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Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress. / Gibbons, T D; Tymko, M M; Thomas, K N et al.
In: Journal of Physiology, Vol. 598, No. 2, 01.2020, p. 265-284.

Research output: Contribution to journalArticlepeer-review

HarvardHarvard

Gibbons, TD, Tymko, MM, Thomas, KN, Wilson, LC, Stembridge, M, Caldwell, HG, Howe, CA, Hoiland, RL, Akerman, AP, Dawkins, TG, Patrician, A, Coombs, GB, Gasho, C, Stacey, BS, Ainslie, PN & Cotter, JD 2020, 'Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress', Journal of Physiology, vol. 598, no. 2, pp. 265-284. https://doi.org/10.1113/JP278917

APA

Gibbons, T. D., Tymko, M. M., Thomas, K. N., Wilson, L. C., Stembridge, M., Caldwell, H. G., Howe, C. A., Hoiland, R. L., Akerman, A. P., Dawkins, T. G., Patrician, A., Coombs, G. B., Gasho, C., Stacey, B. S., Ainslie, P. N., & Cotter, J. D. (2020). Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress. Journal of Physiology, 598(2), 265-284. https://doi.org/10.1113/JP278917

CBE

Gibbons TD, Tymko MM, Thomas KN, Wilson LC, Stembridge M, Caldwell HG, Howe CA, Hoiland RL, Akerman AP, Dawkins TG, et al. 2020. Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress. Journal of Physiology. 598(2):265-284. https://doi.org/10.1113/JP278917

MLA

VancouverVancouver

Gibbons TD, Tymko MM, Thomas KN, Wilson LC, Stembridge M, Caldwell HG et al. Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress. Journal of Physiology. 2020 Jan;598(2):265-284. doi: 10.1113/JP278917

Author

Gibbons, T D ; Tymko, M M ; Thomas, K N et al. / Global REACH 2018 : The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress. In: Journal of Physiology. 2020 ; Vol. 598, No. 2. pp. 265-284.

RIS

TY - JOUR

T1 - Global REACH 2018

T2 - The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress

AU - Gibbons, T D

AU - Tymko, M M

AU - Thomas, K N

AU - Wilson, L C

AU - Stembridge, M

AU - Caldwell, H G

AU - Howe, C A

AU - Hoiland, R L

AU - Akerman, A P

AU - Dawkins, T G

AU - Patrician, A

AU - Coombs, G B

AU - Gasho, C

AU - Stacey, B S

AU - Ainslie, P N

AU - Cotter, J D

N1 - © 2019 The Authors. The Journal of Physiology © 2019 The Physiological Society.

PY - 2020/1

Y1 - 2020/1

N2 - Thermal and hypoxic stress commonly coexist in environmental, occupational and clinical settings, yet how the brain tolerates these multi-stressor environments is unknown Core cooling by 1.0°C reduced cerebral blood flow (CBF) by 20-30% and cerebral oxygen delivery (CDO2 ) by 12-19% at sea level and high altitude, whereas core heating by 1.5°C did not reliably reduce CBF or CDO2 Oxygen content in arterial blood was fully restored with acclimatisation to 4330 m, but concurrent cold stress reduced CBF and CDO2 Gross indices of cognition were not impaired by any combination of thermal and hypoxic stress despite large reductions in CDO2 Chronic hypoxia renders the brain susceptible to large reductions in oxygen delivery with concurrent cold stress, which might make monitoring core temperature more important in this context ABSTRACT: Real-world settings are composed of multiple environmental stressors, yet the majority of research in environmental physiology investigates these stressors in isolation. The brain is central in both behavioural and physiological responses to threatening stimuli and, given its tight metabolic and haemodynamic requirements, is particularly susceptible to environmental stress. We measured cerebral blood flow (CBF, duplex ultrasound), cerebral oxygen delivery (CDO2 ), oesophageal temperature, and arterial blood gases during exposure to three commonly experienced environmental stressors - heat, cold and hypoxia - in isolation, and in combination. Twelve healthy male subjects (27 ± 11 years) underwent core cooling by 1.0°C and core heating by 1.5°C in randomised order at sea level; acute hypoxia ( PET,O2 = 50 mm Hg) was imposed at baseline and at each thermal extreme. Core cooling and heating protocols were repeated after 16 ± 4 days residing at 4330 m to investigate any interactions with high altitude acclimatisation. Cold stress decreased CBF by 20-30% and CDO2 by 12-19% (both P < 0.01) irrespective of altitude, whereas heating did not reliably change either CBF or CDO2 (both P > 0.08). The increases in CBF with acute hypoxia during thermal stress were appropriate to maintain CDO2 at normothermic, normoxic values. Reaction time was faster and slower by 6-9% with heating and cooling, respectively (both P < 0.01), but central (brain) processes were not impaired by any combination of environmental stressors. These findings highlight the powerful influence of core cooling in reducing CDO2 . Despite these large reductions in CDO2 with cold stress, gross indices of cognition remained stable.

