β-Adrenoceptor Blockade and Exercise An Update
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- Van Baak, M.A. Sports Medicine (1988) 5: 209. doi:10.2165/00007256-198805040-00002
Blockade of β-adrenoceptors interferes with haemodynamic and metabolic adaptations and ion balance during dynamic exercise. After administration of a β-blocker exercise heart rate is reduced. Exercise cardiac output and blood pressure are reduced also, but to a lesser extent than heart rate. At submaximal exercise intensities blood flow to the active skeletal muscle is also reduced. The availability of non-esterified fatty acids for energy production is decreased, due to inhibiton of β-adrenoceptor-mediated adipose tissue lipolysis, and possibly also of intramuscular triglyceride breakdown. During submaximal exercise muscle glycogenolysis is unaffected, but there are indications that the maximal glycogenolytic rate at high exercise intensities is decreased. In normally fed subjects plasma glucose concentration is maintained at a normal level during submaximal endurance exercise after β-blocker administration, although lower glucose concentrations are found in fasting subjects and during high intensity exercise after β-blocker administration. Plasma lactate concentrations tend to be somewhat lower after β-blocker administration while plasma potassium concentration during exercise is increased. β-Blocker administration may also interfere with thermoregulation during prolonged exercise.
Maximal aerobic exercise capacity is reduced in normotensive and probably also in hypertensive subjects after β-blocker administration. Submaximal endurance performance is impaired to a much more important extent in both groups of subjects. In patients with coronary artery disease, on the other hand, symptom-limited exercise capacity is improved during β-blocker treatment. Studies on trainability during β-blocker treatment show inconsistent results in healthy subjects, although the majority of studies suggest a similar training-induced increase in V̇2max max during placebo and β-blocker treatment. In patients with coronary artery disease the training effects are also similar in patients treated with β-blockers and those without.
The negative effects of β-blockers on maximal and especially submaximal exercise capacity should be considered when prescribing β-blockers to physically active hypertensive patients. The negative influence is shared by all types of β-blockers, although the impairment of submaximal exercise capacity is more pronounced with non-selective than with β 1-selective β-blockers. β-Blockers with intrinsic sympathomimetic activity have similar effects during exercise to those without intrinsic sympathomimetic activity.