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This Article Full Text Full Text (PDF) All Versions of this Article: 93/8/994    most recent expphysiol.2008.042143v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Fujii, N. Articles by Nishiyasu, T. PubMed PubMed Citation Articles by Fujii, N. Articles by Nishiyasu, T. Related Collections Human, Environmental & Exercise

¹ Institute of Health and Sports Science, University of Tsukuba, Tsukuba City, Japan ² Faculty of Human Development, Kobe University, Kobe 657-8501, Japan ³ Applied Physiology Laboratory, Kobe Design University, Kobe 651-2196, Japan

We tested the hypothesis that hyperthermic hyperventilation in part reflects enhanced chemoreceptor ventilatory O₂ drive, and that the resultant hypocapnia attenuates ventilatory responses and/or middle cerebral artery mean blood velocity (MCAV_mean) in resting humans. Eleven healthy subjects were passively heated for 50–80 min, causing oesophageal temperature (T_oes) to increase by 1.6°C. During heating, minute ventilation increased (P < 0.05), while end-tidal CO₂ pressure (P_ET,CO2) and MCAV_mean declined. A hyperoxia test in which three breaths of hyperoxic air were inspired was performed once before heating and three times during the heating. When we observed hypocapnia (P_ET,CO2 below 40 mmHg), P_ET,CO2 was restored to the eucapnic level by adding 100% CO₂ to the inspired air immediately before the last two tests. Minute ventilation was significantly reduced by hyperoxia, and that reduction gradually increased with increasing T_oes. However, the percentage decrease in from the normoxic level was small (20–29%) and unchanged during heating. When P_ET,CO2 was restored to eucapnic levels, was unchanged, but MCAV_mean was partly restored to the level seen prior to heating (28.1% restoration at T_oes 37.6°C and 38.1% restoration at T_oes 38.0°C). These findings suggest that although hyperthermia increases chemoreceptor ventilatory O₂ drive in resting humans, the relative contribution of the chemoreceptor ventilatory O₂ drive to hyperthermic hyperventilation is small (20%) and unaffected by increasing core temperature. Moreover, hypocapnia induced by hyperthermic hyperventilation reduces cerebral blood flow but not ventilatory responses.

(Received 24 January 2008; accepted after revision 2 April 2008; first published online 10 April 2008)
Corresponding author T. Nishiyasu: Institute of Health and Sports Science, University of Tsukuba, Tsukuba City, Ibaraki 305-8574, Japan. Email: nisiyasu{at}taiiku.tsukuba.ac.jp