Phytoecdysteroids Do Not Have Anabolic Effects in Skeletal Muscle in Sedentary Aging Mice.

Marcus M Lawrence,Kevin A Zwetsloot,Mary Grace,Chase A Sherman,Joshua R Huot,Mary Ann Lila,Susan T Arthur,David C Nieman,Vladimir Badmaev,R Andrew Shanely

doi:10.3390/ijerph18020370

Abstract

Skeletal muscle mass and strength are lost with aging. Phytoecdysteroids, in particular 20-hydroxyecdysone (20E), increase protein synthesis in C2C12 skeletal muscle cells and muscle strength in young rats. The objective of this study was to determine whether an extract from Ajuga turkestanica (ATE), enriched in phytoecdysteroids, and 20E affect skeletal muscle mass and fiber size, fiber type, activation of the PI3K–Akt signaling pathway, and the mRNA levels of MAFbx, MuRF-1, and myostatin in sedentary aging mice. Aging male C57BL/6 mice (20 months old) received ATE, 20E, or vehicle (CT) once per day for 28 days or a single acute dose. Treatment did not alter body, muscle, or organ mass; fiber cross-sectional area; or fiber type in the triceps brachii or plantaris muscles. Likewise, protein synthesis signaling markers (i.e., phosphorylation of AktSer473 and p70S6kThr389) measured after either 28 days or acutely were unchanged. Neither ATE nor 20E treatment for 28 days affected the mRNA levels of MAFbx, MuRF-1, and myostatin. In conclusion, these data indicate that phytoecdysteroid treatment does not alter muscle mass or fiber type, nor does it activate protein synthesis signaling in the skeletal muscle of sedentary aging mice.

Highlights

The loss of muscle mass and strength with advanced age is associated with decreased physical function, including loss of independence and eventually premature death [1]
The blunted muscle protein synthesis response observed in aged muscle is largely due to impaired activation of the PI3K/Akt/mTOR/p70S6K signaling axis or PI3K–Akt pathway [3,4]
Body mass was determined for each treatment prior to day 1 (D1) and day 28 (D28)

Summary

Introduction

The loss of muscle mass and strength with advanced age (sarcopenia) is associated with decreased physical function, including loss of independence and eventually premature death [1]. Aged skeletal muscle has a blunted ability to stimulate muscle protein synthesis in response to anabolic stimuli, termed anabolic resistance [2]. The blunted muscle protein synthesis response observed in aged muscle is largely due to impaired activation of the PI3K/Akt/mTOR/p70S6K signaling axis or PI3K–Akt pathway [3,4]. Sarcopenia is related to changes in the levels of negative growth regulators, e.g., myostatin, and muscle protein degradation enzymes. Myostatin limits skeletal muscle growth, by attenuating the PI3K–Akt pathway, thereby downregulating muscle protein synthesis [5,6]. Compared to young adult muscle, myostatin expression is elevated in aged

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