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

Purpose: To outline how hypoxia profoundly affects neuronal functionality and thus compromises exercise performance. Methods: Investigations were reviewed and evaluated that used electroencephalography (EEG) and transcranial magnetic stimulation (TMS) to detect neuronal changes at rest and those studying fatiguing effects on whole-body exercise performance in acute (AH) and chronic hypoxia (CH). 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 O-2 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.