The aim of this study was to investigate if enhanced peripheral ammonia production
during exhaustive exercise increases ammonia detoxication in brain mediated by glutamine
synthesis, and subsequently influences glutamate and gammaaminobutyric acid (GABA)
levels. This neurotransmitter production is related to the metabolism of glutamine.
A group of rats was trained for 6 weeks by treadmill running (TR). They were compared
to a group of untrained rats (UN). At the end of training, half of TR and UN rats
were submitted to one session of treadmill running until exhaustion (288 i 12 min
and 62 ± 5 min in TR and UN group, respectively). At exhaustion, running and control
rats were sacrificed in order to collect blood and to take samples of the following
brain structures: cortex, striatum and cerebellum. Treadmill running until exhaustion
induced an increase in blood ammonia by 140 % without significant differences between
TR and UN groups. Brain ammonia increased in both groups. However, TR group exhibited
values 50 % higher than those observed in UN group. Brain glutamine was increased
at exhaustion in all groups of running rats by 30 - 75 % of basal value whereas the
glutamate only decreased in TR rats which were able to run for a longer time. In this
group, the GABA level decreased in striatum. These data confirm that enhanced brain
ammonia level during exercise stimulates glutamine synthesis as a mechanism of detoxication.
After several hours of running, a reduction in brain glutamate levels was observed
in all brain structures in trained rats but only in the striatum in untrained animals.
The reduced availability of this GABA precursor decreases GABA levels only in the
striatum of TR group by 45 % of the resting value. These results suggest a relation
between cerebral changes in neurotransmitters and excitatory amino acids, such as
glutamate and GABA, and central fatigue.
Key words
Brain - exercise - central fatigue - ammonia - glutamine - glutamate - GABA
