We investigated the effect of royal jelly (RJ), a natural secretion from worker bees, on the endurance training-induced mitochondrial adaptations in skeletal muscles of ICR mice. Mice received either RJ (1.0 mg/g body weight) or distilled water for three weeks. The mice in the training group were subjected to endurance training (20 m/min; 60 min; 5 times/week). There was a main effect of endurance training on the maximal activities of the mitochondrial enzymes, citrate synthase (CS), and β-hydroxyacyl coenzyme Adehydrogenase (β-HAD), in the plantaris and tibialis anterior (TA) muscles, while no effect of RJ treatment was observed. In the soleus muscle, CS and β-HAD maximal activities were significantly increased by endurance training in the RJ-treated group, while there was no effect of training in the control group. Furthermore, we investigated the effects of acute RJ treatment on the signaling cascade involved in mitochondrial biogenesis. In the soleus, phosphorylation of 5′-AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) were additively increased by a single RJ treatment and endurance exercise, while only an exercise effect was found in the plantaris and TA muscles. These results indicate that the RJ treatment induced mitochondrial adaptation with endurance training by AMPK activation in the soleus muscles of ICR mice.

We previously reported that taurine (2-aminoethanesulfonic acid; dose: 0.5 mg/g body weight) administration after treadmill running at 25 m/min for 90 min increased the glycogen concentration in the skeletal muscle of ICR mice at 120 min after the exercise (Takahashi et al. 2014). In the current study, we further investigated the effects of taurine administration on glycogen repletion and carbohydrate metabolism in the tibialis anterior muscle after endurance exercise. The metabolomic profiles of the tibialis anterior muscle at 120 min after the exercise were analyzed by a capillary electrophoresis-time-of-flight mass spectrometry (n=6). Fructose-1,6-bisphosphate (F1,6P), a glycogenolytic/glycolytic intermediate produced by phosphofructokinase, was significantly lower in the taurine-treated group than that in the control group (p<0.01). Dihydroxyacetonephosphate (DHAP), a downstream product of F1,6P was lower (p=0.05) and glycerol 3-phosphate, a downstream product of F1,6P and DHAP, tended to be lower (p=0.09) in the taurine-treated group than in the controls. At that time, phosphorylated Ser293 on the E1α subunit of pyruvate dehydrogenase (PDH) tended to be higher in the taurine-treated mice than in the controls (p=0.09, n=5). There was a positive correlation between phosphorylation of the PDH E1α subunit at Ser293 and glycogen concentration (r=0.73, p<0.05). Our results showed that the enhanced glycogen repletion in skeletal muscle by taurine treatment during the post-exercise phase was accompanied by the lower levels of glycogenolytic/glycolytic intermediates.

Exercise training enhances oxidative capacity whereas detraining reduces mitochondrial content in skeletal muscle. The strategy to suppress the detraining‐induced reduction of mitochondrial content has not been fully elucidated. As previous studies reported that branched‐chain amino acid (BCAA) ingestion increased mitochondrial content in skeletal muscle, we evaluated whether BCAA supplementation could suppress the detraining‐induced reduction of mitochondrial content. Six‐week‐old male Institute of Cancer Research (ICR) mice were randomly divided into four groups as follows: control (Con), endurance training (Tr), detraining (DeTr), and detraining with BCAA supplementation (DeTr + BCAA). Mice in Tr, DeTr, and DeTr + BCAA performed treadmill running exercises [20–30 m/min, 60 min, 5 times/week, 4 weeks]. Then, mice in DeTr and DeTr + BCAA were administered with water or BCAA [0.6 mg/g of body weight, twice daily] for 2 weeks of detraining. In whole skeletal muscle, mitochondrial enzyme activities and protein content were decreased after 2 weeks of detraining, but the reduction was suppressed by BCAA supplementation. Peroxisome proliferator‐activated receptor γ coactivator‐1α (PGC‐1α) protein content, a master regulator of mitochondrial biogenesis, was decreased by detraining irrespective of BCAA ingestion. Regarding mitochondrial degradation, BCL2/adenovirus E1B 19 kDa protein‐interacting protein 3 (BNIP3), a mitophagy‐related protein, was significantly higher in the Tr group than in the DeTr + BCAA group, but not different from in the DeTr group. With respect to mitochondrial quality, BCAA ingestion did not affect oxygen consumption rate (OCR) and reactive oxygen species (ROS) production in isolated mitochondria. Our findings suggest that BCAA ingestion suppresses the detraining‐induced reduction of mitochondrial content partly through inhibiting mitophagy.

When a high-carbohydrate diet is ingested, whether as small frequent snacks or as large meals, there is no difference between the two with respect to post-exercise glycogen storage for a period of ...