Abstract

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.

Highlights

  • Mitochondria are important organelles that produce the adenosine triphosphate (ATP) required for the contraction of skeletal muscles

  • The mice were weighed post-treatment and the results suggested that neither the endurance training nor the royal jelly (RJ) treatment had a significant effect on their final body weight at the end of the experiment

  • Was observed in the tibialis anterior (TA) muscle (Figure 5C). These results indicate that a differential phosphorylation status of2018, the10, proteins involved in the mitochondrial biogenesis in different skeletal muscles upon Nutrients treatment and endurance training

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Summary

Introduction

Mitochondria are important organelles that produce the adenosine triphosphate (ATP) required for the contraction of skeletal muscles. It is well known that endurance exercise promotes mitochondrial biogenesis in skeletal muscles [1]. As the mitochondrial oxidative capacity is related to glycogen-sparing [2], many athletes try to stimulate the mitochondrial adaptations in the skeletal muscles with daily training. Decreased mitochondrial content has been associated with some metabolic diseases like insulin resistance and obesity [3] and sarcopenia [4]. It is of general interest to increase mitochondrial content to maintain good health and a high quality of life. Any additional method to increase the mitochondrial content might be greatly beneficial to both the athletes looking to improve their performance, as well as the common people to maintain their health

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