Abstract

With an aim to explore the effects of β‐alanine (β‐A) on spatial memory and fatigue resistance, Kunming mice were treated with different concentrations of β‐A (418, 836, and 2090 mg·kg‐1 ·day‐1). After gavage feeding with β‐A for 10 weeks, results of the maze and MWM tests showed that β‐A can enhance spatial learning and memory in mice. After evaluating the fatigue resistance, biochemical parameters (LG, GG, BUN, SOD, and MDA) showed significant differences in the low concentration treatment group compared to control group. Our data demonstrated that the appropriate dose of β‐A can alleviate the oxidative stress and muscle fatigue in mice. Subsequently, expression of mRNA of key genes involved in cAMP‐PKA pathway (PDE4A, MAPK1, adcy1, cAMP and CREB) was up regulated. Also, expression levels of apoptotic pathway genes were significantly affected as confirmed by qPCR and Western blotting. Our results demonstrated that β‐A can enhance spatial learning and memory in mice via regulation of cAMP‐PKA and apoptotic pathway.

Highlights

  • Beta-alanine (β -A) as a non-essential amino acid (AA) in synergism with L-histidine synthesizes carnosine in vivo [1] and the latter is a dipeptide which is abundant in skeletal muscle. βA is considered to be the rate-limiting precursor for carnosine production in vivo [2]

  • We found that the expression trends of PDE4A, MAPK1, adcy1, and cAMP response element binding protein (CREB) genes were similar with up regulation, with the most pronounced results at medium concentrations (p

  • Through the y-maze test results, we speculate that intragastric administration with β-A may have a positive effect on short-term spatial memory in mice

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Summary

Introduction

Beta-alanine (β -A) as a non-essential amino acid (AA) in synergism with L-histidine synthesizes carnosine in vivo [1] and the latter is a dipeptide which is abundant in skeletal muscle. βA is considered to be the rate-limiting precursor for carnosine production in vivo [2]. ΒA is considered to be the rate-limiting precursor for carnosine production in vivo [2]. The exogenous supplementation with βA is considered to be an effective method for improvement of carnosine content in muscle [2]. Supplementation with β-A has been shown to influence cycle capacity [4], ventilatory threshold, and fatigue time in humans [5]. With the supplementation higher than 800 mg, it can cause abnormalities in the host body [6]. Recovering from fatigue state to normal state is a long process [8], which has a negative impact on the normal process of human body [9]. Muscle fatigue is closely related to the exercise intensity of body and it is often measured by metabolites produced during exercise [10]. The occurrence of muscle fatigue is related to many factors

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