Voluntary suppression of hyperthermia-induced hyperventilation mitigates the reduction in cerebral blood flow velocity during exercise in the heat

Tsuji, Bun; Honda, Yasushi; Ikebe, Yusuke; Fujii, Naoto; Kondo, Narihiko; Nishiyasu, Takeshi

doi:10.1152/ajpregu.00419.2014

Cited by 19 publications

(26 citation statements)

References 47 publications

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“…Passive heating by ß1.3°C generally elicits a hyperventilatory response that reduces P a,CO 2 (Fujii et al 2008;Tsuji et al 2012), but the threshold is highly variable between people (reviewed in Tsuji et al 2016). This hyperthermia-induced hypocapnia is responsible for 50-100% of the decrease in CBF with core heating above ß38.5 o C (Brothers et al 2009;Nelson et al 2011;Bain et al 2013;Tsuji et al 2015Tsuji et al , 2018Tsuji et al , 2019. Countrary to our first hypothesis, because of the generally modest ventilatory response in our participants, core heating by 1.5°C did not decrease CBF.…”

Section: Factors Contributing To Cdo 2 During Isolated Thermal Strainmentioning

confidence: 53%

“…; Tsuji et al . , , ). Countrary to our first hypothesis, because of the generally modest ventilatory response in our participants, core heating by 1.5°C did not decrease CBF.…”

Section: Discussionmentioning

confidence: 99%

“…) restoration of CBF during heat stress when eucapnia is acutely restored or when hyperventilation is voluntarily supressed (Tsuji et al . , ). Functionally, each of these stressors in isolation – hypoxia, cold, and heat – have been shown to impair cognitive function (Simmons et al .…”

Section: Introductionmentioning

confidence: 99%

“…During passive and active heating, CBF and CMRO 2 become uncoupled as CBF tends to decrease (Nybo & Nielsen, 2001;Nelson et al 2011), which can be managed only by elevating oxygen extraction (Nybo et al 2002a). The heat-induced reduction in CBF is mediated primarily by arterial hypocapnia secondary to heat-induced hyperventilation; this observation is evidenced by a partial (Brothers et al 2009) or full (Nelson et al 2011;Bain et al 2013) restoration of CBF during heat stress when eucapnia is acutely restored or when hyperventilation is voluntarily supressed (Tsuji et al 2015(Tsuji et al , 2019. Functionally, each of these stressors in isolation -hypoxia, cold, and heat -have been shown to impair cognitive function (Simmons et al 2008;Muller et al 2012;Paulauskas et al 2015;Piil et al 2017).…”

Section: Introductionmentioning

confidence: 99%

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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

Tymko

Thomas

et al. 2020

The Journal of Physiology

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Key points 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.

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Section: Factors Contributing To Cdo 2 During Isolated Thermal Strainmentioning

confidence: 53%

“…; Tsuji et al . , , ). Countrary to our first hypothesis, because of the generally modest ventilatory response in our participants, core heating by 1.5°C did not decrease CBF.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress

Gibbons

Tymko

Thomas

et al. 2020

The Journal of Physiology

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“…A rise in core temperature reportedly leads to increased minute ventilation ( ) (hyperthermic hyperventilation) at rest (10,17,20,40) and during exercise (18,33,45,48).…”

Section: Introductionmentioning

confidence: 99%

Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans

Tsuji

Filingeri

Honda

et al. 2018

Journal of Applied Physiology

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Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (T) to reach 39°C. During heating in two separate trials, end-tidal CO partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) ( P = 0.005) in the Control trial. This decrease was prevented by breathing CO-enriched air throughout the heating such that end-tidal CO partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating ( P = 1.00). The sensitivity to rising T (i.e., slope of the T - V̇ relation) did not differ between the Control and CO-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min·°C, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO breathing increased MCAV relative to Control at the end of heating ( P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia. NEW & NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The last may underlie central fatigue. We are the first to demonstrate that hyperthermia-induced hyperventilation is not suppressed by the resultant hypocapnia and that hypocapnia explains only 36% of cerebral hypoperfusion elicited by hyperthermia. These new findings advance our understanding of the mechanisms controlling ventilation and cerebral blood flow during heat stress, which may be useful for developing interventions aimed at preventing central fatigue during hyperthermia.

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Middle cerebral artery blood flow velocity during a 4 km cycling time trial

et al. 2017

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Changes in MCA appear to depend on the pacing strategy adopted, with a positive pacing strategy likely to contribute to a hyperventilatory drop in PCO and subsequent reduction in MCA. Although lower cerebral blood flow cannot be directly linked to an inability to raise or maintain power output during the closing stages of the time trial, this potential contributor to fatigue is worth further investigation.

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Voluntary suppression of hyperthermia-induced hyperventilation mitigates the reduction in cerebral blood flow velocity during exercise in the heat

Cited by 19 publications

References 47 publications

Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress

Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress

Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans

Middle cerebral artery blood flow velocity during a 4 km cycling time trial

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