Effects of post-exercise glucose ingestion at different solution temperatures on glycogen repletion in mice.

Carbohydrate ingestion is essential for glycogen recovery after exercise. Although studies have investigated methods for enhancement of glycogen repletion with regard to nutrients and their amounts, no studies have examined the effect of temperature of the ingested solution on glycogen recovery. Therefore, this study aimed to investigate the effect of the temperature of glucose solution ingested after exercise on glycogen recovery. Seven-week-old male ICR mice were fasted for 16 h and subjected to treadmill running exercise (20 m/min for 60 min) to decrease glycogen storage. Then, the mice were administered glucose (1.5 mg/g body weight) at three different solution temperatures: 4°C, cold solution group (Cold); 37°C, mild solution group (Mild); and 55°C, hot solution group (Hot). Our results revealed that blood glucose, plasma insulin, and muscle glycogen concentrations did not differ among the three groups. In contrast, liver glycogen concentration in the Hot group was significantly higher than that in the post-exercise and Cold groups (p < 0.05). Furthermore, portal glucose concentration was significantly higher in the Hot group than in the Cold group (p < 0.01). These observations suggest that postexercise muscle glycogen repletion occurs regardless of glucose solution temperature, and that ingesting hot glucose solution after exercise can be an effective means for liver glycogen repletion compared with cold glucose solution ingestion.

High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery.

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.

Enhanced skeletal muscle glycogen repletion after endurance exercise is associated with higher plasma insulin and skeletal muscle hexokinase 2 protein levels in mice: comparison of level running and downhill running model.

To identify factors that influence post-exercise muscle glycogen repletion, we compared the glycogen recovery after level running with downhill running, an experimental model of impaired post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice performed endurance level running (no inclination) or downhill running (-5° inclination) on a treadmill. In Experiment 1, to determine whether these two types of exercise resulted in different post-exercise glycogen repletion patterns, tissues were harvested immediately post-exercise or 2 days post-exercise. Compared to the control (sedentary) group, level running induced significant glycogen supercompensation in the soleus muscle at 2 days post-exercise (p = 0.002). Downhill running did not induce glycogen supercompensation. In Experiment 2, mice were orally administered glucose 1 day post-exercise; this induced glycogen supercompensation in soleus and plantaris muscle only in the level running group (soleus: p = 0.005, plantaris: p = 0.003). There were significant positive main effects of level running compared to downhill running on the plasma insulin (p = 0.017) and C-peptide concentration (p = 0.011). There was no difference in the glucose transporter 4 level or the phosphorylated states of proteins related to insulin signaling and metabolism in skeletal muscle. The level running group showed significantly higher hexokinase 2 (HK2) protein content in both soleus (p = 0.046) and plantaris muscles (p =0.044) at 1 day after exercise compared to the downhill running group. Our findings suggest that post-exercise skeletal muscle glycogen repletion might be partly influenced by plasma insulin and skeletal muscle HK2 protein levels.