BACKGROUND: beta-blockade controls the ventricular response to exercise in chronic atrial fibrillation (AF), but the effects of beta-blockers on exercise capacity in AF have been debated. METHODS:Twelve men with AF (65+/-8 years) participated in a randomized, double-blind, placebo-controlled study of betaxolol (20 mg daily). Patients underwent maximal exercise testing with ventilatory gas exchange analysis, and a separate, submaximal test (50% of maximum) during which cardiac output was measured by a CO2 rebreathing technique. RESULTS: After betaxolol therapy, heart rate was reduced both at rest (92+/-27 vs 62+/-12 beats/min; p < 0.001) and at peak exercise (173+/-22 vs 116+/-24 beats/min; p < 0.001). Maximal oxygen uptake (VO2) was reduced by 19% after betaxolol (21.8+/-5.3 with placebo vs 17.6+/-5.1 mL/kg/min with betaxolol; p < 0.05), with similar reductions observed for maximal exercise time, minute ventilation, and CO2 production. VO2 was reduced by a similar extent (19%) at the ventilatory threshold. Submaximal cardiac output was reduced by 15% during betaxolol therapy (12.9+/-2.3 vs 10.9+/-1.3 L/min; p < 0.05), and stroke volume was higher (88.0+/-21 vs 105.6+/-19 mL/beat; p < 0.05). CONCLUSION:Betaxolol therapy in patients with AF effectively controlled the ventricular rate at rest and during exercise, but also caused considerable reductions in maximal VO2 and cardiac output during exercise. The observed increase in stroke volume could not adequately compensate for reduced heart rate to maintain VO2 during exercise.
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BACKGROUND: beta-blockade controls the ventricular response to exercise in chronic atrial fibrillation (AF), but the effects of beta-blockers on exercise capacity in AF have been debated. METHODS: Twelve men with AF (65+/-8 years) participated in a randomized, double-blind, placebo-controlled study of betaxolol (20 mg daily). Patients underwent maximal exercise testing with ventilatory gas exchange analysis, and a separate, submaximal test (50% of maximum) during which cardiac output was measured by a CO2 rebreathing technique. RESULTS: After betaxolol therapy, heart rate was reduced both at rest (92+/-27 vs 62+/-12 beats/min; p < 0.001) and at peak exercise (173+/-22 vs 116+/-24 beats/min; p < 0.001). Maximal oxygen uptake (VO2) was reduced by 19% after betaxolol (21.8+/-5.3 with placebo vs 17.6+/-5.1 mL/kg/min with betaxolol; p < 0.05), with similar reductions observed for maximal exercise time, minute ventilation, and CO2 production. VO2 was reduced by a similar extent (19%) at the ventilatory threshold. Submaximal cardiac output was reduced by 15% during betaxolol therapy (12.9+/-2.3 vs 10.9+/-1.3 L/min; p < 0.05), and stroke volume was higher (88.0+/-21 vs 105.6+/-19 mL/beat; p < 0.05). CONCLUSION:Betaxolol therapy in patients with AF effectively controlled the ventricular rate at rest and during exercise, but also caused considerable reductions in maximal VO2 and cardiac output during exercise. The observed increase in stroke volume could not adequately compensate for reduced heart rate to maintain VO2 during exercise.
Authors: H F Groenveld; H J G M Crijns; J G P Tijssen; M Alings; H L Hillege; Y S Tuininga; M P Van den Berg; D J Van Veldhuisen; I C Van Gelder Journal: Neth Heart J Date: 2013-04 Impact factor: 2.380