POST-SLAUGHTER CHANGES IN CARCASS AND CARCASS EVALUATION

1. POST-SLAUGHTER CHANGES IN CARCASS AND CARCASS EVALUATION Meat and Slaughter By-Products Technology

2. The major change which occur in the animal after slaughter is RIGOR MORTIS. RIGOR MORTIS ▪ The rigor mortis is a permanent contraction of all the skeletal muscles after death beginning from muscles of head and neck and appearing gradually over the whole body. ▪ It is accompanied with stiffening of joints and rise of temperature by 3 °F. This state of stiffening after death is called rigor mortis.

3. Rigor Mortis • The muscles are soft when the animal is slaughtered. • After death a series of highly complicated chemico-physical changes takes place in the body which end up in stiffening or rigor mortis. • The basis of rigor mortis is the muscle protein “Actomyosin” which is a complex of • Actin and Myosin.

4. Rigor Mortis • The precise manner in which myosin and actin molecules react to cause contraction is not known. • But it is believed that contraction is caused by sliding of the chain of actin molecules with the chain of myosin molecules.

5. Rigor Mortis The break down of actomyosin into its component parts actin and myosin does not take place. And the changes which occur in the meat after death favour this process.

6. The sequence of changes are as under. 1- Immediately after death of animal, adenosine triphosphate (ATP) is broken down to ADP by enzyme ATPase of myosin. This forms the onset of rigor mortis. 2- Because of the presence of oxygen in the tissues on account of recent death, the regeneration of ATP remains continue. Hence no stiffening is seen in the initial time after death.

7. 3- The interruption of blood circulation through the muscle now reduces the ability of muscle to maintain aerobic oxidation of lactic acid and removal of CO2 . 4- Anaerobic metabolism takes over and accumulation of lactic acid concentration is seen at the height of rigor mortis which is almost ten times more than in the living condition of the animal.

9. In living conditions, the muscle is alkaline or neutral but it turns acidic in 3- 6 hours after death. • Concentration of lactic acid reduces the pH of muscle at 5.6 to 5.3. • The decrease in pH retards anaerobic metabolism because the enzymes involved are no longer at their optimum pH for activity.

10. 7- Because of the residual metabolism of the muscle, the concentration of ATP continues decreasing and leading to gradual hardening of the muscle until it becomes quite stiff and dull in appearance.

11. Post-mortem Acidification and Rigor Development • At the death of the animal the supply of oxygen and glucose and free fatty acids to the muscles ceases when the blood circulatory system fails. Any subsequent metabolism must be anaerobic and ATP can only be regenerated through breakdown of glycogen by glycolysis since oxidative phosphorylation will no longer operate

12. As glycogen is broken down so lactic acid accumulates. Because this is not removed by the blood system the muscle gradually acidifies. • The process of acidification normally takes 2–24 h in sheep and 15–36 h in cattle. • In poultry meat the initial pH fall may be relatively rapidly.

13. . For example, in turkeys the pH in the breast muscle can have fallen to 6 by 10–15 min post mortem.

14. Importance of acidification to the characteristics of meat • The muscle proteins tend to denature as the pH falls. This leads to a reduction in their power to bind water. Also, the myofibrillar proteins, myosin and actin, reach their isoelectric point. • This is the pH at which the protein molecules have no net electrical charge and tend to lose the water that is normally bound to them.

15. Both these phenomena lead to exudation of fluid from the muscle fibres. When the meat is cut the fluid also exudes onto the cut surface, which becomes moist. Eventually this exudate may produce drip, which can collect in the meat container or be lost, leading to weight loss.

17. The development of rigor mortis • In a resting muscle, ATP serves to keep the muscle in a relaxed state by preventing the formation of actomyosin. • Only when ATP is hydrolysed to ADP does contraction occur. • The ATP concentration is maintained by the breakdown of glycogen until lack of substrate or unsuitability of conditions e.g. low PH which inhibit glycolysis

18. Rigor mortis occurs when the ATP level falls below the very low level. • When this happens, the actin and myosin molecules of the thin and thick filaments combine irreversibly to form actomyosin and extensibility of the muscle is lost.

