutr. 1986 Sep;116(9):1841-52. doi: 10.1093/jn/116.9.1841.
This study was designed to determine if treadmill training of the male obese Zucker rat could reverse its deficit in muscle accretion, expose a possible latent defect in its muscle oxidative capacity or significantly alter its food intake and lipid deposition. At 12 wk of age muscle mass and myofibrillar protein concentration were significantly lower and body lipid and food intake were significantly higher in the sedentary obese than in the nonobese rat. Exercise, by both inducing hypophagia and increasing energy output, led to a lower body weight, body lipid, and muscle mass in the exercised than in the nonexercised rats. This response to exercise did not differ between both phenotypes, except for body lipid. In that case the reduction of body lipid was greater for the obese rats. Muscle mitochondrial enzyme activities and rates of mitochondrial respiration in the obese rats were not different or greater than those of their sedentary or pair-exercised nonobese counterparts. Taken together these data indicate that oxidative capacity per unit of muscle is not significantly lower in the obese rats than in nonobese rats in both sedentary and exercised states, but that total muscle oxidative capacity is lower on a whole-animal basis since total muscle mass is lower. Further, exercise reduces, but does not prevent the enhanced weight gain and lipid accretion that characterizes the obese rat.
本研究旨在确定对雄性肥胖 Zucker 大鼠进行跑步机训练是否能逆转其肌肉增长不足的情况,揭示其肌肉氧化能力可能存在的潜在缺陷,或者显著改变其食物摄入量和脂质沉积。12 周龄时,久坐不动的肥胖大鼠的肌肉质量和肌原纤维蛋白浓度显著低于非肥胖大鼠,而身体脂质和食物摄入量则显著高于非肥胖大鼠。运动通过诱导食欲减退和增加能量输出,导致运动组大鼠的体重、身体脂质和肌肉质量低于未运动组大鼠。除了身体脂质外,两种表型对运动的反应没有差异。在这种情况下,肥胖大鼠的身体脂质减少幅度更大。肥胖大鼠的肌肉线粒体酶活性和线粒体呼吸速率与久坐或配对运动的非肥胖对照组大鼠相比,没有差异或更高。综合这些数据表明,在久坐和运动状态下,肥胖大鼠每单位肌肉的氧化能力并不显著低于非肥胖大鼠,但由于总肌肉质量较低,从全动物水平来看,总肌肉氧化能力较低。此外,运动可以减少但不能阻止肥胖大鼠典型的体重增加和脂质积累增加。