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Extreme Physiology & Medicine

Open Access

Effect of rising body temperature on respiratory chemosensitivity to CO2

Extreme Physiology & Medicine20154(Suppl 1):A152

https://doi.org/10.1186/2046-7648-4-S1-A152

Published: 14 September 2015

Keywords

Body TemperatureTidal VolumeInitial WaterExperiment SubjectMinute Ventilation

Introduction

A rise in body temperature (Tb) is known to cause minute ventilation (VE) to increase. However, the mechanism of the ventilatory response to rising Tb is still unclear. In the context of the relationship between VE and Tb, it is known that respiratory chemosensitivity is influenced by Tb, and that a rise in Tb of more than 0.7 °C enhances respiratory chemosensitivity [1]. It is not known, however, whether increases in Tb less than 0.7 °C also influence respiratory chemosensitivity. The aim of this study was to clarify the effect of mild hyperthermia (0.3 °C and 0.7 °C) on respiratory chemosensitivity.

Methods

Eight persons (five males and three females, mean (SD) age 25 (10) years, height 171.5 (8.9) cm, weight 66.9 (8.7) kg) participated in the study. All were lowlanders and had not been exposed to altitude above 1,000 m within the 6 months prior the study. We measured sublingual temperature (Tsl) as an index of Tb, and measured respiratory chemosensitivity to CO2 using a rebreathing method [2]. The subjects wore a mask connected to a closed one-way circuit with a rubber bag containing the test gas (7 % CO2, 43 % O2, 50 % N2). Rebreathing was terminated when the inspired CO2 fraction reached 9.2 %. This test was performed before heating (ΔTsl = 0 °C) and during heating (ΔTsl = 0.3 °C and 0.7 °C). Measurements were made twice with a 15-min interval between tests at ΔTsl = 0°C, 0.3°C and 0.7°C. During the experiment subjects wore a water-perfused suit. The initial water temperature was 35 °C and was increased to 45 °C.

Results

Before heating mean (SD) Tsl was 36.15 (0.22) °C (ΔTsl = 0 °C) and rose to 36.47 (0.21) °C at ΔTsl = 0.3 °C and then to 36.87 (0.21) °C at ΔTsl = 0.7 °C during heating. While subjects breathed the CO2-rich mixture, VE was 1.49 (0.68) L.min-1.mmHg-1 (ΔTsl = 0 °C), 1.52 (0.75) L.min-1.mmHg-1 (ΔTsl = 0.3°C) and 1.75 ± 0.98 L.min-1.mmHg-1 (ΔTsl = 0.7°C). The tidal volume was 44.7 (12.4) mL.mmHg-1 (ΔTsl = 0°C), 55.4 (24.9) mL.mmHg-1 (ΔTsl = 0.3 °C) and 61.9 (19.5) mL.mmHg-1 (ΔTsl = 0.7 °C) (P < 0.06). The respiratory frequency was 0.47 (0.38) breaths.min-1.mmHg-1 (ΔTsl = 0 °C), 0.40 (0.42) breaths.min-1.mmHg-1 (ΔTsl = 0.3 °C) and 0.37 (0.41) breaths.min-1.mmHg-1 (ΔTsl = 0.7 °C).

Discussion

These results suggest that increases in Tsl less than 0.7 °C do not influence respiratory chemosensitivity to CO2, though the respiratory pattern did tend to change. The ventilatory response to rising Tb has a threshold around 38 °C (esophageal temperature) in the resting state [3]. Moreover, we suggest that increasing the inspired CO2 fraction did not reduce that threshold to the temperatures reached in the present study (Tsl around 37 °C).

Conclusion

Our findings suggest that respiratory chemosensitivity is not affected by mild hyperthermia (~0.7 °C rise in body temperature). It is possible that there is a Tb threshold for changes in respiratory chemosensitivity that is greater than around 37 °C.

Authors’ Affiliations

(1)
Junior College, University of Shizuoka, Shizuoka, Japan
(2)
Osaka Kyoiku University, Osaka, Japan
(3)
Faculty of Education, Shizuoka University, Shizuoka, Japan

References

  1. Natalino MR, Zwillich CW, Weil JV: Effects of hyperthermia on hypoxic ventilatory response in normal man. J Lab Clin Med. 1977, 89: 564-572.PubMedGoogle Scholar
  2. Read DJA: Clinical method for assessing the ventilatory response to carbon dioxide. Australas Ann Med. 1967, 16: 20-32.PubMedGoogle Scholar
  3. Fujii N, Honda Y, Hayashi K, Soya H, Kondo N, Nishiyasu T: Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise. J Appl Physiol. 2008, 104: 998-1005. 10.1152/japplphysiol.00146.2007.View ArticlePubMedGoogle Scholar

Copyright

© Hayashi et al.; 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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