Impact of Genetic Selection on Skeletal Muscle in Meat-Type Poultry. Héctor L. Santiago

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1 Impact of Genetic Selection on Skeletal Muscle in Meat-Type Poultry Héctor L. Santiago Department of Animal and Poultry Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA (Key words: poultry, skeletal muscle, genetic selection, myopathy) ABSTRACT The growth and success of the poultry industry can be attributed at least in part to the significant improvements in growth and feed efficiency that resulted from genetic selection. However, those improvements have resulted in the appearance of morphological disorders in skeletal muscle. The impact of selection for rapid growth and body composition and the related alterations and abnormalities that have occurred in skeletal muscle of meat-type poultry will be reviewed. INTRODUCTION Genetic selection based on important economic traits such as growth rate, body size, edible meat yield, and feed conversion has resulted in gross changes in commercial meat poultry (Havenstein et al., 1994a,b; Anthony, 1998; Pollock, 1999). The age to reach market weight, the amount of feed necessary to produce a kilogram of meat, and the age at which slaughter occurs has been reduced continuously during the last 50 years (Gous, 1986). However, during the last decade, intense selection pressure has been applied to improve breast meat yield and muscle mass in response to a shift in the market from whole birds to further processed products and an increasing demand for white meat by consumers (Ewart, 1993). Consequently, the growth of the Pectoralis major muscle of broilers and turkeys has increased at a rate that has exceeded body weight growth (Lilburn, 1994). Unfortunately, along with this progress has been a concomitant increase in muscle abnormalities and problems. Genetic selection has resulted in profound changes in muscle fibers and vascular structure of poultry skeletal muscle (Wilson et al, 1990; Dransfield and Sosnicki, 1999; Hoving-Bolink et al., 2000; Remignon et al., 2000;). These alterations have lead to an increase incidence of muscular problems such as leg weakness and edema, focal myopathy, deep pectoral myopathy, and muscular dystrophy in broilers and turkeys (Martindale et al., 1979; Siller and Wight, 1979; Wight and Siller, 1980; Grunder et al, 1984; Siller, 1985; Sosnicki et al, 1988; Wilson et al., 1990; Wilson, 1990; Sosnicki and Wilson, 1991). 1

2 LITERATURE REVIEW Dunnington (1990) stated that in all animal systems, the force of natural selection balances the changes produced by artificial selection. However, radical changes in body composition and production ability may disrupt the biological balance of the animal and a limit can be reached. It appears that such a limit might be close in terms of breast muscle growth. It may be that long-term selection for traits such as body weight or muscular mass will ultimately lead to muscles that exceed some metabolic or anatomical limits, resulting in animals predisposed for muscle abnormalities (Wilson et al., 1990). It may also be that the physiological status of turkey skeletal muscle had not kept in pace with the size of the animal (Sosnicki and Wilson, 1991). