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Introduction and objective Populations at high altitude (HA) face a higher incidence and severity of traumatic brain injury (TBI). This pilot study utilized longitudinal 1 H-MRS to identify neurochemical biomarkers of HA adaptation and the subsequent metabolic response to mild TBI (mTBI). Methods Male C57BL/6J mice were exposed to simulated HA (5,000 m) or sea level (SL) for 12 weeks. Following adaptation, a unilateral mTBI was induced via closed head injury (CHI). Mice were then monitored for an additional 2 weeks at HA (total duration of 14 weeks). In vivo 1 H-MRS spectra (7 T) were collected from the frontal cortex, hippocampi, and cerebellum at weeks 0, 4, 12 to assess HA adaptation. Following the CHI, subsequent measurements were collected at week 12 (post-injury) and week 14 to monitor longitudinal neurochemical responses to the mTBI. Results Chronic HA exposure induced significant reductions in myo-inositol (Ins) and total choline (tCho) in the hippocampus, establishing a baseline of metabolic fragility that sensitized the brain to subsequent traumatic insult. Post-mTBI, the HA group exhibited a profound “metabolic crisis,” characterized by significantly lower tCho and failed recovery of total N-acetylaspartate (tNAA) compared to SL controls. Total creatine (tCr) was the most acutely affected metabolite, underscoring a depletion of the bioenergetic reserve. Conclusion Chronic hypobaric hypoxia fundamentally alters baseline brain metabolism and impairs the neurochemical recovery from mTBI. These findings suggest that standard recovery protocols may be insufficient for HA-adapted populations and highlight 1 H-MRS as a critical tool for detecting “invisible” metabolic vulnerability in extreme environments.
Park et al. (Thu,) studied this question.