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Beta‐blockade and binding of digoxin to skeletal muscle

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Summary. The effect of beta‐blockade and a 1‐h bicycle exercise test on the digoxin concentration in skeletal muscle (thigh) and serum was studied in 10 healthy men, who had ingested 0·5 mg digoxin daily for 2 weeks. Each subject performed two exercise tests at 100–140 W during maintenance digoxin treatment and 24 h after the latest dose. They rested in the supine position for 2·5 h before the exercise. Sixty minutes before the start of the exercise 0·25 mg/kg b.w. propranolol or saline (control) were injected (single‐blind). At the end of the exercise the mean heart rate was 30% lower with beta‐blockade (P < 0·001). During exercise the mean skeletal muscle digoxin concentration increased by 29% (P<0·01) in the control situation and by 12% (NS) with beta‐blockade. The results indicate that propranolol partly inhibits the exercise‐induced increase in skeletal muscle digoxin binding. This might be due to inhibition of a catecholamine‐induced stimulation of Na+‐K+ATPase during exercise.
Title: Beta‐blockade and binding of digoxin to skeletal muscle
Description:
Summary.
The effect of beta‐blockade and a 1‐h bicycle exercise test on the digoxin concentration in skeletal muscle (thigh) and serum was studied in 10 healthy men, who had ingested 0·5 mg digoxin daily for 2 weeks.
Each subject performed two exercise tests at 100–140 W during maintenance digoxin treatment and 24 h after the latest dose.
They rested in the supine position for 2·5 h before the exercise.
Sixty minutes before the start of the exercise 0·25 mg/kg b.
w.
propranolol or saline (control) were injected (single‐blind).
At the end of the exercise the mean heart rate was 30% lower with beta‐blockade (P < 0·001).
During exercise the mean skeletal muscle digoxin concentration increased by 29% (P<0·01) in the control situation and by 12% (NS) with beta‐blockade.
The results indicate that propranolol partly inhibits the exercise‐induced increase in skeletal muscle digoxin binding.
This might be due to inhibition of a catecholamine‐induced stimulation of Na+‐K+ATPase during exercise.

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