The shortening of rabbit muscles during rigor mortis: its relation to the breakdown of adenosine triphosphate and creatine phosphate and to muscular contraction

Abstract

In a recent paper (Bate-Smith & Bendall, 1949) it was shown that the timecourse of rigor mortis in rabbit muscle was determined principally by the glycogen-reserve of the muscle at death. As it had previously been shown (Bate-Smith & Bendall, 1947) that the 20-to 40-fold increase in the modulus of elasticity of the muscle, characteristic of the rapid phase of rigor, coincided with the rapid disappearance of adenosine triphosphate (ATP) from the muscle, the conclusion was drawn that the glycogen was merely acting as a reserve of energy for the resynthesis of ATP. In neither of these papers, however, was the role of creatine phosphate (CP), as a reserve of energyrich phosphate, fully taken into account, nor was direct evidence offered that it did not disappear from the muscle coincidentally with the ATP. In the present paper it will be shown that in well-rested and relaxed animals, the CP level is high immediately postmortem, but decreases rapidly thereafter, being reduced to less than 30 % of its initial level before there is any appreciable loss of ATP. This occurs whatever the rate of glycolysis, although the rate of breakdown of CP depends to some extent on the glycogen reserve at death.For well-fed, rested animals, the chief chemical events related to the onset of rigor mortis are (a) more or less rapid glycolysis from the moment of death, the rate depending on the pH-range traversed (cf. Bate-Smith & Bendall, 1949), (b) the disappearance of CP from the moment of death, the CP falling to 30 % of the resting level when the pH has fallen to about 6-8, (c) the disappearance of ATP, which begins when the CP has fallen below the 30 % level, and continues at a steady rate until it reaches 20 % of its resting level. At this point glycolysis is almost at a standstill, and the rate of ATP disappearance falls off markedly. As in the previous paper, the rate-determining factor in all these reactions is taken to be the breakdown of ATP by the ATP-ADP-ase systems in muscle,

Comparing human skeletal muscle architectural parameters of cadavers with in vivo ultrasonographic measurements

“…Postmortem skeletal muscle undergoes rigor mortis, a process that has been shown to cause a slow contraction in muscle fibres (Bendall, 1951 ;Davies, 1963). However, Bendall (1973) explained that this contraction is minimal in comparison with a living contraction, yielding only a small fraction of the total work which can be performed by the living tissue.…”

“…Cadaveric tissue also undergoes postmortem changes, one of which is rigor mortis. It has been shown that this change can produce a slow contraction in skeletal muscle (Bendall, 1951 ;Davies, 1963). This process may therefore have some effect on the internal fibre architecture.…”

The onset of rigor mortis in various muscles of the draught horse

“…The maintenance of a high ATP level, and hence of pre-rigor extensibility, depends not only on the resynthesis of ATP by glycolysis: the level of creatine phosphate (CP), which serves as a reservoir for the formation of ATP from ADP, is also important. This is apparent from the fact that, irrespective of the glycogen reserves, the ATP level apparently diminishes rapidly as soon as 80 % of the CP initially present has been broken down (Bendall, 1951).In the present study, comparative observations have been made on the onset of rigor mortis in the longissimus dorsi, psoas, diaphragm and heart muscles of the horse. It has been confirmed that the loss of extensibility, characteristic of rigor mortis, is associated with a decrease of ATP in all four muscles.…”

Active State of Muscle in Iodoacetate Rigor

“…Thus irreversible splitting of ATP as such is not sufficient to set up the active state of rigor, for, if it were, this response should develop in relation to the hydrolysis of the first 50 per cent of the muscle's ATP. However, this may signify that during this part of the change the net rate of ATP breakdown is not high enough to activate a mechanical change, as seems to be the case for initiation of shortening in rigor morris (27); or possibly a relaxation mechanism is maintained that prevents the ATP splitting from engendering the active state, as suggested by Weber (25). But still another interpretation is that in IAA rigor even the delayed breakdown of the ATP is merely coincidental with and not causally related to rigor production, and that therefore a reaction of some other substance, e.g.…”