Impaired cardiac "acceleration" at the onset of exercise in patients with coronary disease.
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.
D000328:Adult; D001775:Blood Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006706:Homeostasis; D006801:Humans; D008875:Middle Aged; D008954:Models, Biological; D005082:Physical Exertion; D012119:Respiration; D012146:Rest