Description
Normally, calcium ions are used by the body to activate muscles, composed of myofibril cells. Ca2+ is transported out of the sarcoplasmic reticulum surrounding muscle fiber cells, and leads to metabolism and contractions of the myofibers. Under PSE conditions, twice the amount of Ca2+ is released post-mortem, which causes excessive muscle glycolysis, and the buildup of lactic acid. This lactate accumulates in the postmortem muscle, and leads to a very low pH.
As the pH drops, proteins in the myofibers are denatured, leading to abnormal cell structure and function. The result is a pale tissue color, and a soft, almost mushy texture. The muscle cells shrink, and less water is held within the cell membrane. Subsequently, the myofibers will continue to lose water content as the meat is cooled and stored, leading to excessive drip loss.
Pigs susceptible to porcine stress syndrome, or PSS, have an increased likelihood of developing PSE meat. These animals become easily stressed pre-slaughter, which leads to exaggerated glycolysis, an increase in body temperature, and higher production of lactic acid. In particular, the Halothane gene, Hal, induces PSS in swine. It is a single point mutation in this gene that causes abnormal calcium channels within the muscle. Hal+ pigs are five times more likely to develop PSE meat than Hal- hogs.
The incidence of PSE in poultry meat is believed to have increased over the past several decades because of the incredible advancements in growth rates. Intense breeding selection for breast size and feed efficiency is likely responsible for the increase in meat quality issues. Conditions behind the PSE poultry meat are believed to be the same as observed in pork; higher rates of glycolysis postmortem lead to a sudden pH drop, which in turn causes protein denaturation and a loss of function.
Read more about this topic: PSE Meat
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