Rigor mortis is Latin for "stiffness of death". It is used medically to describe the stiffness of skeletal muscles that appears soon after death. Fully developed rigor mortis in muscle is characterized by maximum loss of extensibility. Regor mortis can be classified in to three phases, the first phase, when a well-marked rigidity was established in the muscles, the second phase, when the complete rigidity was established and the third phase, where the rigor begin to pass off. Cold-shortening occurs when muscles are exposed to low temperatures (below 10 °C to 15 °C) early post mortem, when ATP and pH levels are still high (pH above 6.2). On the other hand, rigor tension occurs much later and at any temperature between 0 ºC and 37 ºC, reaching maximum values when ATP levels have been depleted and pH is at a minimum value. Cold shortening decreases tenderness which is due to muscle fiber contractions that occur before the onset of rigor. Different carcasses in the same chiller can undergo cold shortening that deteriorate the tenderness of meat. Toughening due to cold shortening cannot be eliminated by aging of meat. A thumb rule to avoid cold shortening is that the temperature of the muscle should be kept high i-e above 10ºC till the pH of meat which is initially 7.0-7.2 at the time of death falls below 6.0.
TABLE OF CONTENTS
EXCUTIVE SUMMERY
1. INTRODUCTION
2. LITRATURE REVIEW
2.1. Rigor Mortis In Meat
2.1.1. Delay Period
2.1.2. Onset of Rigor
2.1.3. Rigor (Irreversible phase)
2.1.4. Resolution of Rigor Mortis
2.2. Effects of Rigor Mortis on Appearance
2.3. Effects of Thaw Rigor on Tenderness
2.4. Cold Shortening In Meat
2.4.1. Effects of cold shortening on tenderness
3. REFERENCES
EXCUTIVE SUMMERY
Rigor mortis is Latin for "stiffness of death". It is used medically to describe the stiffness of skeletal muscles that appears soon after death. Fully developed rigor mortis in muscle is characterized by maximum loss of extensibility. Regor mortis can be classified in to three phases, the first phase, when a well-marked rigidity was established in the muscles, the second phase, when the complete rigidity was established and the third phase, where the rigor begin to pass off. Cold-shortening occurs when muscles are exposed to low temperatures (below 10 °C to 15 °C) early post mortem, when ATP and pH levels are still high (pH above 6.2). On the other hand, rigor tension occurs much later and at any temperature between 0 ºC and 37 ºC, reaching maximum values when ATP levels have been depleted and pH is at a minimum value. Cold shortening decreases tenderness which is due to muscle fiber contractions that occur before the onset of rigor. Different carcasses in the same chiller can undergo cold shortening that deteriorate the tenderness of meat. Toughening due to cold shortening cannot be eliminated by aging of meat. A thumb rule to avoid cold shortening is that the temperature of the muscle should be kept high i-e above 10ºC till the pH of meat which is initially 7.0-7.2 at the time of death falls below 6.0.
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1. INTRODUCTION
At the time of slaughter the muscles of the animal are predominantly metabolizing aerobically (generating energy through biochemical pathways that consume oxygen). At the time of exsanguination (bleeding out) the blood supply to the muscles ceases. This means that the oxygen supply is cut off and the products of metabolism in the muscle cannot be removed via the bloodstream. These therefore accumulate in the muscle. The normal response of tissues to oxygen deprivation is to attempt to maintain cellular energy (ATP) levels. Tissues with a high oxygen requirement, such as the brain, will die very quickly, but some other tissues, particularly muscle, can have a high anaerobic capacity. This means that they are capable of producing ATP from glucose without the need for oxygen (glycolysis). One of the products of this anaerobic metabolism is lactic acid. This accumulates in the tissue and gradually reduces the pH of the muscle from about 7.2 in a normal resting live muscle to an ultimate pH (pHu) of about 5.4 to 5.7 in normal meat. Muscle can generate energy from glucose until all the glucose is used up or until the accumulation of acid in the muscle destroys the metabolic processes (Board, 2011). Rigor mortis is Latin for "stiffness of death". It is used medically to describe the stiffness of skeletal muscles that appears soon after death (Abdou, 2001). This ability to generate energy even after slaughter means that muscle can continue to contract, for example in response to an external electrical stimulation (ES), for a considerable time after the animal’s central nervous system is dead. When all of the available energy is exhausted in the post mortem muscle the myosin and actin molecules bind firmly together and the muscle loses its extensibility and flexibility. This point is termed rigor mortis (Board, 2011). During the development of rigor mortis muscles become inextensible due to the sum of each muscle fiber going into full rigor, with irreversible cross-bridge formation (actomyosin) of the contractile components, actin and myosin (Hwang et al., 2003; Botha, Hoffman and Britz, 2008). The rigor process involves first a delay period, when the level of ATP (adenosine triphosphate) is constant, CP (creatine phosphate) is decreasing rapidly, and there is a slow production of lactate and no onset of rigor development. This is followed by a rapid phase when CP is low enough to initiate a rapid decline in ATP concentration, which is accompanied by a decreasing extensibility of the muscle due to irreversible cross-bridge formation of actin and myosin (Bendall, 1973). Shortening of muscles occurs before the onset of rigor mortis since contraction requires a minimum ATP concentration and an increased level of Ca2+ ions around the myofibrils (Honikel et al., 1983; Botha, Hoffman and Britz, 2008). A consequence of ATP disappearance in postmortem muscle is the development of rigor mortis. Rigor mortis develops due to the formation of irreversible cross bridges between myosin and actin by a similar reaction that forms actomyosin during muscle contraction (Haard 1992; Adebisi & Virginia, 2012).
