TY - JOUR

T1 - Severity-dependent influence of isocapnic hypoxia on reaction time is independent of neurovascular coupling

AU - Caldwell, Hannah Grace

AU - Coombs, Geoff B

AU - Tymko, Michael M

AU - Nowak-Flück, Daniela

AU - Ainslie, Philip N

N1 - (Ekstern)

PY - 2018

Y1 - 2018

N2 - With exposure to acute normobaric hypoxia, global cerebral oxygen delivery is maintained via increases in cerebral blood flow (CBF); therefore, regional and localized changes in oxygen tension may explain neurocognitive impairment. Neurovascular coupling (NVC) is the close temporal and regional relationship of CBF to changes in neural activity and may aid in explaining the localized CBF response with cognitive activation. High-altitude related cognitive impairment is likely affected by hypocapnic cerebral vasoconstriction that may influence regional CBF regulation independent of hypoxia. We assessed neurocognition and NVC following 30 min of acute exposure to isocapnic hypoxia (decreased partial pressure of end-tidal oxygen; PETO2) during moderate hypoxia (MOD HX; 55 mm Hg PETO2), and severe hypoxia (SEV HX; 45 mm Hg PETO2) in 10 healthy individuals (25.5 ± 3.3 yrs). Transcranial Doppler ultrasound was used to assess mean posterior and middle cerebral blood velocity (PCAv and MCAv, respectively) and neurocognitive performance was assessed via validated computerized tests. The main finding was that reaction time (i.e., kinesthetic and visual-motor ability via Stroop test) was selectively impaired in SEV HX (−4.6 ± 5.2%, P = 0.04), but not MOD HX, while complex cognitive performance (e.g., psychomotor speed, cognitive flexibility, processing speed, executive function, and motor speed) was unaffected with hypoxia (P > 0.05). Additionally, severity of hypoxia had no effect on NVC (PCAv CON vs. SEV HX relative peak response 13.7 ± 6.4% vs. 16.2 ± 11.5%, P = 0.71, respectively). In summary, severe isocapnic hypoxia impaired reaction time, but not complex cognitive performance or NVC. These findings have implications for recreational and military personnel who may experience acute hypoxia.

AB - With exposure to acute normobaric hypoxia, global cerebral oxygen delivery is maintained via increases in cerebral blood flow (CBF); therefore, regional and localized changes in oxygen tension may explain neurocognitive impairment. Neurovascular coupling (NVC) is the close temporal and regional relationship of CBF to changes in neural activity and may aid in explaining the localized CBF response with cognitive activation. High-altitude related cognitive impairment is likely affected by hypocapnic cerebral vasoconstriction that may influence regional CBF regulation independent of hypoxia. We assessed neurocognition and NVC following 30 min of acute exposure to isocapnic hypoxia (decreased partial pressure of end-tidal oxygen; PETO2) during moderate hypoxia (MOD HX; 55 mm Hg PETO2), and severe hypoxia (SEV HX; 45 mm Hg PETO2) in 10 healthy individuals (25.5 ± 3.3 yrs). Transcranial Doppler ultrasound was used to assess mean posterior and middle cerebral blood velocity (PCAv and MCAv, respectively) and neurocognitive performance was assessed via validated computerized tests. The main finding was that reaction time (i.e., kinesthetic and visual-motor ability via Stroop test) was selectively impaired in SEV HX (−4.6 ± 5.2%, P = 0.04), but not MOD HX, while complex cognitive performance (e.g., psychomotor speed, cognitive flexibility, processing speed, executive function, and motor speed) was unaffected with hypoxia (P > 0.05). Additionally, severity of hypoxia had no effect on NVC (PCAv CON vs. SEV HX relative peak response 13.7 ± 6.4% vs. 16.2 ± 11.5%, P = 0.71, respectively). In summary, severe isocapnic hypoxia impaired reaction time, but not complex cognitive performance or NVC. These findings have implications for recreational and military personnel who may experience acute hypoxia.

KW - Cerebral blood flow

KW - Hypoxia

KW - Neurocognition

KW - Neurovascular coupling

KW - Reaction time

UR - http://www.scopus.com/inward/record.url?scp=85042207966&partnerID=8YFLogxK

U2 - 10.1016/j.physbeh.2018.02.035

DO - 10.1016/j.physbeh.2018.02.035

M3 - Journal article

C2 - 29458114

AN - SCOPUS:85042207966

VL - 188

SP - 262

EP - 269

JO - Physiology & Behavior

JF - Physiology & Behavior

SN - 0031-9384

ER -