Department of Health and Nutrition, Niigata University of Health and Welfare, Niigata, Japan.
J Physiol Sci. 2012 Jan;62(1):1-9. doi: 10.1007/s12576-011-0170-y. Epub 2011 Oct 8.
A single bout of prolonged endurance exercise stimulates glucose transport in skeletal muscles, leading to post-exercise muscle glycogen supercompensation if sufficient carbohydrate is provided after the cessation of exercise. Although we recently found that short-term sprint interval exercise also stimulates muscle glucose transport, the effect of this type of exercise on glycogen supercompensation is uncertain. Therefore, we compared the extent of muscle glycogen accumulation in response to carbohydrate feeding following sprint interval exercise with that following endurance exercise. In this study, 16-h-fasted rats underwent a bout of high-intensity intermittent swimming (HIS) as a model of sprint interval exercise or low-intensity prolonged swimming (LIS) as a model of endurance exercise. During HIS, the rats swam for eight 20-s sessions while burdened with a weight equal to 18% of their body weight. The LIS rats swam with no load for 3 h. The exercised rats were then refed for 4, 8, 12, or 16 h. Glycogen levels were almost depleted in the epitrochlearis muscles of HIS- or LIS-exercised rats immediately after the cessation of exercise. A rapid increase in muscle glycogen levels occurred during 4 h of refeeding, and glycogen levels had peaked at the end of 8 h of refeeding in each group of exercised refed rats. The peak glycogen levels during refeeding were not different between HIS- and LIS-exercised refed rats. Furthermore, although a large accumulation of muscle glycogen in response to carbohydrate refeeding is known to be associated with decreased insulin responsiveness of glucose transport, and despite the fact that muscle glycogen supercompensation was observed in the muscles of our exercised rats at the end of 4 h of refeeding, insulin responsiveness was not decreased in the muscles of either HIS- or LIS-exercised refed rats compared with non-exercised fasted control rats at this time point. These results suggest that sprint interval exercise enhances muscle glycogen supercompensation in response to carbohydrate refeeding as well as prolonged endurance exercise does. Furthermore, in this study, both HIS and LIS exercise prevented insulin resistance of glucose transport in glycogen supercompensated muscle during the early phase of carbohydrate refeeding. This probably led to the enhanced muscle glycogen supercompensation after exercise.
单次长时间耐力运动刺激骨骼肌葡萄糖转运,若运动停止后摄入足够的碳水化合物,会导致运动后肌肉糖原超补偿。虽然我们最近发现短期冲刺间歇运动也能刺激肌肉葡萄糖转运,但这种运动对糖原超补偿的影响尚不确定。因此,我们比较了冲刺间歇运动和耐力运动后碳水化合物喂养对肌肉糖原积累的影响。在这项研究中,16 小时禁食的大鼠进行高强度间歇游泳(HIS)作为冲刺间歇运动的模型,或进行低强度持续游泳(LIS)作为耐力运动的模型。在 HIS 中,大鼠在负重 18%体重的情况下,每 20 秒游泳 8 次。LIS 大鼠无负荷游泳 3 小时。然后,让运动后的大鼠再进食 4、8、12 或 16 小时。运动后 HIS 或 LIS 大鼠的比目鱼肌中的糖原水平在运动停止后几乎耗尽。在再进食的 4 小时内,肌肉糖原水平迅速增加,并且在每组运动后再进食的大鼠中,糖原水平在再进食 8 小时时达到峰值。再进食期间,HIS 和 LIS 运动后的再进食大鼠的峰值糖原水平没有差异。此外,尽管已知大量的肌肉糖原积累对葡萄糖转运的胰岛素反应性降低,并且尽管我们的运动后的大鼠在再进食 4 小时时肌肉中观察到糖原超补偿,但在这个时间点,与非运动禁食对照大鼠相比,HIS 或 LIS 运动后的再进食大鼠的肌肉胰岛素反应性并没有降低。这些结果表明,与持续耐力运动一样,冲刺间歇运动也能增强碳水化合物再进食后的肌肉糖原超补偿。此外,在这项研究中,HIS 和 LIS 运动都能防止碳水化合物再进食早期糖原超补偿肌肉的胰岛素抵抗,这可能导致运动后肌肉糖原的超补偿增强。