Abstract

Although clinical doses of beta-blockade may reduce heart rate by 30 to 35, during maximal exercise cardiac output is not equally reduced. Accordingly, most studies have demonstrated increased stroke volume after beta-blockade. This reduction in heart rate is typically accompanied by a decreased VO2max (5 to 15) in both patients and healthy, trained subjects. This smaller reduction in VO2max, as compared with the decrease in cardiac output, is the result of a partly compensating increased arteriovenous O2 difference. Work capacity as reflected by the ability to perform intense short term or more prolonged steady-state exercise is also impaired following beta-blockade, beta-Adrenoceptors can be subdivided into types beta1- and beta2-Blockers which are specific for either beta1-receptors (beta1-selective blockers) or both beta1- and beta2 receptors (non-selective blockers) differ with regard to their effect on exercise performance. Exercise performance ability, irrespective of exercise intensity and duration, is impaired to a greater extent following non-selective than beta1-selective blockade at equal reductions in heart rate. This response systems from a decreased energy flux through glycogenolysis during non-selective blockade treatment. Individuals receiving beta-blockade medication therefore show greater adaptive response conditioning during treatment with beta1-selective than non-selective blockade probably because of greater training intensity with the former therapy. Neither psychomotor performance nor muscular strength and power is negatively affected by beta-blockade. Nevertheless, the ability to perform athletic events requiring high levels of motor control under emotional stress but not high levels of aerobic or anaerobic energy release, is probably increased during beta-blockade. Verf.-Referat