Metabolic effects in muscle during antihypertensive therapy with β1- and β1/β2-adrenoceptor Blockers

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Abstract
The hemodynamic and metabolic consequences of long-term antihypertensive treatment with .beta.1- and .beta.1/.beta.2-adrenoceptor blockade was investigated in 5 young men with mild essential arterial hypertension (WHO stages I and II) at rest and during submaximal exercise in a single-blind crossover study. The drugs (atenolol and alprenolol) were given in equipotent doses as estimated from their effects on blood pressure. Leg blood flow and O2 uptake were the same during both treatment periods. Muscle glycogen decreased by 40% during exercise, irrespective of the drug. There was a positive relationship between muscle lactate release and concentration but for a given muscle lactate concentration the release tended to be lower during treatment with alprenolol. A negative correlation was observed between the percentage of slow-twitch fibers vs. lactate release and muscle lactate concentration. The results demonstrate that during exercise muscle glycogen breaks down despite .beta.-blockade and is neither reduced when both .beta.1- and .beta.2-receptors are blocked, nor when only the .beta.1-receptors are blocked. It is also shown that .beta. blockade impairs the translocation of lactate from the muscle cell to the blood and this is greater with alprenolol than with atenolol, probably due to a membrane effect.