Cold-shortening occurs when muscles are exposed to low temperatures (below 10 °C to 15 °C) early post mortem, when ATP and pH levels are still high (pH above 6.2). On the other hand, rigor tension occurs much later and at any temperature between 0 ºC and 37 ºC, reaching maximum values when ATP levels have been depleted and pH is at a minimum value. The stiffness characteristic of rigor mortis is then maintained by continuous tension exerted by the cross-bridges between myosin and actin filaments (Botha, Hoffman and Britz, 2008). In both pork and beef a muscle shortening is a major determinant of tenderness when the tissue has not yet entered rigor mortis and when the rate of muscle pH decline is rapid. Knowledge of the course of rigor mortis and post mortem pH changes, as well as the influence of temperature, on the onset of rigor mortis, might help to reduce purge and initial toughness (Botha, Hoffman and Britz, 2008). Muscle will contract (shorten) naturally as it goes into rigor mortis if it is not restrained from doing so. Most muscles are under tension when the skeleton of the carcass is in its normal posture. If muscle is restrained it will develop tension as it goes into rigor but will not be able to shorten in its overall length. The extent to which muscles are able to shorten depends on the remaining energy (ATP) available at the time of shortening, the load on the muscle and the temperature of the muscle when these events occur. A shortened muscle will have shorter sarcomere lengths, ie shorter repeating units within the contractile myofibrils and a greater overlap between the contractile filaments (Board, 2011).The aim of this study was therefore to review rigor mortis and cold shortening in meat.
2. LITRATURE REVIEW
2.1. Rigor Mortis in Meat
Regor mortis can be classified in to three phases, the first phase, when a well-marked rigidity was established in the muscles, the second phase, when the complete rigidity was established and the third phase, where the rigor begin to pass off (Abdou, 2001). Rigor mortis course and sequences was as the same in the all cadaver with only few differences were showed despite of the cause of death. Rigor mortis was began in all muscles of the cadaver (voluntary & involuntary) after death but it first noticed in the lower lip (depressor labiimandibularis) followed by the upper lip (levator labiimaxillaris) and in the small muscles of the eyelids followed by the jaw muscles, first in the lower mandible and in the cheek muscles (massetter muscle) (Abdou, 2001) . The temperature effect on the ability to shorten during rigor is particularly interesting, with the extent of beef muscle shortening varying with temperature at which rigor occurred according to the sequence 1 > 37 > 5 > 20 °C. From this and similar observations, the notion emerged that there were two types of shortening and that for minimum shortening muscle should be at about 15°C as it enters rigor mortis. This can never be achieved in practice for all muscle fibres because of the different rates of cooling in different locations of the carcass and the different rates of rigor development in different fibres. It is however a useful guideline. The shortening that occurs with rigor above 20°C occurs as the energy supply is being exhausted and it is, therefore, generally quite weak. This form of rigor shortening is sometimes termed ‘hot’ shortening. It does have the potential to affect meat quality but its importance is still debated. ‘Cold’ shortening is quite different. It occurs if the muscle is exposed to low temperature prior to the development of rigor. Under these conditions the muscle spontaneously contracts and, since it does so at higher levels of ATP and pH than rigor shortening, the degree of contraction can be considerable (Board, 2011). The sarcoplasmic ATPase become hyperactive and ultimately ATP are degraded. With progressive decomposition and disappearance of ATP from muscle due to dephosphorylation and deamination down to critical level, overlapping arrays of actin and myosin filaments combining as rigid links action myosin, forms viscous, inextensible dehydrated stiff gel like state which accounts for the rigidity and stiffness of muscle in rigor mortis, when the muscle do not respond to electrical or any other stimulus. Thus this irresponsive stiff rigid contracted state of body musculature constitutes the rigor mortis. With this explanation, it is easy to understand the mechanism of development of cadaveric rigidity, which unfolds in four different phases (Kori, 2018).
