Diminished central fatigue by inhibition of the L-system transporter for the uptake of tryptophan.

Nagase genetically analbuminemic rats (NAR) were run to fatigue. Administration of branched chain amino acids (BCAA) before exhaustive exercise, resulted in a post-fatigue decreased tryptophan uptake (-22%, p < 0.05) and 5-hydroxytryptophan (5-HTP) uptake (-29%, p < 0.01) into the synaptosomes isolated from the striatum when compared with saline administration. At the same time, NAR who received either BCAA or 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid (BCH, a specific inhibitor for the L-system transporter) had a considerably prolonged run time to exhaustion (by twofold), compared to those who received either saline or albumin treatments. When classified by run time, it was of interest that, when the data for BCAA and BCH treatments for the longer run time NAR (Group B) was combined, it gave rise to a significant decrease in synaptosomal tryptophan and 5-HTP of a similar magnitude to that observed with BCAA alone. These levels were lower than those observed in NAR in the shorter run time group (Group A) for all treatments. These results support the view that an activated serotonergic function may be involved in central fatigue, which can be diminished by inhibition of the L-system transporter.