g8 PHYSIOLOGICAL TRIGGERS 



length of the cross-structure could then be reflected in a small, longitudinally- 

 oriented relaxation. It can be supposed that calcium is released in sufficient 

 quantity to inactivate relaxing factor maximally and does so briefly, establishing 

 the fully active state. During this period the contractile protein is free to 

 develop tension and to function as an enzyme. Calcium can thus be considered 

 here as a triggering device in that the performance of the contractile protein 

 following its release from relaxing factor is independent of the releasing mecha- 

 nism. A rapid removal of free calcium by readsorption or combination with other 

 anions brings about an early decline in the active state. If more calcium is 

 initially released due to a prolongation of the activating process initiated at the 

 fiber membrane, a greater relaxation of bridge protein, and a more pronounced 

 latency relaxation, would be expected. In addition, the active state would be 

 maintained for a longer period and full development of tension in the fiber 

 could be realized. 



REFERENCES 



1. Abbott, B. C. and J. Lowy. Transparency changes of unstriated squid muscle during 

 contraction. Abstr. XXth Internat. Physiol. Congr., Brussels, 1956, pp. 8-9. 



2. AcHESON, G. H. Physiology of neuro-muscular junctions: Chemical aspects. Federation 

 Proc. 7:447-457, 1948. 



3. Bailey, K. Tropomyosin: a new asymmetric protein component of the muscle fibril. 

 Biochem. J. 43: 271-279, 1948. 



4. Bailey, K. Structure Proteins. II. Muscle. In: The Proteins, vol. II. Edited by H. Neu- 

 RATH and K. Bailey. New York: Acad. Press, 1954. 



5. Bendall, J. R. Relaxing effect of myokinase on muscle fibers: its identity with the Marsh 

 factor. Proc. Roy. Soc. London, s. B 142: 409-426, 1954- 



6. Born, G. V. R. and E. Bulbring. Movement of potassium between smooth muscle and 

 the surrounding fluid. /. Physiol. 131: 690-703, 1956. 



7. Boyle, P. J. and E. J. Conway. Potassium accumulation in muscle and associated 

 changes. J. Physiol. 100: 1-63, 1941. 



8. Bozler, E. Interactions between magnesium, pyrophosphate, and the contractile ele- 

 ments. /. Gen. Physiol. 38: 53-58, 1954- 



9. Bozler, E. Relaxation in extracted muscle fibers. J. Gen. Physiol. 38: 149-159, 1954. 



10. Brown, D. E. S. Effect of rapid changes in hydrostatic pressure upon the contraction of 

 skeletal muscle. ./. Cell. & Com p. Physiol. 4: 257-281, 1934. 



11. Brown, D. E. S. Effect of rapid compression upon events in the isometric contraction of 

 skeletal muscle. J. Cell. & Com p. Physiol. 8: 141-157, 1936. 



12. BucHTHAL, F. and J. LiNDHARD. Direct application of acetylcholine to motor end-plates 

 of voluntary muscle fibers. J. Physiol. 90: 82-83P, 1937- 



13. BiJLBRiNG, E., M. E. Holman and H. LiJLLMAN. Membrane potential and spontaneous 

 activity in calcium-deficient striated muscle of the frog. /. Physiol. 132: 12P, 1956. 



14. Cavanaugh, D. J. AND J. Z. Hearon. Kinetics of acetylcholine action on skeletal muscle. 

 Arch, intern, pharmacodynamie 100: 68-78, 1954- 



15. Conway, E. J. and P. T. Moore. Cation and anion permeahilil) constants for the muscle 

 fiber membrane. Nature 156: 1 70-1 71, 1945- 



16. Creese, R. Measurement of cation fluxes in rat diajjhragm. I'roc. Roy. Soc. London, s. B 

 142: 497-513, 1954. 



