Pale, soft, exudative meat, or PSE meat, describes a carcass quality condition known to occur in pork, beef, and poultry. It is characterized by an abnormal color, consistency, and water holding capacity, making the meat dry and unattractive to consumers. The condition is believed to be caused by abnormal muscle metabolism following slaughter, due to an altered rate of glycolysis and a low pH within the muscle fibers. A mutation point in the ryanodine receptor gene (RYR1) in pork, associated to stress levels prior to slaughter are known to increase the incidence of PSE meat. Although the term "soft" may look positive, it refers to raw meat. When cooked, there is higher cook loss and the final product is hard, not juicy. The malignant hyperthermia (MH) or porcine stress syndrome (PSS) are the terms used to refer to the state pigs are found before slaughter, which will result in PSE. The other related defect is the dark, firm, dry (DFD) condition, or dark-cutter meat; it is also related to muscle glycogen metabolism and is the opposite result of PSE, i.e., it occurs if the post-mortem muscle pH is high.
Description Normally, calcium ions are used by the body to activate muscle cells, composed of myofibril. Ca2+ is transported out of the sarcoplasmic reticulum by ryanodine channels to the cytoplasm of muscle fibers/cells (called sarcoplasm), the process responsible for contractions of the myofibers. Under PSE conditions, twice the amount of Ca2+ can be released post-mortem, which causes excessive glycolysis and the buildup of lactic acid since the metabolism post-mortem is anaerobic. 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. The result is a pale tissue color, and a soft, almost mushy texture. The sarcomeres collapse excessively, and less water is held within the cell membrane and proteins. 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 functionality, important factor to create meaty products, such as sausages. Although the same ryanodine mutation found in pork was not found in poultry, differences in α-ryanodine and β-ryanodine were found. Avian species have lower quantities of the β isoform. This isoform of the channel is more reactive to Ca2+ accumulation, and once activated, remains opened for a longer period in which it is irresponsive, therefore, relatively higher number of α-channels pumps higher calcium ions to the sarcoplasm at a higher speed, contributing to pH lowering. For this similarity, PSE in other species than pork can be referred to as "PSE-like".
Predisposing factors
Stress Acute stress immediately prior to slaughter may result in the abnormal Ca2+ diffusion seen in PSE postmortem muscle. This in turn will induce the increase in glycolysis and cause the decline in pH. Stressful conditions may include handling, transportation, loading and unloading from a truck, mixing with unfamiliar animals and individuals, entering an unfamiliar facility, and stunning. It has also been suggested that excessive heat during summer months results in higher rates of poultry meat quality problems. Transport is one of the most critical moments before slaughter, taking up most of the time of the process, and the incidence of PSE is related to the position of birds in the truck and the design of the lorry/truck. For these reasons, animal welfare often correlates to the incidence of PSE meat or other carcass quality issues. The length of transport, time period between loading and unloading, and the rest time in lairage are known to affect meat quality. Physical activity and psychological stress associated with transportation, as well as incidence of fighting between individuals in lairage, can confound these factors. Hogs susceptible to porcine stress syndrome (PSS) commonly develop PSE meat postmortem.
Genetics In the swine industry, the RYR1 gene, which encodes the ryanodine receptor protein, RyR1, was found to influence the incidence of PSE meat conditions. Upon discovery, this gene was named the Halothane gene, Hal, because researchers noticed that pigs with this specific genotype developed PSE meat after being anesthetized with the halothane drug. The RyR1 protein is the channel responsible for controlling the Ca2+ release from the sarcoplasmic reticulum in skeletal muscle. A mutation found in this gene is likely responsible for the majority of PSE pork problems. However, the Hal gene is only responsible for about 25-35% of the PSE meat processed at abattoirs. Another gene, PRKAG3, commonly also known as the Rendement Napole (RN) gene, affects pork quality in a similar way but through a different mechanism. The RN- dominant allele increases the glycogen content of the muscle, resulting in lower ultimate pH, a phenomen known as 'acid meat' or the 'Hampshire effect'. The poultry industry is still currently trying to identify and eliminate genes that may be responsible for predisposing birds to PSE meat.
Potential solutions
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