Literature DB >> 25593787

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance.

Stuart Goodall1, Rosie Twomey2, Markus Amann3.   

Abstract

PURPOSE: To outline how hypoxia profoundly affects neuronal functionality and thus compromise exercise-performance.
METHODS: Investigations using electroencephalography (EEG) and transcranial magnetic stimulation (TMS) detecting neuronal changes at rest and those studying fatiguing effects on whole-body exercise performance in acute (AH) and chronic hypoxia (CH) were evaluated.
RESULTS: At rest during very early hypoxia (<1-h), slowing of cerebral neuronal activity is evident despite no change in corticospinal excitability. As time in hypoxia progresses (3-h), increased corticospinal excitability becomes evident; however, changes in neuronal activity are unknown. Prolonged exposure (3-5 d) causes a respiratory alkalosis which modulates Na+ channels, potentially explaining reduced neuronal excitability. Locomotor exercise in AH exacerbates the development of peripheral-fatigue; as the severity of hypoxia increases, mechanisms of peripheral-fatigue become less dominant and CNS hypoxia becomes the predominant factor. The greatest central-fatigue in AH occurs when SaO2 is ≤75%, a level that coincides with increasing impairments in neuronal activity. CH does not improve the level of peripheral-fatigue observed in AH; however, it attenuates the development of central-fatigue paralleling increases in cerebral O2 availability and corticospinal excitability.
CONCLUSIONS: The attenuated development of central-fatigue in CH might explain, the improvements in locomotor exercise-performance commonly observed after acclimatisation to high altitude.

Entities:  

Keywords:  brain; exercise; hypoxia; muscle; oxygen

Year:  2014        PMID: 25593787      PMCID: PMC4292893          DOI: 10.1080/21641846.2014.909963

Source DB:  PubMed          Journal:  Fatigue        ISSN: 2164-1846


  111 in total

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