Acute Normobaric Hypoxia Lowers Executive Functions among Young Men despite Increase of BDNF Concentration

Decreased SpO₂ during hypoxia can cause cognitive function impairment, and the effects of acute hypoxia on high-order brain functions such as executive processing remain unclear. This study's goal was to examine the impact of an acute normobaric hypoxia breathing session on executive function and biological markers.

Thirty-two healthy subjects participated in a blind study performing two sessions of single 30 min breathing bouts under two conditions (normoxia (NOR) and normobaric hypoxia (NH), FIO₂ = 0.135). The Stroop test was applied to assess cognitive function.

No significant difference was observed in the Stroop interference in the "reading" part of the test in either condition; however, there was a significant increase in the "naming" part under NH conditions (p = 0.003), which corresponded to a significant decrease in SpO₂ (p < 0.001). There was a significant increase (p < 0.013) in the brain-derived neurotrophic factor (BDNF) level after NH conditions compared to the baseline, which was not seen in NOR. In addition, a significant drop (p < 0.001) in cortisol levels in the NOR group and a slight elevation in the NH group was noticed.

According to these findings, acute hypoxia delayed cognitive processing for motor execution and reduced the neural activity in motor executive and inhibitory processing. We also noted that this negative effect was associated with decreased SpO₂ irrespective of a rise in BDNF.