74 TEXT-BOOK OF PHYSIOLOGY. 



of a tetanized muscle shows that it contains less glycogen than a resting 

 muscle, and that it contains a larger amount of water. Coincident with 

 the muscle contraction, the blood-vessels become widely dilated, leading to a 

 large increase in the blood-supply and a rapid removal of the products of 

 decomposition. 



Rigor Mortis. A short time after death the muscles pass into a condi- 

 tion of extreme rigidity or contraction known as death stiffening or rigor 

 mortis, which lasts from one to five days. In this state they offer great 

 resistance to extension. At the same time their tonicity disappears, their 

 cohesion diminishes, and their irritability ceases. The time of the appear- 

 ance of this post-mortem rigidity varies from a quarter of an hour to seven 

 hours. Its onset and duration are influenced by the condition of the muscle 

 irritability at the time of death. When the irritability is impaired from any 

 cause, such as chronic disease or defective blood-supply, the rigidity appears 

 promptly but is of short duration. After death from acute diseases it is apt 

 to be delayed, but will continue for a longer period. The rigidity first 

 appears in the muscles of the lower jaw and neck; next in the muscles 

 of the abdomen and upper extremities; finally in the trunk and lower ex- 

 tremities. It disappears in practically the same order. Chemic changes 

 of a marked character accompany this process. The muscle becomes acid 

 in reaction from the development of sarcolactic acid and there is a large 

 increase in the amount of carbon dioxid given off. The immediate cause 

 of the rigidity appears to be coagulation of the myosin and myogen within 

 the sarcolemma with the formation of two insoluble proteins, myosin fibrin 

 and myogen fibrin. In the early stages of the coagulation restitution is 

 possible by the circulation of arterial blood through the vessels. The final 

 disappearance of this post-mortem rigidity is due probably to the action of 

 acids which render the myosin and myogen fibrins soluble, and possibly 

 to the action of various microorganisms which give rise to putrefactive 

 changes. 



Source of the Muscle Energy. Notwithstanding many investigations, 

 the nature of the materials which are the immediate source of the muscle 

 energy is not known. The absence of any noticeable increase in the quan- 

 tity of urea or other nitrogen-holding compounds excreted renders it prob- 

 able that the energy does not come from the metabolism of protein materials. 

 The marked production of carbon dioxid and sarcolactic acid points to the 

 decomposition of some unstable compound, of a carbohydrate character, 

 rich in carbon and oxygen. It has been suggested that glycogen furnishes 

 the energy, inasmuch as this substance, generally present in muscle, dis- 

 appears during activity. A muscle which has been tetanized contains less 

 glycogen than the corresponding muscle at rest. A muscle which has been 

 separated from the nervous system by division of its nerves and thus pre- 

 vented from contracting accumulates glycogen. Bunge is of the opinion 

 that though the carbohydrates are the main, they are not the only sources of 

 muscle energy. If there is a deficiency or absence of carbohydrate food, 

 the muscle will utilize fat and protein, for experiment has shown that the 

 available glycogen is entirely consumed by the second or third day. The 

 mechanism by which the energy is liberated, whether by direct oxidation or 

 decomposition is uncertain. The general trend of experimental investigation 



