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Research Article Free access | 10.1172/JCI107814
Cardiology Section, Portland Veterans Administration Hospital, University of Oregon Medical School, Portland, Oregon 97207
Find articles by Sim, D. in: JCI | PubMed | Google Scholar
Cardiology Section, Portland Veterans Administration Hospital, University of Oregon Medical School, Portland, Oregon 97207
Find articles by Neill, W. in: JCI | PubMed | Google Scholar
Published September 1, 1974 - More info
Eight patients with coronary heart disease and exertional angina pectoris successfully completed an 11-15 wk program of endurance exercise conditioning. Angina threshold was determined by upright bicycle ergometer exercise and by atrial pacing. The product of heart rate and arterial systolic blood pressure at the exercise angina threshold was higher after conditioning. suggesting that conditioning increased the maximum myocardial O2 supply during exercise. However, when angina was induced by atrial pacing, heart rate, arterial blood pressure, coronary blood flow, and myocardial O2 consumption at the angina threshold were the same before and after conditioning. Myocardial lactate extraction during atrial pacing was abnormal in the same five patients before and after conditioning. Conditioning caused no detectable changes in coronary collaterals as judged by coronary arteriograms.
The increase in exercise angina threshold appeared to be due to a functional adaptation in either myocardial O2 supply or the relationship between hemodynamic work and myocardial O2 consumption. The adaptation was limited to exercise, and did not occur during a different stress to myocardial O2 supply, atrial pacing.