Rigor mortis

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Rigor mortis is one of the recognizable signs of death (Latin mors, mortis) that is caused by a chemical change in the muscles after death, causing the limbs of the corpse to become stiff (Latin rigor) and difficult to move or manipulate.[1] Eerily, during rigor mortis, muscles may contract in seemingly random and bizarre ways even though the body is dead.

Biochemistry

this is really really stupid that i can edit this so easily!!!, the body experiences different, physical, things after death. There is a reason for it and here is the technical anwser.

After a muscle contracts, ATP expenditure is required to release the myosin head of a thick filament from its binding site on the thin filament[1]. Since all metabolic processes have come to a halt in a dead body, no ATP is being produced. Therefore, because of a lack of ATP, the myosin head cannot be released from the actin filament, and the sarcomere cannot relax. Because this happens in muscles all over the body, they become "stiff" and "locked" into place.

ATP is required to reuptake calcium into the sarcomere's sarcoplasmic reticulum (SR). Additionally, when a muscle is relaxed, the myosin heads are returned to their "high energy" position, ready and waiting for a binding site on the actin filament to become available. Because there is no ATP available, previously released calcium ions cannot return to the SR. These leftover calcium ions move around inside the sarcomere and may eventually find their way to a binding site on the thin filament's regulatory protein. Since the myosin head is already ready to bind, no additional ATP expenditure is required and the sarcomere contracts. When this process occurs on a larger scale, the disturbing twitches and gruesome postures associated with rigor mortis can occur.

Rigor mortis begins to manifest after about 3 hours after death, and lasts about 72 hours. It then disappears as proteolytic enzymes from lysosomes break down the crossbridges; that is the myosin heads detach from the actin filaments. This is known as resolution of rigor.

More specifically, what happens is that the membranes of muscle cells become more permeable to calcium ions. Living muscle cells expend energy to transport calcium ions to the outside of the cells. The calcium ions that flow into the muscle cells promote the cross-bridge attachment between actin and myosin, two types of fibers that work together in muscle contraction. The muscle fibers ratchet shorter and shorter until they are fully contracted or as long as the neurotransmitter acetylcholine and the energy molecule adenosine triphosphate (ATP) are present. However, muscles need ATP in order to release from a contracted state (it is used to pump the calcium out of the cells so the fibers can unlatch from each other). ATP reserves are quickly exhausted from the muscle contraction and other cellular processes. This means that the actin and myosin fibers will remain linked until the muscles themselves start to decompose.[1]

Rigor mortis and the meat industry

Rigor mortis is very important in meat technology. The onset of rigor mortis and its resolution partially determines the tenderness of meat. If the post-slaughter meat is immediately chilled to 15 °C, a phenomenon known as cold shortening occurs, where the muscle shrinks to a third of its original size. This will lead to the loss of water from the meat along with many of the vitamins, minerals, and water soluble proteins. The loss of water makes the meat hard and interferes with the manufacturing of several meat products like cutlet and sausage.

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 carcass, 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.

References

  • Neuroscience, Exploring the Brain 3rd ed. Bear, Connors and Paradiso

See also