Abstract

It has been reported that abundant nitric oxide content in endothelial cells can increase exercise performance. The 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. The 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.

Highlights

  • Nitric oxide (NO) is known as the “endothelium-derived relaxing factor” for the maintenance of cardiovascular homeostasis

  • Morphological Data. e morphological data from each experimental group are summarized in Table 2. ere were no significant differences in initial or final body weight (BW) or in daily intake of diet and water among the vehicle, LVFG-1X, LVFG-2X, and LVFG-5X groups

  • We observed that LVFG supplementation had no effect on water and diet intake, with BW in each group steadily increasing throughout the experimental period

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Summary

Introduction

Nitric oxide (NO) is known as the “endothelium-derived relaxing factor” for the maintenance of cardiovascular homeostasis. It has become increasingly evident that the decreased bioavailability of NO plays a role in several cardiovascular disorders such as atherosclerosis [3] and hypertension [4]. It is well known that exercise causes an increase in reactive oxygen production (ROS), in active skeletal muscle. A synergistic relationship between the cytotoxic effects of nitric oxide and these active oxygen species is frequently assumed [5]. A previous study has demonstrated that the effect of aerobic exercise on endothelial function is mainly related to improved NO bioavailability due to increased production and/or decreased inactivation by superoxide [6]. Some studies suggest that L-arginine supplementation can reduce skeletal muscle

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