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The effect of chronic beta-adrenergic blockade on central circulatory adaptations to physical training was investigated. 16 healthy sedentary males (20-31 yrs) trained on cycle ergometers 40 min/day, 4 days a week for 8 weeks at a work load that during the last 5 weeks corresponded to 75% of the pretraining VO2 max. In a single blind way, 8 subjects were during the training period treated with the beta-adrenergic receptor blocker propranolol (160 mg/day), while the remaining 8 received placebo tablets. Pretraining tests were performed before the start of medication and posttraining tests were performed 6 days after the last day of training and medication. The training program resulted in a similar increase (8%) in VO2 max in both groups (p less than 0.01). The resting heart rate (-4 beats/min; p less than 0.05) as well as the exercise heart rate at a moderate work load (120 W: -11 beats/min; p less than 0.01) decreased with training, and no significant difference was seen between the 2 groups. At a high work load (180 W), however, the heart rate decreased significantly more with training in the placebo group as compared with the beta-blockade group (-19 vs. -7 beats/min; p less than 0.05). The oxygen pulse (VO2/HR) increased in both groups at 120 W (+6%; p less than 0.01). At 180 W the oxygen pulse increased only in the placebo group (+8%; p less than 0.05). The estimated stroke volume at 120 and 180 W, as determined by impedance cardiography, did not change significantly with training although there was a tendency towards an increase in the placebo group only. The resting left ventricular wall thickness and diameter, as determined by echocardiography, did not change significantly with training in either group.--In conclusion, the present study indicates that a moderate degree of beta-adrenergic blockade does not prevent or impair the training-induced increase in the maximal oxygen uptake. During submaximal work, however, the circulatory adaptation may be less apparent if training has been performed during partial blockade of the sympatho-adrenal system.
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