The mechanisms of the manifestation of central fatigue were studied. In the cerebrospinal fluid (CSF) from exercise-fatigued rats there was a factor that depressed the spontaneous motor activity (SMA) of the animals and caused the kind of behavior that is observed in exhausted animals. A bioassay which utilized hydra, a freshwater coelenterate, strongly suggested the existence of transforming growth factor-β (TGF-β) in the CSF. Because the immunoneutralizing treatment of the CSF from fatigued rats with anti-TGF-β antibody eliminated the factor that depresses the SMA of animals, the identity of this factor was shown to be TGF-β. The findings that the intracisternal administration of purified TGF-β depressed the SMA in a dose-dependent manner, and that the concentration of TGF-β in the CSF increased with an increase in the intensity of the exercise which was being used to cause fatigue, supported the speculation that this factor was responsible for the manifestation of central fatigue. In addition, we also demonstrated that TGF-β acted on the brain and modulated the activities of neurons, and that this changed the whole body metabolism to utilize more fat and enhanced the oxidation of fatty acid.
KeywordsChronic Fatigue Syndrome Depressive Effect Bioactive Peptide Respiratory Exchange Ratio Central Fatigue
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