Background and purpose: Acute hypoxia is associated with impairment of cerebral autoregulation (CA), but it is unclear if altered CA during prolonged hypoxia is pivotal to the development of cerebral pathology, such as that seen in acute mountain sickness (AMS). This investigation evaluated relationship between CA and AMS over 9 hours of hypobaric hypoxia.
Methods: Fifty-five subjects (41 males, 14 females) were studied in normoxia (PB=625 mm Hg) and after 4 and 9 hours of hypobaric hypoxia (PB=425 mm Hg; approximately 4875 m). Resting, beat-by-beat changes in arterial blood pressure, and middle cerebral artery blood flow velocity were recorded at each time point while breathing room air. Transfer function analyses were used to estimate autoregulation indices (ARI). In 29 subjects, ARI during isocapnic hyperoxia and cerebral vasomotor reactivity during modified rebreathing were also determined to isolate effects of hypoxia and CO2 reactivity on CA.
Results: Self-reported Lake Louise AMS Questionnaire scores > or = 3 with headache were used to differentiate between AMS-positive (n=27) and AMS-negative (n=28) subjects (P<0.01). ARI decreased and CO2 reactivity increased in both groups at 4 hours (P<0.01) and did not progress at 9 hours, despite increased incidence and severity of AMS (P<0.01). Impairments in ARI were alleviated with isocapnic hyperoxia at 4 and 9 hours (P<0.01) and were not related to CO2 reactivity.
Conclusions: These results indicate that hypoxia directly impairs CA but that impaired CA does not play a pivotal role in the development of AMS.