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The development of pale, soft, and exudative (PSE) breast fillet meat has become an economic burden for the poultry industry worldwide. PSE meat results in 1.0-1.5% loss in moisture and carcass weight, and a 2010 estimate of the Brazilian annual production put the economic loss due to PSE at over US$30 million. In the USA, PSE has caused an annual loss of up to US$200 million to the poultry industries. The underlying causes of the color abnormality in PSE meat are not fully understood. However, the likely physiological origin of PSE broiler meat is an excessive release of Ca(2+) promoted by a genetic mutation of the ryanodine receptor (RYR), a Ca(2+)-channel protein in the skeletal muscle sarcoplasmic reticulum. In pigs, the genetic cause of PSE meat has been identified as a point mutation in the RYR1 gene at nucleotide 1843, which causes an amino acid substitution (Arg615 to Cys615) in the RYR. This mutation leads to an alteration in Ca(2+) homeostasis, hypermetabolism, intense muscle contraction, and malignant hyperthermia in pigs susceptible to porcine stress syndrome. An understanding of this process represents the basis for breeding strategies aimed at eliminating the RYR1 mutation from global pig populations, a strategy that the poultry industry intends to emulate. The aim of this study was to review the subject, with an emphasis on the most recent developments in the field.

Skeletal muscle calcium channel ryanodine and the development of pale, soft, and exudative meat in poultry