Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 56: 1335-1339, 1984;
8750-7587/84 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Bennett, F. M.
Right arrow Articles by Grodins, F. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bennett, F. M.
Right arrow Articles by Grodins, F. S.

Journal of Applied Physiology, Vol 56, Issue 5 1335-1339, Copyright © 1984 by American Physiological Society


ARTICLES

Role of VCO2 in control of breathing of awake exercising dogs

F. M. Bennett, R. D. Tallman Jr and F. S. Grodins

Steady-state ventilatory responses to CO2 inhalation, intravenous CO2 loading (loading), and intravenous CO2 unloading (unloading) were measured in chronic awake dogs while they exercised on an air-conditioned treadmill at 3 mph and 0% grade. End-tidal PO2 was maintained at control levels by manipulation of inspired gas. Responses obtained in three dogs demonstrated that the response to CO2 loading [average increase in CO2 output (Vco2) of 216 ml/min or 35%] was a hypercapnic hyperpnea in every instance. Also, the response to CO2 unloading [average decrease in Vco2 of 90 ml/min or 15% decrease] was a hypocapnic hypopnea in every case. Also, the analysis of the data by directional statistics indicates that there was no difference in the slopes of the responses (change in expiratory ventilation divided by change in arterial Pco2) for loading, unloading, and inhalation. These results indicate that the increased CO2 flow to the lung that occurs in exercise does not provide a direct signal to the respiratory controller that accounts for the exercise hyperpnea. Therefore, other mechanisms must be important in the regulation of ventilation during exercise.


This article has been cited by other articles:


Home page
J. Physiol.Home page
P. Haouzi and B. Chenuel
Control of arterial PCO2 by somatic afferents in sheep
J. Physiol., December 15, 2005; 569(3): 975 - 987.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
A. J. Rice, H. C. Nakayama, H. C. Haverkamp, D. F. Pegelow, J. B. Skatrud, and J. A. Dempsey
Controlled versus Assisted Mechanical Ventilation Effects on Respiratory Motor Output in Sleeping Humans
Am. J. Respir. Crit. Care Med., July 1, 2003; 168(1): 92 - 101.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online