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  • Title: Physical performance and muscle metabolism during beta-adrenergic blockade in man.
    Author: Kaiser P.
    Journal: Acta Physiol Scand Suppl; 1984; 536():1-53. PubMed ID: 6151777.
    Abstract:
    The major findings of the present study may be summarized as follows: Muscle strength, measured as maximal isokinetic torque and maximal dynamic muscle power, measured as the highest 5 s power output during a 30 s maximal cycle exercise test, were unaltered by beta-blockade. When maximal exercise was prolonged to 30-60 s, anaerobic endurance, measured both as average power during 30 s maximal cycle exercise and as static endurance time at 65% of maximal voluntary contraction force, was decreased by beta-blockade. On the other hand, anaerobic endurance measured as peak torque decline during 50 repeated maximal isokinetic contractions was unaffected by beta-blockade. Aerobic power, measured as maximal oxygen uptake (VO2max) during cycle exercise, was decreased by beta-blockade. In addition, aerobic endurance was decreased by beta-blockade when measured as both time to fatigue during 10 min cycling and as time for a 2000 m run. When comparing the effects of beta 1-selective and non-selective beta-blockade on work capacity, no differences were demonstrated with regard to muscle strength, muscle power, and aerobic power (VO2max). Aerobic endurance was decreased to a greater extent by non-selective than by beta 1-selective blockade, when similar reductions in heart rate and VO2 max were attained. The difference in aerobic endurance between the two types of blockers indicates that factors other than an effect on oxygen transport, are responsible for the further reduction in endurance induced by the non-selective blockade. These factors are most likely local metabolic factors. Similarly, work capacity was reduced to a greater extent by non-selective than beta 1-selective blockade when similar reduction in blood pressure were attained by both drugs in hypertensive patients. Muscle G-6-P concentration was reduced by non-selective, but not by beta 1-selective blockade, suggesting a beta 2-mediated retardation of glycolysis. The effects of beta-blockade on VO2max and work capacity shown during acute administration persisted during long-term treatment.
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