112 INVERTEBRATE PHYSIOLOGY 



the mechanical response is a single twitch (isolated muscle) or a train of 

 myogenic contractions. 



This first hypothesis has been stated in terms of a complex between 

 actomyosin and the high-energy molecule leading to contraction or the 

 development of tension. According to Weber and Portzehl ( 1954) the evi- 

 dence from the glycerinated muscle model is that tension is produced when 

 ATP bound in the fibers is split ; ATP whose splitting is prevented by 

 — SH poisons is the most effective plasticizing agent for the fiber model. 

 The resting state is with ATP bound to the actomyosin and the fibrils 

 fully plastic and extensible. In the fiber model ATP splitting is inhibited 

 at the concentrations above a certain value but still in the physiological 

 range. Weber supposes that, when the muscle is brought into the active 

 state, ATP splitting starts because of a shift in this critical inhibitory con- 

 centration and tension then develops. 



A second hypothesis may now be stated consistent with the view that 

 tension development accompanies the splitting and not the binding of 

 ATP. Again it must be supposed that the rate of splitting depends on the 

 rate of shortening. A sudden shortening on quick release therefore produces 

 a large and nearly synchronous splitting of ATP, and the re-occupation of 

 the sites gives an initial plasticizing efTect ; the muscle therefore behaves 

 as if it was relaxed for a short interval of time until splitting again occurs. 

 Possibly the sudden stretch of the out click of the tymbal or the opposite 

 stroke of the wing again initiates splitting and the development of tension. 

 It is necessary in order that this cycle of events shall occur that the splitting 

 of ATP with the development of tension does not immediately follow the 

 binding of ATP on the actomysin complex, so that the re-occupation of the 

 sites by ATP shall have time to produce a plasticizing effect before splitting 

 has again proceeded far enough to produce an appreciable tension. There is 

 here no diffusion lag producing the oscillation ; the necessary condition is 

 that the splitting shall follow the binding of ATP with a finite time lag 

 even in the active state. 



A lag between binding of ATP and splitting with development of ten- 

 sion is not inconsistent with the result of experiments on normal striated 

 muscle. When a vertebrate striated muscle is excited by stimulation of its 

 motor nerve, the twitch tension does not appear for several milliseconds. 

 Hill (1949) has explained this lag in terms of the stretching of the series 

 elastic component, and has shown that, if quick stretches are given in 

 addition to stimulation, a change in the mechanical properties of the muscle 

 can be detected much earlier ; he concludes that activation starts almost 

 immediately upon excitation. It would be equally possible to interpret this 

 experiment as indicating a normal slow development of activity in the con- 

 tractile mechanism, but that quick stretch accelerated the activation. There 



