MODIFICATION OF EXCITATION-CONTRACTION COUPLING IN LOCUST SKELETAL MUSLE INDUCED BY CAFFEINE

Potassium contractures were recorded isometrically in locust extensor tibialis muscles. The graphs relating contracture tension to external potassium, and contractute tension to depolarization were of sigmoid shape. In normal circumstances, peak contracture tension was obtained with 100 mM/1 potassium saline at a depolarization level of about −10 mV. At a concentration of 2 mM/1, caffeine considerably lowered the mechanical threshold of the muscle fibres such that peak contracture tension was obtained with 40 mM/1 potassium saline, at a depolarization level of only −30 mV. Withdrawal of calcium ions from caffeine containing salines resulted in a loss of the contractile response to depolarization, and the lowering of the mechanical threshold was abolished. These results are consistent with the view that caffeine may activate muscle in vivo by accelerating calcium release from the sarcoplasmic reticulum and by suppressing active calcium binding by the reticular calcium pump. Since caffeine can activate depolarized muscle it is suggested that caffeine short‐circuits the normal excitation‐contraction coupling channels to initiate a direct release of calcium ions from the sarcoplasmic reticulum without transient depolarization. Copyright © 1969 Wiley‐Liss, Inc., A Wiley Company