Abstract

Lactate is not merely a metabolic intermediate that serves as an oxidizable and glyconeogenic substrate, but it is also a potential signaling molecule. The objectives of this study were to investigate whether lactate administration enhances post-exercise glycogen repletion in association with cellular signaling activation in different types of skeletal muscle. Eight-week-old male ICR mice performed treadmill running (20 m/min for 60 min) following overnight fasting (16 h). Immediately after the exercise, animals received an intraperitoneal injection of phosphate-buffered saline or sodium lactate (equivalent to 1 g/kg body weight), followed by oral ingestion of water or glucose (2 g/kg body weight). At 60 min of recovery, glucose ingestion enhanced glycogen content in the soleus, plantaris, and gastrocnemius muscles. In addition, lactate injection additively increased glycogen content in the plantaris and gastrocnemius muscles, but not in the soleus muscle. Nevertheless, lactate administration did not significantly alter protein levels related to glucose uptake and oxidation in the plantaris muscle, but enhanced phosphorylation of TBC1D1, a distal protein regulating GLUT4 translocation, was observed in the soleus muscle. Muscle FBP2 protein content was significantly higher in the plantaris and gastrocnemius muscles than in the soleus muscle, whereas MCT1 protein content was significantly higher in the soleus muscle than in the plantaris and gastrocnemius muscles. The current findings suggest that an elevated blood lactate concentration and post-exercise glucose ingestion additively enhance glycogen recovery in glycolytic phenotype muscles. This appears to be associated with glyconeogenic protein content, but not with enhanced glucose uptake, attenuated glucose oxidation, or lactate transport protein.

Highlights

  • Glycogen is formed as a branched polymer of glucose serving as an essential energy deposit stored predominantly in skeletal muscle

  • The plasma insulin level did not differ between the PW and LW groups (Fig. 2G), but it was significantly lower in the LG group than in the PG group at 15 min of recovery (Fig. 2G)

  • Lactate injection had no effect on glycogen content in the soleus muscle (Fig. 3A), we found a positive main effect of lactate injection on glycogen concentration in the plantaris muscle (Fig. 3B) and the gastrocnemius muscle (Fig. 3C)

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Summary

Introduction

Glycogen is formed as a branched polymer of glucose serving as an essential energy deposit stored predominantly in skeletal muscle. Lactate had long been considered to be a waste product that is produced in skeletal muscle and accumulated in the circulation as exercise intensity increases (Gladden 2004). Previous studies have provided evidence that skeletal muscle possesses enzymes that catalyze lactate to glycogen (Opie & Newsholme 1967; McLane & Holloszy 1979; Crabtree et al 1972), and that lactate is incorporated into glycogen in skeletal muscle (McLane & Holloszy 1979; Shiota et al 1984; Jin et al 2015; Bonen et al 1990). A previous study reported that lactate infusion enhanced the disappearance of

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