AJP - Regu Watch the video to see how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 283: R1227-R1235, 2002. First published June 20, 2002; doi:10.1152/ajpregu.00036.2002
0363-6119/02 $5.00
This Article
Right arrow Full Text
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
Right arrow Citation Map
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.
Vol. 283, Issue 5, R1227-R1235, November 2002

Role of hypoxemia for the cardiovascular responses to apnea during exercise

Peter Lindholm, Jessica Nordh, and Dag Linnarsson

Section of Environmental Physiology, Department of Physiology and Pharmacology, Karolinska Institutet, SE-171 77 Stockholm, Sweden

We sought to define the role of hypoxemia in eliciting the cardiovascular responses to apnea during exercise. Eleven men performed repeated apneas during 100-W 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 interindividual 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 was reduced by 33% with air and by 11% with oxygen (P < 0.001 for air vs. oxygen). We conclude that the hypoxemia component cannot account for the wide interindividual 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.

hypertension; bradycardia; oxygen; diving response; hypoxia


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
P. Lindholm and C. E. Lundgren
The physiology and pathophysiology of human breath-hold diving
J Appl Physiol, January 1, 2009; 106(1): 284 - 292.
[Abstract] [Full Text] [PDF]

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 TABLE OF CONTENTS
Visit Other APS Journals Online