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BioMed Research International
Volume 2017 (2017), Article ID 8182020, 12 pages
Research Article

Detection of Urine Metabolites in a Rat Model of Chronic Fatigue Syndrome before and after Exercise

1College of Arts and Sciences, Shanghai Maritime University, Shanghai 201306, China
2Laboratory of Nutrition and Hygiene, Shaanxi Normal University, Xi’an 710119, China
3School of Sports, Hebei Normal University, Shijiazhuang 050090, China

Correspondence should be addressed to Aiping Chi

Received 17 November 2016; Accepted 5 March 2017; Published 22 March 2017

Academic Editor: Isabelle Chevalot

Copyright © 2017 Changzhuan Shao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Purpose. The aim of the present study was to elucidate the metabolic mechanisms associated with chronic fatigue syndrome (CFS) via an analysis of urine metabolites prior to and following exercise in a rat model. Methods. A rat model of CFS was established using restraint-stress, forced exercise, and crowded and noisy environments over a period of 4 weeks. Behavioral experiments were conducted in order to evaluate the model. Urine metabolites were analyzed via gas chromatography-mass spectrometry (GC-MS) in combination with multivariate statistical analysis before and after exercise. Results. A total of 20 metabolites were detected in CFS rats before and after exercise. Three metabolic pathways (TCA cycle; alanine, aspartate, and glutamate metabolism; steroid hormone biosynthesis) were significantly impacted before and after exercise, while sphingolipid metabolism alone exhibited significant alterations after exercise only. Conclusion. In addition to metabolic disturbances involving some energy substances, alterations in steroid hormone biosynthesis and sphingolipid metabolism were detected in CFS rats. Sphingosine and 21-hydroxypregnenolone may be key biomarkers of CFS, potentially offering evidence in support of immune dysfunction and hypothalamic-pituitary-adrenal (HPA) axis hypoactivity in patients with CFS.