AJP - Regu Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol (June 20, 2002). doi:10.1152/ajpregu.00036.2002
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/5/R1227    most recent
00036.2002v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lindholm, P.
Right arrow Articles by Linnarsson, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lindholm, P.
Right arrow Articles by Linnarsson, D.

Articles in PresS, published online ahead of print June 20, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00036.2002
Submitted on January 22, 2002
Accepted on June 19, 2002

Role of hypoxemia for the cardiovascular responses to apnea during exercise

Peter Lindholm1*, Jessica Nordh1, and Dag Linnarsson1

1 Physiology and Pharmacology, Karolinska Institutet, Section of Environmental Physiology, Stockholm, Stockholm, Sweden

* To whom correspondence should be addressed. E-mail: peter.lindholm{at}fyfa.ki.se.

We sought to define the role of hypoxemia in eliciting the cardiovascular responses to apnea during exercise. Eleven men performed repeated apneas during 100W steady-state exercise, either with normoxic gas (air) or 95% oxygen (oxygen). Beat-by-beat arterial blood pressure, arterial oxygen saturation, and heart rate (HR) were determined, and stroke volume (SV) was estimated from impedance cardiography calibrated with soluble-gas rebreathing. There were large inter-individual variabilities of HR, mean arterial pressure (MAP), and total peripheral resistance (TPR) at end-apnea (ea). However, for each individual HRea, MAPea, and TPRea were highly correlated between air and oxygen (R=0.94, 0.78 and 0.93). HR decreased and MAP increased faster during apnea with air than with oxygen (ANOVA, p<0.05) but MAPea was not different between conditions. Cardiac output (COea) was reduced by 33% with air and 11% with oxygen (p<0.001 for air vs. oxygen). We conclude that the hypoxemia component cannot account for the wide inter-individual differences of HR and TPR responses to apnea. However, hypoxemia augments the HR and TPR responses and may limit the MAP response to apnea by preventing a bradycardia-associated increase of SV.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
A. Pingitore, A. Gemignani, D. Menicucci, G. Di Bella, D. De Marchi, M. Passera, R. Bedini, B. Ghelarducci, and A. L'Abbate
Cardiovascular response to acute hypoxemia induced by prolonged breath holding in air
Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H449 - H455.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
J. P. A. Andersson, M. H. Liner, A. Fredsted, and E. K. A. Schagatay
Cardiovascular and respiratory responses to apneas with and without face immersion in exercising humans
J Appl Physiol, March 1, 2004; 96(3): 1005 - 1010.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2002 by the American Physiological Society.