Abstract

We evaluated the effects of long-term beta-blocker treatment on the balance between oxygen delivery and extraction at peak oxygen uptake (VO2) and at target heart rate training (anaerobic threshold). Fifteen patients with coronary artery disease performed paired peak cardiopulmonary and submaximal exercise tests on a cycle ergometer with and without atenolol treatment. Thirty minutes following the submaximal tests, participants pedaled 10 minutes at a workload corresponding to that of the anaerobic threshold attained. Arterial oxygen was defined from echocardiography and venous oxygen content. At rest, stroke volume, heart rate, and cardiac output were lower (P < .05), whereas arteriovenous oxygen difference [(a - v)O2] was higher with the use of atenolol (P < .05). At peak exercise, heart rate, lactate, and systolic blood pressure were lower (P < .05), whereas (a - v)O2 was higher (P < .05) with the use of atenolol. At anaerobic threshold, stroke volume, heart rate, cardiac output, and systolic blood pressure were lower (P < .05), whereas (a - v)O2 was higher (P < .05) with the use of atenolol. Absolute VO2 and workload during maximal (P = .67 and P = .49, respectively) and submaximal (P = .13 and P = .44, respectively) exercises were similar between conditions. Results demonstrate that atenolol treatment in patients with coronary artery disease does not alter VO2 and workload at the anaerobic threshold and peak exercise because of an increase in oxygen extraction and stroke volume in the face of reduced heart rate. These findings indicate that with long-term beta-adrenergic receptor blockade, there is interplay between oxygen delivery and extraction, suggesting a link between cardiac hemodynamic responses and skeletal muscle metabolic adaptations.

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