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


     


J Appl Physiol 52: 71-78, 1982;
8750-7587/82 $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 Google Scholar
Google Scholar
Right arrow Articles by Zimmerman, P.
Right arrow Articles by Jones, N. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zimmerman, P.
Right arrow Articles by Jones, N. L.

Journal of Applied Physiology, Vol 52, Issue 1 71-78, Copyright © 1982 by American Physiological Society


ARTICLES

Impaired cardiac "acceleration" at the onset of exercise in patients with coronary disease

P. Zimmerman, G. J. Heigenhauser, N. McCartney, J. R. Sutton and N. L. Jones

The responses to two levels of exercise (400 and 800 kpm/min) were studied in nine untrained healthy subjects and seven patients with coronary artery disease. Measurements were made over 20-s time intervals to obtain the half times (t1/2) of the asymptotic rise in cardiac frequency (fc), O2 intake (VO2), CO2 output (VCO2), and ventilation (VE). Complete data were obtained in both groups at 400 kpm/min, but only in healthy subjects at 800 kpm/min, as patients were unable to exercise for longer than 2 min at this power. At the onset of 400 kpm/min, t1/2 for VO2 was similar, but t1/2 for fc, VCO2, and VE were all longer in the patients. At 800 kpm/min there was a delay in VO2 in the patients before stopping exercise. In patients and healthy subjects t1/2 for VCO2 and VE, but not VO2, were related to t1/2 for fc. The results emphasized the importance of tissue CO2 storage in attenuating the delivery of CO2 to the lungs and thus delayed the ventilatory response to a step increase in power output.





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