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Effects of selective beta 2-adrenoceptor blockade on serum potassium and exercise performance in normal men
L Gullestad1, K Birkeland, G Nordby
1Department of Medicine, Baerum Hospital, Sandvika, Norway.
Abstract:
1. The differential effects of beta-adrenoceptor subtypes on potassium fluxes and exercise capacity were compared in eight healthy young men using single oral doses of the selective beta 2-adrenoceptor antagonist ICI-118551, the selective beta 1-adrenoceptor antagonist atenolol or the non-selective beta-adrenoceptor antagonist propranolol. The study was randomized, double-blind and placebo controlled. 2. Potassium in the venous effluent from the exercising muscles increased progressively with increasing exercise intensity. This response was augmented by propranolol, whereas neither atenolol nor ICI-118551 modified the response. After exercise potassium concentration fell exponentially with no difference between the treatment regimens. 3. Cumulative work was significantly reduced by ICI-118551 (6.4%, P = 0.04) and by propranolol (12.4%, P less than 0.01), whereas the reduction with atenolol (5.6%) did not reach statistical significance. 4. Atenolol and propranolol reduced peak heart rate by 23% and 29%, and peak systolic blood pressure by 9% and 11% respectively during maximal exercise. ICI-118551 caused a non-significant reduction in heart rate during submaximal exercise, with a significant reduction at maximum exercise (6% reduction), whereas systolic blood pressure was not different from placebo. Diastolic blood pressures were similar across all treatment regimens. 5. Similar glucose concentrations were obtained at baseline and at exhaustion during all treatment regimens. Lactate concentrations were comparable for any given exercise intensity irrespective of treatment regimens. Propranolol reduced lactate concentrations from the exercising muscles at maximum exercise in proportion to the reduction of maximal exercise capacity. 6. The subjective perception of fatigue was not affected by either beta 1- or beta 2-adrenoceptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Beta-blockers affect exercise differently. Propranolol and a beta 2-antagonist reduced exercise capacity, while propranolol also increased muscle potassium release during intense exercise. Beta 1-blockade had minimal impact.
Area of Science:
- Exercise Physiology
- Pharmacology
- Cardiovascular Research
Background:
- Beta-adrenoceptors play a role in regulating physiological responses during exercise.
- Understanding the specific roles of beta 1- and beta 2-adrenoceptor subtypes is crucial for optimizing exercise performance and managing cardiovascular responses.
Purpose of the Study:
- To investigate the differential effects of selective beta 1- and beta 2-adrenoceptor blockade, as well as non-selective blockade, on potassium fluxes and exercise capacity in healthy young men.
Main Methods:
- A randomized, double-blind, placebo-controlled study involving eight healthy young men.
- Administration of single oral doses of selective beta 2-adrenoceptor antagonist (ICI-118551), selective beta 1-adrenoceptor antagonist (atenolol), or non-selective beta-adrenoceptor antagonist (propranolol).
- Measurement of potassium concentration in venous effluent from exercising muscles, cumulative work, heart rate, blood pressure, glucose, lactate, and subjective fatigue during graded exercise.
Main Results:
- Propranolol augmented the exercise-induced increase in muscle potassium release, while atenolol and ICI-118551 did not.
- Cumulative work was significantly reduced by ICI-118551 and propranolol, but not by atenolol.
- Atenolol and propranolol significantly reduced peak heart rate and systolic blood pressure during maximal exercise, while ICI-118551 had a smaller effect on heart rate.
Conclusions:
- Beta 2-adrenoceptor blockade, but not beta 1-blockade alone, significantly impairs exercise capacity.
- Non-selective beta-blockade with propranolol affects both potassium handling and exercise capacity.
- Subjective perception of fatigue was not altered by either beta 1- or beta 2-adrenoceptor blockade.