Abstract
Pale, soft, and exudative (PSE) pork is primarily caused by an accelerated rate of postmortem glycolysis resulting in low muscle pH while carcass temperature remains high, thus causing protein denaturation. Numerous factors influence the rate of postmortem metabolism and may be responsible for the rapid pH decline characteristic of PSE pork during the 1st h postmortem. Release of high levels of Ca 2+ from the sarcoplasmic reticulum into the sarcoplasm triggers an accelerated rate of postmortem glycolysis and is responsible for the high incidence of PSE observed in halothane pigs. Because total muscle ATPase activity is closely associated with rate of glycolysis, differences in myosin ATPase activity may explain in part the accelerated glycolysis in PSE development. Although important in determining the overall rate of glycolysis, differences in glycolytic enzyme activities have failed to explain discrepancies in postmortem metabolism between PSE and normal muscle. Elevated muscle glycogen content and an extended duration of postmortem glycolysis can also result in PSE-like characteristics, as seen in RN – pigs. Shifts in muscle fiber type toward higher proportions of glycolytic fibers may help explain the incidence of PSE. Inherent differences in mATPase activity, Ca 2+ regulation, glycolytic enzyme profiles, and glycogen content between muscle fiber types integrate various mechanisms responsible for the abnormal postmortem glycolysis in PSE muscle. In an effort to delineate potential mechanisms responsible for PSE, models to artificially induce PSE, such as retarding temperature decline and electrical stimulation, provide useful tools. The value and limitations of these models stem from their abilities to alter postmortem temperature and pH declines and to effectively simulate the protein denaturation typical of PSE pork.
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