Effects and adverse effects of autonomic blockade in physical exercise

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Abstract

Training bradycardia during autonomic blockade has been studied in rats and humans. The heart rate after autonomic blockade (intrinsic heart rate) is also lowered as a part of the adaptation to training. However, this nonautonomic component of the cardiac adaptation requires a long duration of intense endurance training to appear. This is in contrast to the autonomic component of the training bradycardia. From animal studies we have concluded that even if the training bradycardia is due to an adaptation within the heart itself, the adrenergic nerves are important for the development of a slow intrinsic heart rate. Neither the β-receptor stimulation nor the degree of the heart rate increase during exercise is the main stimulus for the development of a training-induced bradycardia.

Well-trained bicyclists had an intrinsic heart rate 20 beats lower than untrained normal control subjects. The heart rate at rest and the maximal heart rate were also on an average 20 beats lower for the bicyclists. There was no significant difference between propranolol and the β1 selective metoprolol in this study regarding their effects on heart rate and on deterioration of the maximal oxygen consumption after blockade. This deterioration was more marked in the well-trained than in the sedentary group. Based upon studies both in normal subjects and patients a careful rating of symptoms including physical exertion, fatigue or pain in the legs, dyspnea and chest pain using a Borg scale is recommended during exercise testing with β blockade. This should facilitate a more optimal and individual prescription and avoid use of β blockers in subgroups of patients with such symptoms as leg fatigue, pain or breathlessness during exercise and β blockade.

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