AB - Thermal and hypoxic stress commonly coexist in environmental, occupational and clinical settings, yet how the brain tolerates these multi-stressor environments is unknown Core cooling by 1.0°C reduced cerebral blood flow (CBF) by 20-30% and cerebral oxygen delivery (CDO2 ) by 12-19% at sea level and high altitude, whereas core heating by 1.5°C did not reliably reduce CBF or CDO2 Oxygen content in arterial blood was fully restored with acclimatisation to 4330 m, but concurrent cold stress reduced CBF and CDO2 Gross indices of cognition were not impaired by any combination of thermal and hypoxic stress despite large reductions in CDO2 Chronic hypoxia renders the brain susceptible to large reductions in oxygen delivery with concurrent cold stress, which might make monitoring core temperature more important in this context ABSTRACT: Real-world settings are composed of multiple environmental stressors, yet the majority of research in environmental physiology investigates these stressors in isolation. The brain is central in both behavioural and physiological responses to threatening stimuli and, given its tight metabolic and haemodynamic requirements, is particularly susceptible to environmental stress. We measured cerebral blood flow (CBF, duplex ultrasound), cerebral oxygen delivery (CDO2 ), oesophageal temperature, and arterial blood gases during exposure to three commonly experienced environmental stressors - heat, cold and hypoxia - in isolation, and in combination. Twelve healthy male subjects (27 ± 11 years) underwent core cooling by 1.0°C and core heating by 1.5°C in randomised order at sea level; acute hypoxia ( PET,O2 = 50 mm Hg) was imposed at baseline and at each thermal extreme. Core cooling and heating protocols were repeated after 16 ± 4 days residing at 4330 m to investigate any interactions with high altitude acclimatisation. Cold stress decreased CBF by 20-30% and CDO2 by 12-19% (both P < 0.01) irrespective of altitude, whereas heating did not reliably change either CBF or CDO2 (both P > 0.08). The increases in CBF with acute hypoxia during thermal stress were appropriate to maintain CDO2 at normothermic, normoxic values. Reaction time was faster and slower by 6-9% with heating and cooling, respectively (both P < 0.01), but central (brain) processes were not impaired by any combination of environmental stressors. These findings highlight the powerful influence of core cooling in reducing CDO2 . Despite these large reductions in CDO2 with cold stress, gross indices of cognition remained stable.

KW - Adolescent

KW - Adult

KW - Altitude

KW - Cerebrovascular Circulation

KW - Cold-Shock Response

KW - Heat-Shock Response

KW - Hemodynamics

KW - Humans

KW - Hypoxia/physiopathology

KW - Male

KW - Young Adult

U2 - 10.1113/JP278917

DO - 10.1113/JP278917

M3 - Article

C2 - 31696936

VL - 598

SP - 265

EP - 284

JO - Journal of Physiology

JF - Journal of Physiology

SN - 0022-3751

IS - 2

ER -