202 1. lODOACETATE AND lODOACETAMIDE 



the muscle and responsible for the rigor. Eelaxation from rigor has been 

 studied most thoroughly by Sandow and Schneyer (1955) and is one of their 

 evidences that rigor involves a cyclical process like a normal contraction, 

 rather than being entirely different. They believe that rigor is due to the 

 activation of some contractile process instead of the development of the 

 inability to relax. One important question that remains unanswered is: 

 what is the state of the pulled-out extended muscle? It is inexcitable, but 

 can it be contracted by any means? Is it neither contracted nor relaxed, 

 but in a third state, which we might call extension? Is rigor relaxation simply 

 a mechanical luxation of intracellular bonding on a molecular level? It ap- 

 pears that more work must be done before one can accept that this type of 

 relaxation is comparable to that from a normal contraction. 



(C) Certain metabolic characteristics of iodoacetate rigor. The problem of 

 high-energy substances, EM pathway intermediates, and the accumulation 

 of various substances will be taken up later, but here it is pertinent to in- 

 quire into several more general metabolic relationships. For example, is 

 the development of rigor dependent solely on a block of the EM pathway? 

 Very little study of the effects of pyruvate on rigor has been done. Grimlund 

 (1936) showed that pyruvate and lactate prevent, or appreciably delay, 

 the rigor of muscles in 1 milf bromoacetate, whereas succinate, fumarate, 

 and glycerophosphate have no effect, but I know of no work in which pyru- 

 vate or lactate has been added after rigor has occurred. What slight evi- 

 dence we have thus suggests that at least the onset of rigor is due to a 

 glycolytic depression. 



If this is so and the basis for rigor is metabolic, one might expect certain 

 other inhibitors also to induce rigor. Anyone who has used a number of 

 inhibitors on muscle gets the impression that iodoacetate is particularly 

 prone to cause rigor, but this may be due only to the fact that iodoacetate 

 is able to su])i)ress more effectively all the energy-supplying processes. 

 Fluoride should also produce rigor and indeed Lipmann (1930) has shown 

 that in frog muscle it does; it does not so readily in cardiac muscle (see 

 page 221). There seems to be no mention of rigor from 2-deoxyglucose, but 

 the block in most cases is perhaps not complete enough. Mercurials and 2,4- 

 dinitrophenol may bring about rigor of frog muscle (Krueger, 1950; Kutscha, 

 1961). The rigor of rat diaphragm induced by 2,4-dinitrophenol is very 

 marked; the maximal shortening is greater than in a single contraction, 

 develops quite rapidly, and is reversible (Barnes and Duff, 1954). However, 

 in other muscles, as the heart, 2,4-dinitrophenol is occasionally rather inef- 

 fective in causing rigor, and we shall delay final decision on this matter 

 until we have discussed these other tissues. 



The metabolic changes occurring during the development of rigor have 

 not yet been generally characterized. Wright (1932) reported some rise in 

 the respiration following the onset of rigor, but claimed that this does not 



