The effect of endurance training on regional serotonin metabolism in the brain during early stage of detraining period in the female rat.

Abstract

1. The effect was examined of a single bout of nonexhaustive endurance exercise on tryptophan (Try), serotonin (5-HT), 5-hydroxyindolacetic acid (5-HIAA), and tryptophan hydroxylase (TpH) levels in different parts of rat brain (brain cortex, cerebellum, hypothalamus, midbrain striatum, medulla) on the last day of endurance training and 48 h later (detraining period). 2. Female rats were subjected to a 6-week endurance training programme. The effectiveness of the training was evaluated by measuring anaerobic threshold (AT). High performance liquid chromatography (HPLC) was used to determine regional Try, 5-HT, and 5-HIAA contents in the brain, and thin layer chromatography followed by gas-liquid chromatography was used to determine blood levels of free fatty acids. Regional TpH levels were measured by Western blot analysis. 3. In the two rat groups subjected to endurance training, in all brain regions studied but cerebellum, 5-HT content was significantly lower after the last bout of nonexhaustive endurance exercise than in resting control rats that were not subjected to the training. Similarly, the cortical and striatal, but not cerebellar, 5-HT/Try ratios were significantly lower in the trained rats at the end of the last training session and at the end of a single bout of nonexhaustive exercise administered after a 48-h detraining period than in the controls. TpH protein level was decreased by 15-25% after the last bout of exercise either during the training process or after the and 1 h bout of endurance exercise performed 48 h after cessation of endurance training in brain cortex and striatum but not cerebellar.4. These results indicate that the reduction in 5-HT level was the adaptive response to endurance training. The lowered 5-HT/Try ratio and lowered TpH protein level attained after the training process suggests and that this change may be, at least partially, attributed to downregulation of TpH activity.