論文

査読有り
2014年3月

Response of end tidal CO2 pressure to impulse exercise

ACTA PHYSIOLOGICA HUNGARICA
  • T. Yano
  • ,
  • R. Afroundeh
  • ,
  • R. Yamanak
  • ,
  • T. Arimitsu
  • ,
  • C-S Lian
  • ,
  • K. Shirkawa
  • ,
  • T. Yunoki

101
1
開始ページ
103
終了ページ
111
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1556/APhysiol.100.2013.018
出版者・発行元
AKADEMIAI KIADO RT

The purpose of the present study was to examine how end tidal CO2 pressure (PETCO2) is controlled in impulse exercise. After pre-exercise at 25 watts for 5 min, impulse exercise for 10 sec with 200 watts followed by post exercise at 25 watts was performed. Ventilation ((V) over dotE) significantly increased until the end of impulse exercise and significantly re-increased after a sudden decrease. Heart rate (HR) significantly increased until the end of impulse exercise and then decreased to the pre-exercise level. PETCO2 remained constant during impulse exercise. PETCO2 significantly increased momentarily after impulse exercise and then significantly decreased to the pre-exercise level. PETCO2 showed oscillation. The average peak frequency of power spectral density in PETCO2 appeared at 0.0078 Hz. Cross correlations were obtained after impulse exercise. The peak cross correlations between (V) over dotE and PETCO2, HR and PETCO2, and (V) over dotE and HR were 0.834 with a time delay of -7 sec, 0.813 with a time delay of 7 sec and 0.701 with a time delay of -15 sec, respectively. We demonstrated that PETCO2 homeodynamics was interactively maintained by PETCO2 itself, CO2 transportation (product of cardiac output and mixed venous CO2 content) into the lungs by heart pumping and CO2 elimination by ventilation, and it oscillates as a result of their interactions.

リンク情報
DOI
https://doi.org/10.1556/APhysiol.100.2013.018
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/24311228
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000332946400011&DestApp=WOS_CPL
ID情報
  • DOI : 10.1556/APhysiol.100.2013.018
  • ISSN : 0231-424X
  • eISSN : 1588-2683
  • PubMed ID : 24311228
  • Web of Science ID : WOS:000332946400011

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