During prolonged endurance exercise within the heat catecholamine turnover is increased compared to the same exercise in a temperate environment (i.e. the former accelerates fatigue compared to the latter, in part due to central catecholamine depletion of their major precursor TYR).^{2, 3}

During acute stress, there is an observed increase in the activation of noradrenergic neurons in the frontal cortex, which release neurotransmitter as a response to stress.⁴ The continued release of neurotransmitter is fundamental in the ability to cope with stress, and thus as concentrations begin to deplete, aspects of cognitive function start to deteriorate.⁵ Therefore, oral supplementation of TYR is proposed to increase its ratio to other large neutral amino acids (LNAA) for competitive transport across the blood brain barrier, thus resulting in a greater cerebral uptake and an increase in dopamine (DA) synthesis in the brain^{6, 7}; i.e. facilitative of prolonging/maintaining ‘optimal’/’minimal’ catecholamine/neurotransmitter presence/function. It is suggested that similar to the effects of physical/exercise/ mental stress and/or heat-stress, catecholamine concentrations also become depleted during exposure to other environmental stressors (e.g. cold and/or hypoxia).⁸