2.1.1. Delay Period
The delay period prior to rigor onset is the first stage of postmortem changes. This period is called the pre-rigor period or lag period. The time lag from death to onset of rigor mortis is called “Lag of initiation” (Adebisi & Virginia, 2012). After clinical death, the muscles survives in a normal state for a short time and relaxed as long as the ATP content remains sufficient enough to permit the splitting of actin-myosin cross-bridges. Here decrease in ATP levels was matched by an increase in the hardness. The rate of ATP depletion depends on its contents at time of death, on the possibility of postmortem ATP production and the rate of ATP hydrolysis (Kori, 2018).
2.1.2. Onset of Rigor
Rigor mortis is the first postmortem process that has a major effect on the appearance and structure of muscle. When creatine phosphate and ATP reach the same concentration, ATP content begins to decrease resulting in the stiffness of muscle (Watabe and others 1991) and muscle enters full rigor mortis (Iwamoto and others 1987). The onset of rigor mortis occurs when ATP content of the muscle drops below a critical level. Rigor mortis occurs upon depletion of ATP in the muscle to the point where cross-bridge cycling between actin and myosin filaments stop, and therefore, detachment of the filaments is halted (Adebisi & Virginia, 2012) . The ATP content of the muscles falls below a critical threshold. The cross bridges remain intact and rigidity appears. However, this state is still reversible. The addition of ATP or oxygen results in a relaxation, indicating that the muscle is still able to function (Kori, 2018).
2.1.3. Rigor (Irreversible phase)
Is also known as 3rd phase. Rigidity is fully developed and become irreversible. Postmortem modifications of muscle fiber destroy their ability to relax (Kori, 2018).
2.1.4. Resolution of Rigor Mortis
During the resolution of rigor mortis muscle gradually loses its stiffness and softens. Softening continues until fillet firmness returns to its original level or becomes softer. Rigor mortis is said to be completely resolved when fish tissue softness reaches the original level. Gradual muscle softening continues unabated even after termination of rigor mortis, resulting in muscle softness beyond the original level (Adebisi & Virginia, 2012). 4th phase: Rigidity disappears and the muscles become limp (Kori, 2018).
2.2. Effects of Rigor Mortis on Appearance
Meat palatability is affected by rigor mortis however there is no way by which the whole process of onset and resolution of rigor mortis can be explored. It has been confirmed that ambient temperature effect the process of rigor mortis and struggle at the time of slaughter can also accelerate the process of rigor (Li et al., 2010; Saleem and Majeed, 2014).
If meat freezes before the onset of rigor then a very large amount of drip is lost at thawing which is called thaw rigor (Warriss, 2000). If meat is frozen before the onset of rigor it exhibits thaw rigor that makes its texture very hard when thawed. Thaw rigor suppression is very important as large amount of drip loss and stiffness of muscles decreases the commercial value of meat (Imamura et al., 2012) so, temperature and thawing process must be controlled to avoid thaw rigor (Cook et al., 2009). Lowering of temperature during storage suppresses thaw rigor but can lead to changes in meat color from red to brown due to formation of metmyoglobin that is oxidized form of ferric or hemin. Therefore thawing and freezing should be optimized for preventing thaw rigor and metmyoglobin formation in meat. A temperature shift technique that prevents thaw-rigor and metmyoglobin formation is storage before thawing at -7ºC and -10ºC for 1 day and 7 days respectively (Imamura et al., 2012).
2.3. Effects of Thaw Rigor on Tenderness
The organoleptic trait that effects consumer’s satisfaction is tenderness. Due to thaw rigor development toughening of meat can occur because of sarcomere shortening. Thawed meat is less tender than non-frozen meat, but freezing is the most common method used for meat storage. Microbiological spoilage of meat is demolished by freezing, but fluctuations in temperature during transportation, storage (Xia et al., 2009) and repeated thaw freeze cycles can cause alterations in the tenderness of meat quality that causes financial concerns to the industry (Qi et al., 2012).
Cutting and deboning of meat in slaughtering plants has to be done quickly due to economic and hygienic conditions (Thielke et al., 2005). When muscles are frozen pre-rigor, upon thawing a very severe form of rigor takes place and if thawing is done rapidly meat can suffer from defects due to high temperature. It has been suggested that immediate freezing of carcass after slaughter and then storing it at a temperature below freezing point prevents toughness and thaw rigor development. Moreover tenderness of thaw rigor muscle can be increased by increasing the holding time at -3ºC (Yu et al., 2005)
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- Quote paper
- Tajudin Denur (Author), 2020, "Regor mortis" as "Stiffness of Death" and the Cold Shorting in Meat, Munich, GRIN Verlag, https://www.grin.com/document/982807
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