Kuipers H, Costill D L, Porter D A, Fink W J, Morse W M
J Appl Physiol (1985). 1986 Sep;61(3):859-63. doi: 10.1152/jappl.1986.61.3.859.
This investigation studied the effect of an oral glucose feeding on glycogen sparing during exercise in non-glycogen-depleted and glycogen-depleted endurance-trained rats. The non-glycogen-depleted rats received via a stomach tube 2 ml of a 20% glucose solution labeled with [U-14C]glucose just prior to exercise (1 h at 25 m/min). Another group of rats ran for 40 min at higher intensity to deplete glycogen stores, after which they received the same glucose feeding and continued running for 1 h at 25 m/min. The initial 40-min run depleted glycogen in heart, skeletal muscle, and liver. In the non-glycogen-depleted rats the glucose feeding spared glycogen in the liver, primarily from the oxidation of blood-borne glucose in muscle. In the glycogen-depleted rats, muscle glycogen was repleted after the feeding, but sources other than the administered glucose also contributed to glycogen synthesis. The results suggest that glycogen depletion rather than the glucose feeding per se stimulates glycogen resynthesis in muscle during exercise in endurance-trained rats.
本研究调查了口服葡萄糖对非糖原耗尽和糖原耗尽的耐力训练大鼠运动期间糖原节约的影响。非糖原耗尽的大鼠在运动前(以25米/分钟的速度运动1小时)通过胃管接受2毫升含有[U-14C]葡萄糖的20%葡萄糖溶液。另一组大鼠以更高强度跑40分钟以耗尽糖原储备,之后它们接受相同的葡萄糖喂食,并继续以25米/分钟的速度跑1小时。最初的40分钟跑步耗尽了心脏、骨骼肌和肝脏中的糖原。在非糖原耗尽的大鼠中,葡萄糖喂食使肝脏中的糖原得以节约,主要是通过肌肉中血源性葡萄糖的氧化。在糖原耗尽的大鼠中,喂食后肌肉糖原得到补充,但除了给予的葡萄糖外,其他来源也有助于糖原合成。结果表明,在耐力训练大鼠运动期间,糖原耗竭而非葡萄糖喂食本身刺激了肌肉中的糖原再合成。