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Understanding Rigor Mortis: The Process of Muscle Stiffening After Death, Exercises of Forensics

An in-depth explanation of rigor mortis, a post-mortem physiological process that causes muscles to stiffen and become inextensible. the causes, mechanisms, and characteristics of rigor mortis, as well as its classification and factors affecting its onset. It also discusses the phenomena of cold shortening and thaw rigor, which can affect meat quality.

Typology: Exercises

2021/2022

Uploaded on 09/12/2022

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Bhavana Gupta
Assistant Professor
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RIGOR MORTIES
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Download Understanding Rigor Mortis: The Process of Muscle Stiffening After Death and more Exercises Forensics in PDF only on Docsity!

Bhavana Gupta Assistant Professor 1

RIGOR MORTIES

Rigor mortis- Muscle - Meat CONVERSION involves a series of complex physico-chemical changes.The first and most important change that occurs in muscles is- rigor mortis. Proteins form the most important solid constituent and consist of myofibrillar, sarcoplasmic and connective tissue proteins. About two-thirds of the proteins are myofibrillar,most important types being actin and myosin which form actomyosin complex after rigor mortis and give rigidity to the muscles. Troponin A, B and T, and tropomyosin are the other proteins present in variable quantities. Sarcoplasmic proteins which are water soluble include myoglobin, haemoglobin and some glycolytic enzymes.

Process of rigor mortis

  1. After death/slaughter of an animal, blood supply of the muscles ceases leading to severe deficiency of oxygen, energy and vital elements essential for cellular activity and an anaerobic environment in the muscles is created.
  2. During normal glycolysis in presence of oxygen through a series of biochemical changes, the muscle glycogen is converted into adenosine triphosphate (ATP), carbon dioxide and water. However, absence of oxygen favours anaerobic glycolysis and due to action of lactic dehydrogenase glycogen is converted into lactic acid thereby causing drastic reduction in ATP production.
  1. The lactic acid formed during the glycolysis goes on accumulating and lowering the pH of muscles. The pH begins to decline from about
  2. 0 till 5. 3 to 5. 5. With reduction in pH, ATP content of the muscle starts declining from its pre-rigor concentration of 5. 9 micromoles/gm at pH 7. 0 - 7. 2 to near zero at pH 5. 3 - 5. 5.
  1. Ca++ gets bound to troponin and causes conformational changes in the tropomyosin resulting into release of the Mg++ activated ATPase enzyme
  2. Due to action of this ATPase enzyme, ATP at actin- combining site on myosin and ATP at myosin combining site on actin are hydrolysed. As a result, myosin and actin interact together to form cross-linkage as actomyosin complex which cannot be dissociated. This actomyosin complex results in inextensibility and toughening of the muscles making them rigid and noncontractile

. This rigidity and toughening to the muscles is termed as rigor mortis. The loss of extensibility due to actomyosin formation proceeds slowly at first (the delay period), then with rapidity (the fast phase) after which it remains at a low level. The onset of rigor mortis is accompanied by lowering of water holding capacity of muscles.

The onset patterns of rigor mortis can be classified as acid rigor which is characterised (in immobilised animals) by a long delay period and a short fast phase and in struggling animals by a drastic curtailment of the delay period; alkaline rigor which is characterised by a rapid onset of stiffening and by marked shortening of muscles; and intermediate rigor characterised (in starved animals) by a curtailment of the delay period but not of the rapid phase.

  • Rigor mortis starts from muscles of head and neck and then extends to rest of the body and finally the legs. In healthy animals it starts after 9 - 12 hours of slaughter, stays for 20 - 24 hours and then passes off.
  • After 20 - 24 hours, the rigidity of the muscles cannot be maintained due to lowering of ATP concentration since it is also required to maintain the stromal integrity of the proteins.
  • Besides, lowering of pH by lactic acid denatures the proteins that are attacked by proteases and cathepsins of muscles. These all complex activities ultimately increase the pH of meat which results in enhancing impermeability of sarcoplasmic reticulum to Ca++ ions.

The heart, however, is affected very early in the process

  • normally within an hour of slaughter. Factors affecting rigor mortis. - Species of animal. - Type of muscle - Amount of glycogen - Initial level of ATP and creatinine phosphate

Intrinsic

factors

  • Atmospheric temperature
  • Health and condition of an animal
  • Administration of drugs-drugs such as sodium salicylate, alcohol and ether tend to encourage the early onset of rigor mortis.

Extrinsic

factors

Affections induced in meat during rigor mortis. (a) Cold shortening. Cold shortening is described as the excessive shortening that occurs in muscles during glycolysis when the temperature of carcass is maintained in the range of 0 - 10 °C pre-rigor. Exposure of meat to low temperatures immediately after slaughter results in excessive contraction of muscles (may be up to 40 %) thereby resulting in pronounced increase in the toughness of meat. This change usually occurs in more active muscles of legs. Muscles having incomplete development of acidity (pH usually more than 6. 7 ) and high ATP levels are more prone to cold shortening.

b) Thaw rigor / Freezing shortening - This phenomenon results when the muscle is frozen pre-rigor and subsequently thawed. Massive contractions of muscles occur (up to a 50 % of its initial length) when frozen and which upon thawing release substantial amount of drip resulting in tough muscles. Fine crystals of ice formed inside the cells break the sarcoplasmic reticulum resulting in an abundant release of Ca++ on thawing. Increased concentration of Ca++ produces toughness in muscles on thawing.