Neural responses to acute hypoxia and hyperoxia

The brain's high metabolic demands make it highly sensitive to oxygen level changes, with both hypoxia and hyperoxia affecting cognitive and neural function. However, the underlying neural mechanisms remain unclear. This study aimed to characterise the effects of acute normobaric hypoxia and hyperoxia on neural function and perceptual thresholds using EEG, visual evoked potentials (VEPs), and critical flicker fusion (CFF) thresholds. In a single-blind, randomised, crossover design, thirty participants inhaled 10.5%, 21%, or 100% oxygen while resting-state EEG, VEPs, and CFF thresholds were recorded. Hypoxia reduced CFF thresholds in an exposure-dependent manner, while hyperoxia produced a smaller, transient reduction. Resting-state EEG revealed significantly increased power across delta, theta, and beta bands in response to hypoxia. Whereas hyperoxia induced smaller increases in theta and alpha and decreases in gamma power and a reduction in beta power over the sensorimotor area. Hypoxia increased spectral entropy, indicating impaired network synchronisation, while hyperoxia increased fuzzy entropy, particularly in eyes-closed states, potentially reflecting enhanced neural complexity. In VEPs, hypoxia reduced P1 amplitude and increased N2 deflections, reflecting disrupted early and late sensory processing, with sustained effects across blocks. Hyperoxia transiently increased P1 amplitude and showed minor effects on other components. These findings demonstrate the impact of altered cerebral oxygen on fundamental neural processing and the associated state- and time-dependent effects on brain function. This provides insight into the mechanisms underlying oxygen-induced neuromodulation and highlights the value of EEG and CFF as biomarkers for tracking neural responses to oxygen variability.