Abstract

Antrodia cinnamomea, a folk medicinal mushroom, has numerous biological effects. In this study, we aim to assess whether the antifatigue effects of A. cinnamomea mycelia (AC) and its underlying mechanisms are related to oxidative stress signaling using behavioral mouse models and biochemical indices detection. Mice were orally treated with AC at doses of 0.1, 0.3, and 0.9 g/kg for three weeks. AC had no effect on the spontaneous activities of mice indicating its safety on central nervous system. Furthermore, results obtained from weight-loaded forced swimming test, rotary rod test, and exhausted running test confirmed that AC significantly enhanced exercise tolerance of mice. Biochemical indices levels showed that these effects were closely correlated with inhibiting the depletion of glycogen and adenosine triphosphate stores, regulating oxidative stress-related parameters (superoxide dismutase, glutathione peroxidase, reactive oxygen species, and malondialdehyde) in serum, skeletal muscle, and liver of mice. Moreover, the effects of AC may be related with its regulation on the activations of AMP-activated protein kinase, protein kinase B, and mammalian target of rapamycin in liver and skeletal muscle of mice. Altogether, our data suggest that the antifatigue properties of AC may be one such modulation mechanism via oxidative stress-related signaling in mice.

Highlights

  • Fatigue, a complex symptom, is accompanied by difficulty in initiating or sustaining activities, resulting from severe stress, mental work, and/or hard physical labour [1]

  • The present study provided evidence that the oxidative stress may be the potential mechanism responsible for the antifatigue properties of A. cinnamomea mycelia (AC)

  • Strenuous exercise is accompanied by the increased generation of free radical productions which contribute to oxidative stress [34]

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Summary

Introduction

A complex symptom, is accompanied by difficulty in initiating or sustaining activities, resulting from severe stress, mental work, and/or hard physical labour [1]. Liver serves as a reservoir for blood, glycogen, fats, carbohydrates, and even proteins, where protein synthesis and substance metabolism are performed. Due to the high intensity or exhaustive exercise, free radicals are reportedly formed in limb muscle and in vitro contraction [5]. ROS leads to fatigue by damaging muscles, especially in the diaphragm [5]. Evidence provided further supports that depressing depletion of energy source had positive effects on antifatigue, and inhibiting free radical generation enhanced exercise performance [7]. Adenosine 5󸀠-monophosphate- (AMP-) activated protein kinase (AMPK) is very sensitive to the ratio of AMP/ATP, leading to regulating the absorption of glucose and fatty acids [8]. High glucose activates mammalian target of rapamycin (mTOR) signaling, enhances the anabolic response of protein and lipid [9]

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