Abstract

Fatigue is a self-limiting response arising from physical and/or mental weariness, with a consequent personal and economic morbidity on work performance and social relationships. Anti-fatigue intervention is therefore urgently sought. “Qi-invigorating” Chinese tonic herbs, which can improve the energy status in the body according to the theory of traditional Chinese medicine, may produce beneficial effects in fatigue individuals. The herbal formula V-Vital capsule (VVC), which comprises 3 “Qi-invigorating” herbs, namely the root of Rhodiola rosea, Eleutherococcus senticosus and Panax quinquefolium, may produce anti-fatigue effect. In the present study, we investigated the effect of acute/long-term VVC treatment (acute: 0.75, 0.2 and 3.75 kg/day × 1 dose; long-term: 0.075 and 0.25 g/kg/day × 14 doses) on weight-loaded swimming female ICR mice. The weight-loaded swimming time until exhaustion, indicative of exercise endurance capacity, was recorded. Plasma levels of glucose, non-esterified fatty acid (NEFA), lactate and reactive oxygen metabolites (ROM) were measured in the exhausted mice. Glycogen levels in skeletal muscle and liver tissues were also measured. Mitochondrial function status [such as adenine nucleotide translocase (ANT) activity and coupling efficiency] was assayed. Results showed that acute VVC treatment increased the exercise endurance capacity in weight-loaded swimming mice. The ability of acute VVC treatment to enhance the exercise endurance was associated with increases in plasma glucose levels as well as glycogen levels in skeletal muscles and liver tissues, presumably due to the utilization of plasma lactate for gluconeogenesis and/or glycogen synthesis in the liver. While acute VVC treatment reduced the plasma ROM level in weight-loaded swimming mice, it increased the ANT activity. In this regard, the enhancement in exercise endurance afforded by acute VVC treatment might be due to an increase in the glucose supply to the skeletal muscle, the amelioration of systemic oxidative stress and the improvement in mitochondrial function of skeletal muscle. Consistent with the results obtained in acute VVC treatment experiment, the long-term VVC treatment enhances the exercise endurance in weight-loaded swimming mice. The ensemble of results suggests that VVC may offer a promising prospect for enhancing the exercise endurance and alleviating fatigue in humans.

Highlights

  • Fatigue, which is a self-limiting response arising from physical and/or mental weariness, can be classified into three categories, namely secondary fatigue, physiologic fatigue and chronic fatigue [1]

  • The ensemble of results suggests that V-Vital capsule (VVC) may offer a promising prospect for enhancing the exercise endurance and alleviating fatigue in humans

  • While physiologic fatigue refers to an unbalance status of work and rest that can be recovered by taking rest, chronic fatigue is a pathological condition characterized by a persistent debilitating and clinically unexplained fatigue that leads to a substantial impairment in functional status [2]

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Summary

Introduction

Fatigue, which is a self-limiting response arising from physical and/or mental weariness, can be classified into three categories, namely secondary fatigue, physiologic fatigue and chronic fatigue [1]. Secondary fatigue refers to the weariness secondary to medical condition. While physiologic fatigue refers to an unbalance status of work and rest that can be recovered by taking rest, chronic fatigue is a pathological condition characterized by a persistent (or relapsing) debilitating and clinically unexplained fatigue that leads to a substantial impairment in functional status [2]. Despite the diversity of these pathophysiological anomalies, the disruption of structural and functional integrity of mitochondria has been shown to be crucially involved in the development of chronic fatigue, presumably due to an inadequate/inefficient energy supply to skeletal muscle [3] [4]. In order to sustain the energy demands in cytosol of muscle cells, the ATP synthesized in the mitochondria is exchanged with cytosolic ADP by adenine nucleotide translocase (ANT). In view of the consequent personal and economic morbidity arising from the negative impacts of fatigue on work performance and social relationships [1], anti-fatigue intervention is urgently sought

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