Pale Soft Exudative Pse And Porcine Stress Syndrome Pss In Pigs

An unusual condition occurs in pig muscle postmortem that is referred to as PSE.[5] The muscle is pale in color, soft in texture, and may exude as much as 10% of the muscle weight in liquid (also called drip) (Fig. 2). The condition is genetic in nature and has been linked to a recessive mutation in the ryanodine receptor.[6] The latter is a protein that serves as a calcium channel in the sarcoplasmic reticulum. In normal muscle, this channel releases calcium to activate muscle contraction. However, the mutant protein leaks calcium and thus partially activates the contractile system. Such activation dramatically increases the postmortem ATP splitting and the rate of glycolysis. Muscle pH drops rapidly while the temperature is still high, and this pH temperature combination denatures the myosin, resulting in decreased muscle water binding. The extent of this glycolysis acceleration is highly variable, being affected by numerous antemortem conditions including ambient temperature, climatic change, and stress.[7] The incidence of the PSE condition has remained at about 10 15% of the pig population for many years. Animals with the mutant gene are often leaner and more heavily muscled, so visual breed stock selection has worked against eliminating the mutation. A similar condition occurs in humans and is called ''malignant hyperthermia.'' The name is actually a misnomer; it is unrelated to cancer. Humans containing a ryanodine receptor mutation respond to anesthesia by developing muscle rigidity and extreme increases in body temperature, often leading to death unless the condition can be stopped by drug intervention. More than 20 different ryanodine receptor mutations have been found in humans; it seems fairly likely that additional pig mutations will also be identified in the future.

Porcine stress syndrome is caused by the same ryanodine receptor mutation found in PSE, but occurs in postmortem glycolysis is normal, but the final or ultimate pH in the longissimus muscle is often around 5.3 5.4 instead of the more typical 5.5 to 5.6. This phenotype results from a dominant mutation termed RN-. The letters are an abbreviation for Rendement (French for yield) Napole (name of a test for ham processing yield). The condition is also referred to as ''acid meat'' and the ''Hampshire effect'' since the mutation is prevalent in the Hampshire breed. The lower ultimate pH, along with a lower protein content, causes the water-holding capacity of the meat to be diminished and the processed ham yield to be reduced. Carriers were formerly identified by measuring the ''glycolytic potential'' (the sum of the lactic acid concentration plus 2 x [glycogen glucose+glucose+glucose-6 phosphate content]).[9] Since muscle is a closed system postmortem, the time of sampling after death will not affect the glycolytic potential. Glycolytic potential values are typically around 125 mM/gram in normal muscle, but often range from 180 300 mM/gram in animals with the mutation. The RN- locus is on chromosome 15 in the region coding for the gamma


Fig. 1 Carcass from a double muscled steer. Note the bulging muscles and the minimal external fat covering. (Photograph courtesy of Morse Solomon, United States Department of Agriculture, Beltsville, Maryland.) (View this art in color at

the live animal. PSS pigs under stress may show muscle tremors and rigidity, skin splotchiness, and increased body temperature. In many cases, these conditions will lead to death. Even the stress of loading the animals on a truck to transport them to market may be fatal.

Testing for carriers of the ryanodine receptor mutation was formerly conducted using a challenge with the Pale, Soft Exudative anesthetic halothane; carriers would show muscle tremors and rigidity. A genetic test now is available for the single pig ryanodine receptor mutation identified to date; however, some pigs develop PSE meat in spite of having a normal genetic result.

Some turkeys and chickens also have accelerated postmortem glycolysis that has been termed a PSE-like condition. It is not currently known whether a ryanodine receptor mutation is the causative agent.


Norwegian Double Muscle Steer

Fig. 1 Carcass from a double muscled steer. Note the bulging muscles and the minimal external fat covering. (Photograph courtesy of Morse Solomon, United States Department of Agriculture, Beltsville, Maryland.) (View this art in color at


Fig. 2 Loin chops from a normal and a pale, soft, exudative (PSE) pig. Note that the PSE condition does not affect all muscles equally. (View this art in color at

Certain pigs have unusually high glycogen levels in their muscle at the time of death.[8] The time course of

Fig. 2 Loin chops from a normal and a pale, soft, exudative (PSE) pig. Note that the PSE condition does not affect all muscles equally. (View this art in color at"/>
Fig. 3 Carcasses from normal (L) and callipyge (R) lambs. The extreme muscularity of the hind legs is evident. (Photograph courtesy of Sam Taylor, Texas Tech University.) (View this art in color at

subunit of a muscle-specific adenosine-monophosphate-activated protein kinase PRKAG3.[10] This kinase normally inactivates glycogen synthase, but this inactivation does not occur in the mutant animals.

