Effects of Royal Jelly Administration on Endurance Training-Induced Mitochondrial Adaptations in Skeletal Muscle

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.

Apitherapy for Age-Related Skeletal Muscle Dysfunction (Sarcopenia): A Review on the Effects of Royal Jelly, Propolis, and Bee Pollen

“…Therefore, it is possible that the antioxidant activity demonstrated by bee products, particularly that expressed in the mitochondria, is associated with their metabolic and hypoglycemic activities. For instance, 10-HDA increased expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in skeletal muscle of diabetic mice [ 112 , 119 ]. Similarly, aged mice treated with amino acids similar to those found in royal jelly demonstrated improved size of muscle fiber by increasing PGC-1α mRNA levels.…”

“…Japanese researchers proved that oral consumption of royal jelly and 10-HDA induced mitochondrial adaptation in the soleus muscle when accompanied with endurance training. These compounds also enhanced glucose uptake in skeletal muscle by inducing the phosphorylation of AMPK [ 106 , 112 ], an effect that was mediated by the upstream kinase Ca²⁺/calmodulin-dependent kinaseβ—independently of changes in AMP:ATP ratio and the liver kinase B1 pathway. Activation of AMPK was followed by translocation of GLUT4 to the plasma membrane of L6 myotubes [ 106 ].…”

“…These products increased muscle mass [ 36 , 54 , 95 , 96 ] and restored muscle function in old [ 36 , 38 , 95 , 96 , 97 ] and exhausted [ 54 , 90 , 101 , 106 ] animal models. As shown in Panel ( D ), these effects originated from multiple molecular events that resulted in several therapeutic actions including amelioration of inflammation [ 36 , 38 , 90 , 101 , 107 , 108 ] and oxidative [ 95 , 106 , 109 , 110 ] damages, metabolic regulation [ 69 , 70 , 96 , 100 , 106 , 109 , 111 , 112 ], enhancements of satellite cell responsiveness [ 96 , 97 ], improving muscular blood supply [ 110 ], inhibition of catabolic genes [ 97 ], and promotion of peripheral neuronal regeneration [ 113 ]. However, future studies could examine the involvement of other possible mechanisms in the muscle-enhancing potential of these bee products such as the role of gut microbiome in the absorption of nutrient contents of bee products.…”

Apitherapy for Osteoarthritis: Perspectives from Basic Research

“…Honey prevents activation of the caspases pathway and ROS-induced mitochondrial dysfunction [78]. In an environment of mitochondria hyperactivation, royal jelly facilitates its adaptation to the increase of its function by inducing mitochondrial biogenesis [79].…”

Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy

“…In mice, feeding of RJ increases the serum IGF1 levels and stimulates regeneration of injured muscle via the IGF1-Akt pathway in satellite cells [ 32 ]. Administration of RJ also induces mitochondrial adaptation with endurance training by adenosine monophosphate-activated protein kinase (AMPK) activation in the soleus muscle of ICR mice [ 33 ]. Human clinical trials demonstrated that RJ has the potential to attenuate the age-related decline in grip strength [ 34 ].…”