Rigor mortis

Corpses of victims of the 1991 Bangladesh cyclone in Sandwip displaying signs of rigor mortis

After death, aerobic respiration in an organism ceases, depleting the source of oxygen used in the making of adenosine triphosphate (ATP). ATP is required to cause separation of the actin-myosin cross-bridges during relaxation of muscle.[2] When oxygen is no longer present, the body may continue to produce ATP via anaerobic glycolysis. When the body's glycogen is depleted, the ATP concentration diminishes, and the body enters rigor mortis because it is unable to break those bridges.[3][4]

Calcium enters the cytosol after death. Calcium is released into the cytosol due to the deterioration of the sarcoplasmic reticulum. Also, the breakdown of the sarcolemma causes additional calcium to enter the cytosol. The calcium activates the formation of actin-myosin cross-bridging. Once calcium is introduced into the cytosol, it binds to the troponin of thin filaments, which causes the troponin-tropomyosin complex to change shape and allow the myosin heads to bind to the active sites of actin proteins. In rigor mortis myosin heads continue binding with the active sites of actin proteins via adenosine diphosphate (ADP), and the muscle is unable to relax until further enzyme activity degrades the complex. Normal relaxation would occur by replacing ADP with ATP, which would destabilize the myosin-actin bond and break the cross-bridge. However, as ATP is absent, there must be a breakdown of muscle tissue by enzymes (endogenous or bacterial) during decomposition. As part of the process of decomposition, the myosin heads are degraded by the enzymes, allowing the muscle contraction to release and the body to relax.[5]

Decomposition of the myofilaments occurs 48 to 60 hours after the peak of rigor mortis, which occurs approximately 13 hours after death.[1]

At the time of death, a condition called "primary flaccidity" occurs. Following this, the muscles stiffen in rigor mortis. All muscles in the body are affected. Starting between two and six hours following death, rigor mortis begins with the eyelids, neck, and jaw. The sequence may be due to different lactic acid levels among different muscles, which is directly related to the difference in glycogen levels and different types of muscle fibers.

Rigor mortis then spreads to the other muscles, including the internal organs, within the next four to six hours. The onset of rigor mortis is affected by the individual's age, sex, physical condition, and muscular build. Rigor mortis generally peaks at 12 hours, and dissipates after 48 hours.

Rigor mortis may not be perceivable in many infant and child corpses due to their smaller muscle mass.[6]

Rigor mortis is very important in meat technology. The onset of rigor mortis and its resolution partially determine the tenderness of meat. If the post-slaughter meat is immediately chilled to 15 °C (59 °F), a phenomenon known as cold shortening occurs, whereby the muscle sarcomeres shrink to a third of their original length.

Cold shortening is caused by the release of stored calcium ions from the sarcoplasmic reticulum of muscle fibers, in response to the cold stimulus. The calcium ions trigger powerful muscle contraction aided by ATP molecules. To prevent cold shortening, a process known as electrical stimulation is carried out, especially in beef carcasses, immediately after slaughter and skinning. In this process, the carcass is stimulated with alternating current, causing it to contract and relax, which depletes the ATP reserve from the carcass and prevents cold shortening.[7]

The degree of rigor mortis may be used in forensic pathology, to determine the approximate time of death. A dead body holds its position as rigor mortis sets in. If the body is moved after death, but before rigor mortis begins, forensic techniques such as livor mortis can be applied. If the position in which a body is found does not match the location where it is found (for example, if it is flat on its back with one arm sticking straight up), that could mean someone moved it.

Rigor mortis is known as transient evidence, as the degree to which it affects a body degrades over time. Several factors impact its progression, and investigators take these into account when estimating the time of death. One such factor is the ambient temperature. In warm environments, the onset and pace of rigor mortis are sped up by providing a conducive environment for the metabolic processes that cause decay. Low temperatures, however, slow them down. Therefore, for a person who dies outside in frozen conditions rigor mortis may last several days more than normal, so investigators may have to abandon it as a tool for determining time of death.[8][9]

• Cadaveric spasm

• Bear, Mark F; Connors, Barry W.; Paradiso, Michael A., Neuroscience, Exploring the Brain, Philadelphia : Lippincott Williams & Wilkins; Third Edition (1 February 2006). ISBN 0-7817-6003-8
• Robert G. Mayer, "Embalming: history, theory, and practice", McGraw-Hill Professional, 2005, ISBN 0-07-143950-1
• "Rigor mortis and Other Postmortem Changes - Burial, Body, Life, Cause, Time, Person, Human, Putrefaction." Encyclopedia of Death and Dying. 2011. Web. 4 December 2011. <Rigor mortis and Other Postmortem Changes - burial, body, life, cause, time, person, human, Putrefaction>.
• Saladin, Kenneth. Anatomy and Physiology: The Unity of Form and Function, 6th ed. McGraw-Hill. New York, 2012.
• Peress, Robin. "Discovery Health "Rigor mortis at the Crime Scene"" Discovery Health "Health Guides" Discovery Fit & Health, 2011. Web. 4 December 2011. <What causes Rigor mortis?>.