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Hypobaric Hypoxia: Adaptation and Acclimatization
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
John H. Coote, James S. Milledge
Longer-term disruption in brain function in low-oxygen environments is likely also to be a consequence of impairment of synthesis of neurotransmitters. For example, the synthesis of brain monoamines are rate-limited by the enzyme tyrosine hydroxylase in the case of dopamine, noradrenaline and adrenaline or tryptophan hydroxylase in the case of serotonin, both enzymes requiring molecular oxygen (Siesjo, 1978). In support of this are data from rats showing that measures that improve the synthesis of brain amines protect against the deleterious effects of hypobaric hypoxia (Boismare et al., 1980). Also, the re-uptake of glutamate and formation of the gaseous transmitter nitric oxide, which participate in new tasks, are processes requiring oxidation, and these transmitters are involved in numerous brain pathways. These reactions are severely impaired when the oxygen tensions are reduced to around 50 mm Hg (6.7 kPa). Proof of this has come from experimental animal studies showing that hypoxia altered the content of neurotransmitters, their turnover and synaptic transmission long before axonal conduction was affected (Siesjo, 1978; LaManna, 2007). The high sensitivity (KM – see Figure 7.10) of the oxygen-consuming processes involved in LTP is a likely explanation for the learning deficits demonstrated in subjects exposed to a mild hypoxia of 8,000 feet (2,500 metres) (Denison, 1981), confirmed by Farmer et al. (1991), where the partial pressure of oxygen in the blood will be around 50 mm Hg (6.7 kPa). It is also very likely that this contributes to the marked disturbances of cognitive and psychomotor behaviour reported during exposure to altitudes above 13,000 feet (4,000 metres).
Fatigue: Is it all neurochemistry?
Published in European Journal of Sport Science, 2018
The neurons responsible for the release of serotonin are located along the midline of the brainstem. They are clustered in the raphe nuclei from where they innervate nearly every region of the central nervous system (Frazer & Hensler, 1994; Roelands & Meeusen, 2010). Two enzymatic steps are required in the synthesis of serotonin. First, the amino acid precursor tryptophan is hydroxylized by tryptophan hydroxylase to l-5-hydroxytriptophan, and second, it is decarboxylated to serotonin (Roelands & Meeusen, 2010). Metabolization occurs via aldehyde dehydrogenase and monoamine oxidase to 5-hydroxyindoleacetic acid (5-HIAA) (Meeusen & De Meirleir, 1995). Increases in serotonin are presumed to play an important role in various behavioural functions, such as increased feelings of tiredness, fatigue and pain, and decreases in the level of arousal (Davis & Bailey, 1997).