Effects of conditioned running on plasma, liver and brain tryptophan and on brain 5‐hydroxytryptamine metabolism of the rat

Abstract

An investigation was made into the effects of conditioned running (1 h and 2 h at 20 m min−1), which accelerates lipolysis, on the concentrations of tryptophan (Trp) in plasma, liver and brain and on 5‐hydroxytryptamine (5‐HT) and 5‐hydroxyindoleacetic acid (5‐HIAA) levels in brain. Running caused time‐dependent increases in plasma free Trp and brain Trp of the rat, leading to increased brain 5‐HT turnover as revealed by higher amounts of its metabolite, 5‐HIAA. The ratio of brain Trp to plasma free Trp was decreased after 2 h of running. Liver Trp content rose only after 3 h of running, while liver unesterified fatty acid (UFA) concentrations remained unmodified. A comparison between food deprivation and running (both of which promote lipolysis) was performed. Running for 2 h affected to the same extent plasma Trp disposition when compared with 24 h food deprivation. Nevertheless, the ratio of brain Trp to plasma free Trp was decreased in the food‐deprived rats, when compared to the runners. Valine, an inhibitor of entry of Trp into the brain decreased its level there to the same extent in both controls and 1 h runners. Nicotinic acid, which inhibits fat catabolism, completely abolished the plasma UFA increase induced by 1 h of running. The drug did not affect plasma free Trp, brain Trp, 5‐HT or 5‐HIAA but enhanced plasma total Trp level. Naloxone, an opiate antagonist, which decreased running‐induced lipolysis, did not alter plasma Trp disposition. Desipramine, an antidepressant compound, affected only peripheral Trp concentrations of the runners. Plasma free and total Trp concentrations were increased in desipramine‐treated runners, compared with saline‐treated runners. In addition, desipramine increased the ratio of brain Trp to plasma free Trp of the runners. Brain 5‐HT and 5‐HIAA were increased in both desipramine‐treated controls and runners. The results suggest that running, which like food deprivation accelerates lipolysis, increases brain Trp content and then 5‐HT turnover. Comparison of these two physiological situations suggests that effectiveness of brain Trp entry is much more altered by fasting. 1985 British Pharmacological Society