Effects of CO2 on ventilatory and cerebrovascular responses during passive heating in human

Bun Tsuji (7150787)

Davide Filingeri (1384197)

K. Hayashi (7150793)

N. Honda (7150802)

N. Kondo (7150799)

Naoto Fujii (7150790)

Takeshi Nishiyasu (7150805)

Tsubasa Eguchi (7150796)

English

Loughborough University Institutional Repository

Abstract (ECSS 2014) Effects of CO2 on ventilatory and cerebrovascular responses during passive heating in humans  Tsuji, B.1, Filingeri, D.2, Fujii, N.3, Hayashi, K.4, Eguchi, T.1, Kondo, N.5, Honda, Y.1, Nishiyasu, T.1  1 Institute of Health and Sports Science, University of Tsukuba, Japan 2 Loughborough University, UK 3 University of Ottawa, Canada  4 University of Shizuoka, Japan 5 Kobe University, Japan  Introduction During passive heating of resting humans, minute ventilation (VE) changes little as esophageal temperature (Tes, an index of core temperature) rises until the temperature reaches about 38°C. Above this threshold, VE increases by ~30 L/min with respect to 1°C rise in Tes and results in a decrease in arterial CO2 pressure (PaCO2) (Tsuji et al. 2012). In nornothermic condition, generally, change in PaCO2 can affect both ventilatory and cerebrovascular responses such that the decrease in PaCO2 suppresses VE via central chemoreceptors, and also reduces cerebral blood flow by cerebral vasoconstriction. However, the effect of reduced PaCO2 on ventilatory and cerebrovascular responses during hyperthermia at rest is not well understood. We previously found that, during prolonged moderate exercise in the heat, restoration of PaCO2 to the eucapnic level augmented the ventilatory sensitivity to rising Tes (slope of the Tes-VE relation) by threefold (Hayashi et al. 2011). The present study thus examined the effect of PaCO2 on the ventilatory sensitivity and cerebrovascular response to rinsing Tes at rest. Methods Abstract (ECSS 2014) Fourteen healthy male were passively heated using hot-water immersion (41°C) and a water-perfused suit until Tes reached 39°C or the subjects could no longer tolerate the heating. During the heating on two separate occasions, subjects breathed room air (Control trial) or CO2-enriched air (a mixture of room air and 100% CO2) to prevent a reduction in PETCO2 (an index of PaCO2) (CO2 trial).  Results and Discussion Tes threshold for increase in VE was seen at both trials (Control vs. CO2: 38.4±0.4 vs. 38.1±0.6°C, P = 0.13), and above the thresholds VE increased linearly with rising Tes. In Control trial PETCO2 declined gradually with rising Tes above the threshold, whereas it in CO2 trial remained at eucapnic level. Ventilatory sensitivity to increasing Tes did not differ between Control and CO2 trials (38.1±43.1 vs. 16.5±11.1 L/min/°C, P = 0.15). These suggest that ventilatory response with rising core temperature at rest is unaffected by a decrease in PaCO2. Middle cerebral artery mean blood velocity (MCAVmean) decreased gradually with rising Tes in Control trial (59.9 ± 8.4 and 49.9 ±9.7 sm/s at Tes 36.8 and 38.8°C, respectively), and the reduced MCAVmean was restored by about 40% in CO2 trial (53.8 ± 5.6 cm/s at Tes 38.8°C), but inhaling CO2 had no significant effect on MCAVmean. Furthermore, the restoration of MCAVmean by CO2 inhalation was similar among each Tes revel of 37.2, 37.6, 38.0, 38.4 and 38.8°C. These suggest that the decrease in PaCO2 accounts for the reduction in MCAVmean by 40% at Tes range of 37–39°C during passive heating at rest.  References Tsuji B, Honda Y, Fujii N, Kondo N, Nishiyasu T (2012). J Appl Physiol 113, 1388-1397. Hayashi K, Honda Y, Miyakawa N, Fujii N, Ichinose M, Koga S, Kondo N, Nishiyasu T (2011). J Appl Physiol 110, 1334-41.  

Effects of CO2 on ventilatory and cerebrovascular responses during passive heating in humans

https://repository.lboro.ac.uk/articles/Effects_of_CO2_on_ventilatory_and_cerebrovascular_responses_during_passive_heating_in_humans/9341621/files/16950338.pdf

Effects of CO2 on ventilatory and cerebrovascular responses during passive heating in humans

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