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Post-mortem Changes in Meat
The pH Scale The preceding discussion has outlined the precursors to poor meat quality, viz.
· The possible presence of the Halothane gene · Stress on the individual animal, either acute or chronic
The presence of the Halothane gene is not essential to induce poor meat quality but if it is present then significant quality deterioration is almost certain.
To understand the post-mortem changes in meat one must understand the pH scale.
Figure 3: pH Scale
Distilled water is neither acidic nor alkaline and forms the neutral mid point of the scale. The living animal has a pH of about 7.4 and is slightly alkaline. If we taste our own blood we often say it is salty. Also shown on the scale above is the ultimate pH (pHu) that meat achieves at rigor-mortis. It can be seen that the tissue moves from alkaline (7.4) to acidic (6.2) after slaughter.
The key to the pH scale is that it is logarithmic, in other words pH 4 is ten times more acidic than pH5.
Glycolysis In the mammalian body we “burn” a complex sugar called glycogen to provide energy for our tissues to do any work. The process looks like:
On its breakdown journey glycogen forms lactic acid but this is quickly combined with oxygen to form carbon dioxide and water. The carbon dioxide is rapidly excreted through the lungs.
Figure 5: Anaerobic Glycolysis When an animal is slaughtered however the system changes. As the animal is exsanguinated (bled) there is no longer a blood stream to carry oxygen to the muscles. Glycogen is still broken down in the muscles by the reflex actions of the slaughtered animal but it can no longer get past the lactic acid stage. Eventually nearly all of the glycogen is used up and once this occurs the muscle no longer has an energy source to operate and locks up. We call this condition rigor-mortis, and, depending on temperature, this normally occurs at about 3 hours post-mortem.
The build up of lactic acid of the muscle lowers the pH (i.e. increases the acidity) to about 6.2 at rigor mortis.
When we experience cramp this is in fact a build up of lactic acid in our living muscle.
DFD Meat Where an animal has been exposed to prolonged stress such as heat, starvation or disease, its reserves of glycogen in both the liver and muscle have been depleted. If there are low glycogen levels to begin with then there will be low lactic acid levels at rigor-mortis.
We use lactic acid to preserve (i.e. prevent bacterial growth) yoghurt; we used acetic acid (i.e. vinegar) to do the same with meat and vegetables. The more acidic the environment the fewer bacteria are able to survive.
DFD is not unique to pork and can be seen in any type of red meat (e.g. “Dark Cutting” beef). It is not normally a huge problem in the New Zealand pork sector unless extremely hot conditions are encountered where the producer has not taken steps to cool his pigs.
PSE PSE is perhaps the most significant quality issue facing the pork sector and the understanding of the cause and solution to the problem has been the main thrust of the international meat community for the last decade. The US, Canada and EU have spent millions of dollars understanding the condition and it economic and buyer behaviour implications.
The figure below shows the classic picture of PSE in loin chops selected from a local retail outlet. The centre of the eye muscle is markedly paler than the muscle in the “tail” of the chop, the tissue has torn due to its softness and although the photo cannot show it, there will have been marked water loss from the tissue.
Figure 6: Classic Pale, Soft, Exudative Pork
Muscle is a complex organ that enables animals to move. The complex nature of each muscle fibre is beyond the scope of this document but down at the microscopic functional level the molecules act as a ratchet.
Figure 7: The Actin-Myosin Ratchet of Muscle
As the myosin heads ratchet through, they pull the actin rod along with them. As both ends are attached to the walls of the muscle fibre this has the effect of shrinking the fibre. When millions of fibres shrink simultaneously then the whole muscle contacts. Energy is required for the ratchet action of the myosin and also to release the ratchet – so when they no longer release we have a state of post-mortem rigor-mortis.
In the case of PSS animals, they have arrived at slaughter in a stressed condition bought about by herding, transport, strange environment and strange animals. Their muscle glycogen levels are very high as is their lactic acid content. As soon as these animals are slaughtered the lactic acid production is kept high, building up in the muscle while the carcass is still hot (42-44oC).
In a normal carcass there is some shrinkage of the individual muscle fibres by virtue of the actin-myosin contraction. In a PSE carcass the rapid pH fall while the carcass is still hot causes a breakdown of the myosin heads allowing the myosin and actin strands to compress even closer together.
Figure 8: Excess shrinkage in a cross section of a myofibril after myosin head degeneration
The result is:
· The increased density of the actin and myosin leads to a greater degree of reflection of light - PALENESS
· The water forced out of the myofibril accumulates between the myofibrils tearing the connective tissue – SOFTNESS
· As the muscles are cut during the normal breakdown of the carcass to retail cuts there is excessive loss of water from between the myofibrils – EXUDATION
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