Cerebral perturbations during exercise in hypoxia

Abstract

Reduction of aerobic exercise performance observed under hypoxic conditions is mainly attributed to altered muscle metabolism due to impaired O 2 delivery. It has been recently proposed that hypoxia-induced cerebral perturbations may also contribute to exercise performance limitation. A significant reduction in cerebral oxygenation during whole body exercise has been reported in hypoxia compared with normoxia, while changes in cerebral perfusion may depend on the brain region, the level of arterial oxygenation and hyperventilation induced alterations in arterial CO 2. With the use of transcranial magnetic stimulation, inconsistent changes in cortical excitability have been reported in hypoxia, whereas a greater impairment in maximal voluntary activation following a fatiguing exercise has been suggested when arterial O 2 content is reduced. Electromyographic recordings during exercise showed an accelerated rise in central motor drive in hypoxia, probably to compensate for greater muscle contractile fatigue. This accelerated development of muscle fatigue in moderate hypoxia may be responsible for increased inhibitory afferent signals to the central nervous system leading to impaired central drive. In severe hypoxia (arterial O 2 saturation Ͻ70 -75%), cerebral hypoxia per se may become an important contributor to impaired performance and reduced motor drive during prolonged exercise. This review examines the effects of acute and chronic reduction in arterial O 2 (and CO2) on cerebral blood flow and cerebral oxygenation, neuronal function, and central drive to the muscles. Direct and indirect influences of arterial deoxygenation on central command are separated. Methodological concerns as well as future research avenues are also considered. cerebral perfusion; cerebral oxygenation; cortex excitability; central motor command; endurance WITH THE EXCEPTION of very short or static exercises performed at a high percentage of maximal power (15,19,83), hypoxia deteriorates exercise performance (7, 82). In particular, the maximal aerobic workload (Ẇ max ) that can be sustained during exercise involving large muscle groups (e.g., cycling) is considerably lower in hypoxia compared with normoxia. The difference between these two environmental conditions increases progressively with the reduction in oxygen inspiratory pressure (PI O 2 ) (36) and is affected by subjects' fitness so that subjects with elevated maximal aerobic capacity are more affected by hypoxia (41).The origin of exercise performance limitation in hypoxia is still under debate, since the consequences of reduced blood O 2 affect the whole organism. This limitation has been attributed to a lowered O 2 partial pressure in arterial blood (Pa O 2 ) reducing arterial O 2 content and O 2 delivery to tissues with critical consequences on muscle metabolism and contraction (1, 46). Magnetic nerve stimulation has confirmed the effects of reduced arterial oxygenation on dynamic (12, 111) and static (54) exercise-induced alterations in muscle contractility. Reduced muscle O...

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