Enhanced glycogen repletion in liver and skeletal muscle with citrate orally fed after exhaustive treadmill running and swimming.
A possibility whether an oral feeding of citrate, which has been reported to inhibit phosphofructokinase in vitro, following exercise to exhaustion could increase the rate of glycogen repletion in liver and soleus muscle was tested in treadmill running trained (experiments 1 and 2) and swimming trained rats (experiment 3). An exhaustive running or swimming was loaded at the end of the experiments, resulting in a significant reduction in liver and soleus muscle glycogen stores. The feeding of 1.0 and 0.5 g of citrate per kg of body weight just after the exhaustive running could significantly increase the liver glycogen repletion during a 2-hr recovery period, but this was not observed in soleus muscle (experiment 1). As compared with a single feeding of 3.3 g of glucose per kg of body weight, a mixed feeding of 0.5 g of citrate and 3.0 g of glucose after an exhaustive running (experiment 2) and swimming (experiment 3) could significantly enhance the repletion of glycogen stores in both liver and soleus muscle. These results clearly indicate that the postexercise feeding of citrate can stimulate the glycogen repletion in liver and skeletal muscle during an early period of recovery.
D000284:Administration, Oral; D000818:Animals; D002951:Citrates / Q000008:administration & dosage*; D019343:Citric Acid; D005260:Female; D006003:Glycogen / Q000096:biosynthesis*; D008099:Liver / Q000187:drug effects*; D008112:Liver Glycogen / Q000096:biosynthesis; D009132:Muscles / Q000187:drug effects* / Q000378:metabolism; D005082:Physical Exertion; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D002951:Citrates; D008112:Liver Glycogen; D019343:Citric Acid; D006003:Glycogen