PHYSICAL PERFORMANCE AND MUSCLE METABOLISM DURING BETA-ADRENERGIC-BLOCKADE IN MAN

  • 1 January 1984
    • journal article
    • review article
    • Vol. 536, 1-53
Abstract
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, was 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 O2 uptake (.ovrhdot.VO2 max) 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 nonselective .beta.-blockade on work capacity, no differences were demonstrated with regard to muscle strength, muscle power and aerobic power (.ovrhdot.VO2 max). Aerobic endurance was decreased to a greater extent by nonselective than by .beta.1-selective blockade, when similar reductions in heart rate and .ovrhdot.VO2 max were attained. The difference in aerobic endurance between the 2 types of blockers indicates that factors other than an effect on O2 transport, are responsible for the further reduction in endurance induced by the nonselective blockade. These factors are most likely local metabolic factors. Similarly, work capacity was reduced to a greater extent by nonselective than .beta.1-selective blockade when similar reductions in blood pressure were attained by both drugs in hypertensive patients. Muscle G-6-P concentration was reduced by nonselective, but not by .beta.1-selective blockade, suggesting a .beta.2-mediated retardation of glycolysis. The effects of .beta.-blockade on .ovrhdot.VO2 max and work capacity shown during acute administration persisted during long-term treatment.