may protect against the adverse behavioural
effects of prolonged periods of stress by prevent-
ing the depletion of brain catecholamines that
may counteract mood and performance degra-
dation in soldiers (Owasoyo et al.1992). Most of
this work has focused on noradrenaline deple-
tion, even though good evidence in animals
show that both dopamine and noradrenaline
synthesis can be increased by tyrosine adminis-
tration (see Owasoyo et al.1992). It is thought
that noradrenaline neurones in the locus
coeruleus regulate, in part, behavioural func-
tions like anxiety (tension), vigilance and atten-
tion that are apparently improved following
administration of tyrosine. However, it is also
possible that some of the beneficial effects of
tyrosine can be attributed to prevention of
dopamine depletion, especially in the case
of motivation, wakefulness, motor control and
overall fatigue.
Unlike tryptophan, however, catecholaminer-
gic neurones are not sensitive to the presence of
excess tyrosine while at rest, but become sensi-
tive when the neurones are activated by stress
(Milner & Wurtman 1986). This theory is consis-
tent with work from both human (Growden et al.
1982) and animal research (Lehnert et al.1984).
Research on the possible beneficial effects of
tyrosine on adverse behavioural responses to
stress in humans comes primarily from one
group of investigators headed by H.R.
Lieberman and associates at Massachusetts
Institute of Technology and the US Army
Research Institute of Environmental Medicine.
They initially showed that tyrosine decreased
some of the adverse consequences of a 4.5-h
exposure to cold and hypoxia (Banderet &
Lieberman 1989). Tyrosine (100 mg · kg–1)
returned mood, cognitive performance, vigi-
lance and feelings of fatigue and sleepiness to
baseline levels in subjects who were most
affected by the environmental stressors. They
also found that tyrosine increased tolerance to
lower body negative pressure with an accompa-
nying decrease in depression, tension and
anxiety (Dollins et al.1995) and lessened the
impairments of learning and memory during
severe hypoxia (Shukitt-Hale et al.1996). There is
also one report from another group that showed
that tyrosine improved performance in percep-
tual motor tasks during lower body negative
pressure (Deijen & Orlebeke 1994).
There are no studies that specifically focus on
the possible effects of tyrosine as a means of
delaying fatigue during exercise. This is unfortu-
nate, since there is reasonable information to
hypothesize a possible beneficial effect of tyro-
sine in preventing a depletion of noradrenaline
and dopamine that appears to be essential to
optimal physical performance. It is reasonable to
suspect that tyrosine could limit some of the
negative behavioural consequences of prolonged
stressful exercise including reductions in
alertness, attention, motivation (drive), positive
mood and motor control that would be expected
to limit optimal performance perhaps though an
effect on central fatigue. Special attention needs
to be focused on the possible role of dopamine
since this has essentially not been addressed in
the literature to date.Acetylcholine and CNS fatigue
Acetylcholine is the most abundant neurotrans-
mitter in the body. It is essential for the genera-
tion of muscular force at the neuromuscular
junction, and within the CNS is generally assoc-
iated with memory, awareness, and temperature
regulation.
As with 5-HT and the catecholamines, the rate
of synthesis of acetylcholine is determined by the
availability of its precursor, choline, which is nor-
mally obtained from the diet. ACh is synthesized
in the cytoplasm from choline and acetyl coen-
zyme A via the enzyme choline acetyltransferase
that is not saturated with choline at physiological
concentrations, and ACh does not ‘feed-back’ to
inhibit its own synthesis. There is also some
evidence in animals to suggest that depletion of
ACh may contribute to fatigue during sustained
electrical activity. However, no studies have
investigated the relationship between modified
plasma choline levels and concentrations of ACh
in skeletal muscle, although synthesis of ACh