Poland J L, Trowbridge C, Poland J W
Can J Physiol Pharmacol. 1980 Oct;58(10):1229-33. doi: 10.1139/y80-186.
Carbohydrate and lipid substrates were measured in rats during recovery following exercise or a 24-h fast and compared with values from time-matched control (rested, fed) rats. After exercise muscle glycogen recovered at the expense of liver glycogen repletion. Myocardial glycogen supercompensated whereas soleus, red vastus lateralis (RVL) and white vastus lateralis glycogen merely returned to control levels. A similar recovery pattern occurred after fasting with refeeding promoting glycogen synthesis in the liver, skeletal muscles, and even in the myocardium, where glycogen had already been elevated by the fast. Both soleus and RVL muscles, along with the myocardium, exhibited glycogen supercompensation. Both exercise and fasting increased plasma free fatty acid (FFA) levels which favor myocardial glycogen synthesis. Unchanged tissue triglycerides and relatively stable blood glucose levels suggest that these are unlikely influences on glycogen recovery. It is concluded that exercise per se is unlikely to induce glycogen supercompensation in skeletal muscles though myocardial glycogen supercompensation readily occurs, that food restriction prior to exercise quantitatively affects substrate recovery though its impact could go unnoticed because of the qualitative similarities between substrate recovery following exercise or fasting, and that FFA is the only major energy substrate concurrently changing with glycogen after exercise or fasting which could facilitate glycogen synthesis.
在运动或禁食24小时后的恢复过程中,对大鼠的碳水化合物和脂质底物进行了测量,并与时间匹配的对照(静息、进食)大鼠的值进行了比较。运动后,肌肉糖原以肝糖原补充为代价而恢复。心肌糖原出现超补偿,而比目鱼肌、红色股外侧肌(RVL)和白色股外侧肌糖原仅恢复到对照水平。禁食后再喂食时,肝脏、骨骼肌甚至心肌中糖原合成增加,出现了类似的恢复模式,禁食已使心肌糖原升高。比目鱼肌和RVL肌肉以及心肌均表现出糖原超补偿。运动和禁食均会升高血浆游离脂肪酸(FFA)水平,这有利于心肌糖原合成。组织甘油三酯不变和血糖水平相对稳定表明,这些因素不太可能影响糖原恢复。结论是,运动本身不太可能在骨骼肌中诱导糖原超补偿,尽管心肌糖原超补偿很容易发生;运动前的食物限制会定量影响底物恢复,但其影响可能因运动或禁食后底物恢复的定性相似性而未被注意到;FFA是运动或禁食后唯一与糖原同时变化的主要能量底物,可促进糖原合成。