This randomized controlled trial examined the physiological and cognitive consequences of a 24-hour exposure to simulated high-altitude hypobaric hypoxia equivalent to 3600 m. The primary physiologic outcome was regional cerebral blood flow (CBF) measured with arterial spin labeling (ASL). The study reports compensatory increases in CBF across the examined brain territories in participants exposed to hypobaric hypoxia without stimulation, consistent with an acute hemodynamic response to reduced inspired oxygen.
The study enrolled healthy Han Chinese men aged 18–45 at the Chinese PLA General Hospital between June 2024 and December 2025. Forty-three participants undergoing hypobaric exposure were randomized to receive either transcutaneous vagus nerve stimulation (tVNS) (n = 23) or no tVNS (n = 20). A separate non-exposure cohort (n = 18) was included to correct for cognitive practice or learning effects on repeated testing. Exposure occurred in a specialized hypobaric chamber for 24 hours at a simulated altitude of 3600 m.
CBF quantification used arterial spin labeling to measure perfusion in the anterior, middle, and posterior cerebral artery territories and the hippocampus at three time points: baseline (pre-exposure), during exposure, and post-exposure. Cognitive performance was assessed at the same time points using the Repeatable Battery for the Assessment of Neuropsychological Status, which evaluates domains including visuospatial ability, language, attention, and memory.
Participants in the non-tVNS control group demonstrated statistically significant compensatory increases in regional CBF during hypobaric hypoxia across all examined regions (p < 0.05). These findings indicate an acute cerebrovascular adjustment to hypoxic stress, reflected by elevated perfusion in major arterial territories and the hippocampus relative to baseline.
In participants receiving tVNS, CBF changes were not uniform across brain regions. The frontotemporal regions exhibited higher perfusion at the exposure time point compared with post-exposure, and post-exposure perfusion remained higher than baseline. By contrast, occipital and hippocampal CBF were higher at exposure than at both baseline and post-exposure, while post-exposure values did not differ from baseline in those regions. These patterns indicate that tVNS produced region-specific modulation of hypoxia-associated perfusion changes rather than a generalized augmentation across all territories.
When comparing the randomized groups, the only statistically significant between-group difference reported was in temporal lobe perfusion. Temporal lobe CBF was higher in the tVNS group than in the non-tVNS control group (76.22 ± 7.49 vs. 70.88 ± 8.93, p = 0.039). No other arterial territories or hippocampal perfusion were reported as significantly different between groups in the source abstract.
Across exposed participants, simulated hypobaric hypoxia produced measurable cognitive declines: impairments were observed in visuospatial ability, language, attention, and delayed memory (all reported p < 0.05). Despite the region-specific perfusion effects associated with tVNS, the intervention did not ameliorate these hypoxia-induced cognitive deficits in this study protocol.
The authors conclude that a 24-hour simulated exposure to 3600 m hypobaric hypoxia elicits compensatory increases in regional CBF, and that tVNS selectively increases temporal lobe perfusion under these conditions. However, tVNS did not translate into preserved cognitive performance in the administered protocol. The report notes that further, optimized studies are needed to clarify whether tVNS has a meaningful neuroprotective role against hypoxia-induced cognitive decline and to define the stimulation parameters, timing, and target populations most likely to benefit.
Note: Details reported here are limited to the information provided in the source abstract; full-text methodological, statistical, and safety details were not reported in the excerpt used as the source.