Abstract
Intracerebroventricular administration of the high-molecular-mass fraction of cerebrospinal fluid (CSF) from exercise-exhausted rats to sedentary mice produced a decrease in spontaneous motor activity, whereas CSF from sedentary rats had no such effect. This suggests the presence of a substance regulating the urge for motion as a response to fatigue. A bioassay system using Hydra, a freshwater coelenterate, showed an activity indistinguishable from transforming growth factor beta (TGF-β) in the CSF from exercise fatigued rats, whereas no such activity was present in CSF from sedentary rats. The increase in the concentration of active TGF-β in the CSF from exercise-fatigued rats was also ascertained by another bioassay system using mink lung epithelial cells (Mv1Lu). Injection of TGF-β into the brains of sedentary mice elicited a similar decrease in spontaneous motor activity in a dose-dependent manner. Increasing the exercise load on rats raised both the level of active TGF-β in their CSF and the depressive effect it elicited on the spontaneous motor activity of mice. Taken together, these results suggest that exercise increases the level of active TGF-β in the brain, which creates a feeling of fatigue and thus suppresses spontaneous motor activity.