19. Cross-bridges form permanently and there is very weak contraction. Each muscle fiber goes into rigor very quickly once ATP is depleted, but the variation between individual fibers leads to a more gradual development of stiffness in the whole muscle as more and more fibers become inextensible.

20. ALKALINE RIGOR • Rigor onset is determined only by the availability of ATP, not the pH value of the muscle. It is possible to have rigor in muscle in which the pH is still high if the animal has been exhausted preslaughter. This has been referred to as alkaline rigor.

21. The meat in early rigor, if cooked, is found tough, but if it is kept in a cooler condition for a few days, it will gradually begin to soften again. This period is called “AGEING”. some autolytic changes appear to play role in softening the meat. Lactic acid also tenderizes meat by converting collagen to gelatin.

22. Tenderization results from the activities of proteolytic enzymes present in the muscles. Their normal role is in the breakdown and recycling of proteins which occurs continuously in all living tissues. • There are two main sorts of enzyme involved, cathepsins and calpains.

23. They are known to degrade some collagen cross-links and mucopolysaccharides of the connective tissue ground substance.

25. The duration of rigor mortis is extremely variable. It starts appearing in 7-12 hours and reaches to its peak in 20-24 hours and then starts declining gradually. The earlier it appears, the sooner it passes away and vice versa.

26. Factors Affecting Rigor Mortis 1. Muscular activity: Any exertion before slaughter depletes the glycogen content of the meat thus affecting the onset of rigor mortis. The appearance of rigor mortis is inversely related to the glycogen content of the muscles. The lesser is the glycogen, the quicker and short is the rigor mortis.

27. Hence there will be no or even lesser the rigor mortis in fatigued or exhausted animals. 2. High atmospheric temperature: The onset of rigor mortis is accelerated by high atmospheric temperature and retarded by low temperature.

28. 3. Health condition: Rigor mortis dose not properly develop in sick and debilitated animal. It may be absent or minutely present in the carcass of animals that have suffered from, ♦ Severe febrile conditions ♦ Septic infection & ♦ Emaciation

29. Importance of rigor mortis Great importance must be attached to rigor mortis in meat inspection because it is criterion for judging the quality of meat. Lack of rigor mortis means that the animal was suffering from one or the more of the following conditions/diseases: Fatigue, Exhaustion, Debility Septicemia or Toxemia

30. A carcass showing a lack of rigor mortis due to fatigue may be passed but do not pass carcass, that fail to set rigor mortis otherwise. This might be due to diseased animal. And its meat may contain harmful bacteria or toxins which may cause meat poisoning. The development of acid during rigor mortis retards the growth and multiplication of putrefactive bacteria.

31. Hence it enhances the durability or the keeping quality of the meat. Lack of rigor mortis is an indicative of poor keeping quality of meat.

32. The development of rigor mortis (acid) tenderizes the meat by converting collagen to gelatin. It also improves the flavour of the meat . Full rigor mortis signifies healthy and good quality meat. The very early rigor mortis is an indication for the onset of putrefaction process.

33. Why incomplete rigor mortis in Anthrax?

34. Anthrax - Pathogenesis • Bacillus anthracis, a gram positive bacterium, is the causative agent of anthrax. This organism is capsulogen and toxinogenic. It secretes two toxins which are composed of three proteins: • protective antigen (PA), • lethal factor (LF) • edema factor (EF). • The lethal toxin (PA+LF) provokes a death in animals • edema toxin (PA+EF) induces edema. • The edema and the lethal factors are internalised into the eukaryotic target cells via the protective antigen. • http://www.sciencedirect.com/science/article/pii/S0041010101001611 • Virulence of B. anthracis derives from presence of poly-D-glutamic acid capsule and complex toxin.

35. Anthrax - Pathogenesis • Oedema factor is a calmodulin dependent adenylate cyclase and once inside cells following binding to PA increases cAMP causing the build up of fluid in tissue (tissue swells as seen in clinical disease) • Oedema factor also inhibits neutrophil function, could be leukocidal • LF stimulates macrophages to release cytokines IL-1 beta and TNF alpha. • LF also not allow the Zn to bind with Kinases this effects signaling pathway and ultimately cause apoptosis • Local effects are swelling, darkening of tissue, oedema and necrosis.