title: Exercise performance and beta-blockade.
abstract: beta-Adrenoceptor blockers (beta-blockers) are common first-choice drugs in the treatment of various cardiovascular disorders. Physical exercise performed during single-dose administration of beta-blockers, however, is associated with an increased rate of perceived exertion; an effect which appears to be partly reduced with long term treatment. 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 beta 1- and beta 2. Blockers which are specific for either beta 1-receptors (beta 1-selective blockers) or both beta 1- and beta 2 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 beta 1-selective blockade at equal reductions in heart rate. This response stems from a decreased energy flux through glycogenolysis during non-selective blockade treatment. Individuals receiving beta-blockade medication therefore show greater adaptive response to physical conditioning during treatment with beta 1-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.
authors.forename: P A
authors.initials: PA
authors.lastname: Tesch
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D001786:Blood Glucose / Q000378:metabolism; D050260:Carbohydrate Metabolism; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D004734:Energy Metabolism / Q000187:drug effects; D006003:Glycogen / Q000378:metabolism; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007773:Lactates / Q000378:metabolism; D008066:Lipolysis / Q000187:drug effects; D009132:Muscles / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D010807:Physical Endurance / Q000187:drug effects; D005082:Physical Exertion / Q000187:drug effects*; D011597:Psychomotor Performance / Q000187:drug effects; D012123:Pulmonary Ventilation / Q000187:drug effects; D011943:Receptors, Adrenergic, beta / Q000145:classification; D013997:Time Factors
chemical_list: D000227:Adenine Nucleotides; D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D007773:Lactates; D011943:Receptors, Adrenergic, beta; D006003:Glycogen