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

Abstract

1 An investigation was made into the effects of conditioned running (1 h and 2h at 20mmin-'), 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. 2 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. 3 Liver Trp content rose only after 3 h of running, while liver unesterified fatty acid (UFA) concentrations remained unmodified. 4 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. 5 Valine, an inhibitor ofentry ofTrp into the brain decreased its level there to the same extent in both controls and I h runners. 6 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. 7 Naloxone, an opiate antagonist, which decreased running-induced lipolysis, did not alter plasma Trp disposition.8 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. 9 The results suggest that running, which like food deprivatiQn 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.

A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise

“…In animal studies, running increased plasma free tryptophan, brain tryptophan, and levels of the serotonin metabolite, 5-HIAA (Bailey et al, 1993, Chaouloff et al, 1985. Human trials also provide evidence of exercise and its serotonin-enhancing effects.…”

Effects of Aerobic Exercise on Anxiety Disorders: A Systematic Review

“…Though, these monoamine levels may be increased with regular and systematic practice of physical exercise. Studies have shown that significant levels of noradrenaline and 5TH, as well as the expression of 5HIAA and 5-HT2C receptors in the limbic system have been reported following exercise on a treadmill of chronic form [27][28][29][30][31][32]. Another important mechanism that suffers major adaptations is the hypothalamicpituitary-adrenal system (HPA) subjected to chronic stress has great hyperactivity and elevated levels of glucocorticoids [33,34], which are harmful to the body.…”

Activation of β2- and β3-Adrenergic Receptors Increases Brain Tryptophan

“…CL 316243 had no effect on brain tryptophan in ␤ 3 -receptor knockout mice, whereas clenbuterol increased brain tryptophan, indicating that ␤-adrenergic modulation of brain tryptophan occurs in the absence of ␤ 3 -receptors. We conclude that activation of either ␤ 2 -or ␤ 3 -adrenergic receptors, but not ␤ 1 -adrenergic receptors, increases mouse brain tryptophan content.A wide variety of stressors can increase brain tryptophan content and subsequently affect serotonin (5-HT) metabolism (Curzon et al, 1972;Chaouloff et al, 1985;Dunn, 1988a). Stress-related elevations in brain tryptophan are normal in adrenalectomized animals (Curzon et al, 1972;Dunn and Welch, 1991), but can be blocked by ganglionic blockers and ␤-adrenergic antagonists (Dunn and Welch, 1991), suggesting that the changes are a consequence of peripheral sympathetic activation of ␤-adrenergic receptors.…”