Increased central availability of tryptophan as a result of endurance exercise

Prolonged endurance training results in metabolic changes which have a favourable effect on the central availability of tryp (Chaouloff 1997). Moreover, animal experiments suggest that endurance exercise may stimulate endogenous serotonin synthesis. Administration of tryp prior to endurance exercise leads to a further increase in serotonin synthesis in the brain (Meeusen et al. 1996).

Numerous studies with beta2-sympathomimetic agents (e.g. salbutamol, clenbuterol) have shown that these drugs – probably by activating central beta2-receptors – promote the CNS uptake of tryp (Lenard et al. 2003). By increasing the release of noradrenaline/adrenaline, intense endurance training also leads to physiological activation of beta2-receptors; this mechanism of action is likely to result in the enhanced central availability of tryp.

As the uptake of tryp at the BBB depends, among other things, on the concentration of branched-chain amino acids (BCAA) using the same transport system, the increased uptake of BCAA (leucine, isoleucine, valine) into the working muscles as a result of physical exercise has a favourable effect on the tryp uptake in the brain (Blomstrand et al. 1991). Regardless of the presence or absence of insulin, BCAA are taken up into the muscle cells to provide energy during prolonged endurance exercise. In the course of endurance training, the blood tryp/BCAA ratio shifts increasingly in favour of tryptophan, thus heightening the likelihood of tryp uptake by the brain.
Moreover, tryp competes with free fatty acids (FFA) for binding to albumin in blood. Only the tryp that is not bound to albumin can pass the BBB. Any conditions that increase the FFA in the blood may also raise the concentration of free tryp (Strüder et al. 1996). These observations seem to suggest that low-impact exercise may be particularly suitable to enhance central tryptophan uptake or serotonin synthesis. Various studies, however, indicate that intense exercise is more likely to increase serotonin synthesis (Cuperuto et al. 2009). Therefore, a compromise would be high-intensity exercise, with the bulk of the body’s energy needs still being supplied by fat metabolism (70% - 75% VO2 max). Even under these circumstances the concentration of free fatty acids steadily rises in the course of exercise (Strüder et al. 1997). If exercise duration is 40-60 minutes or more, the fraction of free tryp increases parallel to the concentration of FFA. Moreover, if endurance exercise is initiated on an empty stomach (last meal > 4 hours earlier) FFA levels will be high right from the start. If tryp is administered in this setting at a dose of 1.5 mg 30 minutes prior to the start of exercise, high blood concentrations of free tryp will be achieved early on. Tryp should be taken with at least 100 ml of water (fruit juice is to be avoided, as subsequent release of insulin would reduce FFA levels). It takes approximately 30 minutes until tryp becomes systemically available. Throughout the duration of exercise there are optimal conditions for the uptake of tryptophan by the CNS. As the concentration of FFA is elevated for at least one hour after exercise (Henderson et al. 2007), the next meal should be postponed for some time, in order to maintain optimal conditions for tryp uptake in the brain for as long as possible. Prolonged endurance exercise results in increased uptake of tryp into the CNS, provided no carbohydrates are consumed during exercise (Blomstrand et al. 2005).

Link: Tryptophan Literature