Meat from RN carriers has greater cooking loss and is inferior for use in processed meat products. However, this type of meat is more tender than normal pork.


An unusual genetic condition in sheep results in animals with hypertrophied muscles primarily in their hindquarters. The word callipyge was derived from the Greek calli = beautiful and pyge = buttocks. The phenotypic trait only appears after the lambs are 4 to 6 weeks of age. The callipyge condition is transmitted by a remarkable inheritance mode called polar overdominance, where only heterozygous offspring from carrier males express the phenotype. The mutation locus appears to be a single A- to -G replacement on chromosome 18.[11] Callipyge carcasses have increased muscle content and reduced fat levels.[12] A picture showing a comparison of a normal and callipyge lamb carcass is shown in Fig. 3. Unfortunately, muscles from these animals also have reduced tenderness. Increased calpastatin content has been linked to the tenderness problem.[13]


The influence of genetics on meat quality will continue to be an important area of research. The rapid progress toward sequencing the genomic DNA from the agricultural animal species will speed the identification of new factors affecting muscle foods.


1. Johnson, D.D.; Huffman, R.D.; Williams, S.E.; Hargrove, D.D. Effects of percentage Brahman and Angus breeding, age season of feeding and slaughter end point on meat palatability and muscle characteristics. J. Anim. Sci. 1990, 68, 1980 1986.

2. Ferguson, D.M.; Jiang, S.T.; Hearnshaw, H.; Rymill, S.R.; Thompson, J.M. Effect of electrical stimulation on protease activity and tenderness of M. longissimus from cattle with different proportions of Bos indicus content. Meat Sci. 2000, 55, 265 272.

3. Grobet, L.; Martin, L.J.; Poncelet, D.; Pirottin, D.; Brouwers, B.; Riquet, J.; Schoeberlein, A.; Dunner, S.; Menissier, F.; Massabanda, J.; Fries, R.; Hanset, R.; Georges, M. A deletion in the bovine myostatin gene causes the double muscled phenotype in cattle. Nat. Genet. 1997, 17, 71 74.

4. Wegner, J.; Albrecht, E.; Fiedler, I.; Teuscher, F.; Papstein, H.J.; Ender, K. Growth and breed related changes of muscle fiber characteristics in cattle. J. Anim. Sci. 2000, 78, 1485 1496.

5. Cassens, R.G. Historical perspectives and current aspects of pork meat quality in the USA. Food Chem. 2000, 69, 357 363.

6. Fujii, J.; Otsu, K.; Zorzato, F.; de Leon, S.; Khanna, V.K.; Weiler, J.E.; O'Brien, P.J.; MacLennan, D.H. Identifica tion of a mutation in porcine ryanodine receptor associated with malignant hyperthermia. Science 1991, 253, 448 451.

7. Greaser, M.L. Conversion of Muscle to Meat. In Muscle as Food; Bechtel, P.J., Ed.; Academic Press: New York, 1986; 37 102.

8. Estrade, M.; Vignon, X.; Rock, E.; Monin, G. Glycogen hyperaccumulation in white muscle fibres of RN carrier pigs. A biochemical and ultrastructural study. Comp. Biochem. Physiol. B 1993, 104, 321 326.

9. Monin, G.; Sellier, P. Pork of low technological meat quality with a normal rate of muscle pH fall in the immediate post mortem period. Meat Sci. 1985,13, 49 63.

10. Milan, D.; Jeon, J.T.; Looft, C.; Amarger, V.; Robic, A.; Thelander, M.; Rogel Gaillard, C.; Paul, S.; Iannuccelli, N.; Rask, L.; Ronne, H.; Lundstrom, K.; Reinsch, N.; Gellin, J.; Kalm, E.; Roy, P.L.; Chardon, P.; Andersson, L. A mutation in PRKAG3 associated with excess glycogen content in pig skeletal muscle. Science 2000, 288, 1248 1251.

11. Smit, M.; Segers, K.; Carrascosa, L.G.; Shay, T.; Baraldi, F.; Gyapay, G.; Snowder, G.; Georges, M.; Cockett, N.; Charlier, C. Mosaicism of Solid Gold supports the causality of a noncoding A to G transition in the deter minism of the callipyge phenotype. Genetics 2003, 163, 356 453.

12. Jackson, S.P.; Miller, M.F.; Green, R.D. Phenotypic characterization of rambouillet sheep expressing the callipyge gene: III. Muscle weights and muscle weight distribution. J. Anim. Sci. 1997, 75, 133 138.

13. Koohmaraie, M.; Shackelford, S.D.; Wheeler, T.L.; Lonergan, S.M.; Doumit, M.E. A muscle hypertrophy condition in lamb (callipyge): Characterization of effects on muscle growth and meat quality traits. J. Anim. Sci. 1995, 73, 3596 3607.

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