| Summary: | The central fatigue hypothesis suggests that during prolonged exercise, the increased plasma free-tryptophan (f-Trp) concentration may lead to an increased rate of synthesis of brain serotonin (5-HT). This may impair central nervous system function and cause increased perceptions of fatigue and deteriorate exercise performance. Two-fold increases in plasma concentrations of f-Trp have resulted in a 20% and 53% increase in brain Trp and forebrain Trp respectively. In addition, it has been suggested that 5-HT is involved in the stimulation of PRL release. The aim of the present thesis was to examine the relationship between the main peripheral markers of central fatigue, namely venous concentrations of f-Trp and prolactin (PRL), under three different experimental conditions. It was hypothesised that the changes in venous concentrations of f-Trp and PRL would exhibit similar patterns. Plasma f-Trp concentration increased by 110% after 2 h of cycling in normobaric hypoxia at a workload corresponding to 55% of FO2max determined in normobaric normoxia (P < 0.05). Serum PRL concentration did not differ between trials but the mean concentration increased at 30 min post exercise (P < 0.05). Following highintensity exercise for 30 s, plasma f-Trp concentration decreased by 23.5% (P < 0.05), whereas serum PRL concentration did not change (P > 0.05). Oral administration of L-Trp was followed by an increased plasma f-Trp concentration of 920%, however, plasma PRL concentrations decreased by 32.6% at the same time-point (P < 0.05). Analysis of functional magnetic resonance imaging of the brain demonstrated a different pattern of brain activation while subjects performed the interference task of the counting Stroop test following L-Trp ingestion. From these results it can be proposed that central fatigue is likely not to play any part during high-intensity exercise lasting 30s. However, the 110% and 920% increase in plasma f-Trp concentration during prolonged exercise in normobaric hypoxia and following oral administration of L-Trp respectively may have led to an increased rate of brain 5-HT synthesis, although venous concentrations of PRL were not in support of this increase. There may be many reasons for the lack of relationship between the two peripheral markers of central fatigue, including an effect of the catecholamines on inhibiting PRL secretion. During oral ingestion of L-Trp, the increased plasma f-Trp concentration may also have caused the increased brain activation in the areas known to house 5-HT neurones, and for the unique pattern of brain activation when performing a cognitive task. It remains to be established whether the increased f-Trp concentration, and unique brain activation pattern is evidence of fatigue originating within the brain.
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