HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 89/4/465    most recent expphysiol.2004.027250v1 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 Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Howden, R. Articles by Swaine, I. L. Search for Related Content PubMed PubMed Citation Articles by Howden, R. Articles by Swaine, I. L. Related Collections Cardiovascular control

¹ Physiology of Exercise, De Montfort University, Lansdowne Road, Bedford, UK² Department of Kinesiology, University of North Carolina, 9201 University City Boulevard, Charlotte, NC, USA³ Department of Sport Science, Tourism and Leisure, Canterbury Christ Church University College, North Holmes Road, Canterbury, UK

Breathing carbon dioxide (CO₂) is known to induce hypercapnic acidosis and to affect chemoreceptor regulation of the cardiovascular system. However, there is limited information in the literature regarding the effects of breathing CO₂ upon tolerance to orthostatic stress where cardiovascular regulation is challenged. The purpose of this study was to investigate the effect of breathing 5% CO₂ on presyncopal tolerance to lower body negative pressure (LBNP). Nine subjects (five males and four females; average ±S.D. age 21.9 ± 0.9 years, height 172.4 ± 9.7 cm, mass 70.3 ± 7.1 kg) volunteered to participate in this study. Orthostatic tolerance was determined by exposing subjects to LBNP until the onset of presyncopal signs and symptoms on two occasions each separated by approximately 1 week. On one occasion investigations were carried out while subjects were breathing room air and on the other while subjects were breathing air containing 5% CO₂, inducing hypercapnia and stimulating systemic chemoreceptors. During hypercapnic conditions, as compared with normocapnia, there were significant increases (P < 0.05) in minute ventilation, end-tidal CO₂ and estimated arterial P_CO2. Furthermore, under hypercapnic conditions there was an increase in orthostatic tolerance, peak heart rate and time to peak heart rate during LBNP. The LBNP-induced increase in calf circumference was significantly attenuated at –50 mmHg of LBNP in addition to a further 22.3% reduction in stroke volume under hypercapnic conditions. In conclusion, these results suggest that the possible protective element of presyncope was delayed during hypercapnia at the expense of further reductions in stroke volume. This delayed presyncopal response may have been associated with increases in cerebral blood flow (CBF) induced by the increased arterial P_CO2.

(Received 15 January 2004; accepted after revision 28 April 2004; first published online 29 June 2004)
Corresponding author R. Howden: Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Building 101, Room E-214, Research Triangle Park, NC 27709, USA. Email: howden{at}niehs.nih.gov