PCOL3021 Prac 2: Beta blockers and exercise induced changes in heart rate
Adrenoceptors, in particular β-receptors, play significant roles in the sympathetic nervous system (Furchgott, 1972). β1-receptors, found in the cardiovascular system, regulate cardiac output through heart rate and contractility. Conversely, β2 receptors found on the bronchioles of the lungs regulate bronchial diameter in response to changing blood oxygen requirements (Johnson, 2006). Both the baroreceptor reflex, triggered by the drop in blood pressure upon standing (Pilowskya and Goodchild, 2002), and exercise are well documented as causing β-receptor stimulation, changing cardiac output (Fu and Levine, 2013).
Atenolol is a selective β1 adrenoceptor antagonist used in the treatment of cardiovascular disease. It decreases cardiac output by lowering heart rate and contractility, reducing cardiac oxygen demand and arterial blood pressure (The American Society of Health-System Pharmacists, 2014). While displaying greater affinity for β1 adrenoceptors, β2-binding may still occur with higher doses, contraindicating its use for asthmatics (The American Society of Health-System Pharmacists, 2014). As effectively treating cardiovascular conditions requires a combination of diet change and exercise together with pharmacological intervention, ideal cardiovascular drugs would have no impact on the capacity to exercise (Vanhees et al., 2000). As β-blockers have been implicated with orthostatic hypotension by interfering with the baroreceptor reflex (Logan & Witham, 2012), further investigation was necessary to determine the extent of their ability to interfere with normal cardiac function.
This study examines the effect of atenolol on postural change and exercise induced tachycardia in a group of healthy, young university students. Peak expiratory flow rate (PEFR) was measured to quantify β2 antagonist-mediated bronchoconstriction. It was hypothesised that atenolol would cause...