Background: β-blockade controls the ventricular
response to exercise in chronic atrial fibrillation (AF), but the
effects of β-blockers on exercise capacity in AF have been
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.
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
(V̇o2) 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.
V̇o2 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
V̇o2 and cardiac output during exercise.
The observed increase in stroke volume could not adequately compensate
for reduced heart rate to maintain V̇o2
Abbreviations: AF = atrial fibrillation;
V̇e = minute ventilation;
V̇co2 = carbon dioxide output;
V̇o2 = oxygen uptake