Document Type : Original Article
Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tnnoudai, Tsukuba, Ibaraki, Japan
Faculty of Health and Sport Sciences, University of Tsukuba, Tennodai, Tsukuba, Ibaraki, Japan
Reserch Fellow in Japan Society for Promotion Science, Tokyo, Japan
Kashima Gakuen High School, Kashima Gakuen School Corporation, Tanobe, Kashima, Ibaraki, Japan
Tsukuba Life Science Innovation Program (T-LSI), University of Tsukuba, Tennodai, Tsukuba, Ibaraki, Japan
Background: Maslinic acid (MA) is an olive-derived extract with the structure of pentacyclic triterpenes, which potents anti-inflammatory effects. It has been reported that the combination of MA and resistance exercise increases skeletal muscle mass, but there are many unknowns regarding its detailed molecular mechanism. The present study aimed to clarify the effect of MA supplementation on muscle hypertrophic response to acute muscle contraction-induced resistance exercise using animal model.
Methods: Seven-week-old ICR (Institute of Cancer Research) male mice fed a diet containing 0.27% MA during an acclimatization of 1 week. After an overnight fast, the right gastrocnemius muscle was subjected to acute resistance exercise using percutaneous electrical stimulationinduced muscle contractions, while the left gastrocnemius muscle was saved as control. The muscle was excised at 1, 3, and 6 hours after exercise and protein synthesis-related signaling expressions were examined.
Results: MA was demonstrated to significantly activate the downstream targets of mammalian/mechanistic target of rapamycin (mTOR), phosphorylated ribosomal protein S6 (rpS6) at Ser240/244 site particularly, while Akt/glycogen synthase kinase-3β (GSK-3β) pathway and mitogenactivated protein kinase (MAPK) signaling were unaffected.
Conclusion: Our results suggested that acute resistance exercise-induced muscle protein synthesis-promoting effect of MA is supported by the activation of downstream signaling of mTOR.