Supplementation of L‐Arginine, L‐Glutamine, Vitamin C, Vitamin E, Folic Acid, and Green Tea Extract Enhances Serum Nitric Oxide Content and Antifatigue Activity in Mice

Abstract

It has been reported that abundant nitric oxide content in endothelial cells can increase exercise performance. e purpose of this study was to evaluate the potential beneficial effects of a combined extract comprising L-arginine, L-glutamine, vitamin C, vitamin E, folic acid, and green tea extract (LVFG) on nitric oxide content to decrease exercise fatigue. Male ICR (Institute of Cancer Research) mice were randomly divided into 4 groups and orally administered LVFG for 4 weeks. e 4-week LVFG supplementation significantly increased serum nitric oxide content in the LVFG-1X and LVFG-2X groups. Antifatigue activity and exercise performance were evaluated using forelimb grip strength, exhaustive swimming test, and levels of serum lactate, ammonia, glucose, and creatine kinase (CK) after an acute swimming exercise. LVFG supplementation dose-dependently improved exercise performance and nitric oxide content, and it dose-dependently decreased serum ammonia and CK activity after exhaustive swimming test. LVFG's antifatigue properties appear to manifest by preserving energy storage (as blood glucose) and increasing nitric oxide content. Taken together, our results show that LVFG could have the potential for alleviating physical fatigue due to its pharmacological effect of increasing serum nitric oxide content.

Impact of Optimal Timing of Intake of Multi-Ingredient Performance Supplements on Sports Performance, Muscular Damage, and Hormonal Behavior across a Ten-Week Training Camp in Elite Cyclists: A Randomized Clinical Trial

“…L-Glutamine also appears to have anti-inflammatory properties, a feature associated with a reduction of indirect markers EIMD, a reduction of delayed onset muscle soreness (DOMS), and improved muscular function [78]. It has a synergistic effect on various MIPS by fatigue delay and accelerated elimination of fatiguerelated metabolites [77,79]. Chen et al [79], for example, found enhanced serum total protein (TP) content with MIPS supplementation with only L-Arginine and L-Glutamine stimulated muscle protein synthesis.…”

“…It has a synergistic effect on various MIPS by fatigue delay and accelerated elimination of fatiguerelated metabolites [77,79]. Chen et al [79], for example, found enhanced serum total protein (TP) content with MIPS supplementation with only L-Arginine and L-Glutamine stimulated muscle protein synthesis. In this study [79], lactate, ammonia, glucose, and CK levels were positively modulated by MIPS supplementation and were dose-dependent for ammonia, glucose, and CK.…”

A Novel Formula Comprising Wolfberry, Figs, White Lentils, Raspberries, and Maca (WFWRM) Induced Antifatigue Effects in a Forced Exercise Mouse Model

“…A previous study indicated that patients with amino acid deficiency may develop dysfunctions of the pain-inhibitory mechanisms together with fatigue [ 23 ]. Consistent with this conclusion, Chen et al recently showed that L-arginine supplementation could minimize skeletal muscle damage and reduce the accumulation of free radicals to decrease the occurrence of fatigue in rats [ 24 ]. Moreover, L-phenylalanine is a potential lipophilic antioxidant.…”

Suitability of Banana and Plantain Fruits in Modulating Neurodegenerative Diseases: Implicating the In Vitro and In Vivo Evidence from Neuroactive Narratives of Constituent Biomolecules

“…It is involved in physiological processes, such as metabolic regulation and hormonal biosynthesis [ 152 ]. Deficiency in copper levels induces the depletion of several enzyme activities, with precursory implications in the Menkes neurological disorder [ 112 ]. For instance, dopamine-β-hydroxylase (DBH) enzyme is dependent on copper for its neurotransmission role in translating dopamine to norepinephrine [ 112 ].…”

“…Deficiency in copper levels induces the depletion of several enzyme activities, with precursory implications in the Menkes neurological disorder [ 112 ]. For instance, dopamine-β-hydroxylase (DBH) enzyme is dependent on copper for its neurotransmission role in translating dopamine to norepinephrine [ 112 ]. Abnormal neurochemical trends in Menkes disease result when the copper-dependent DBH enzyme activity is altered [ 153 , 154 ].…”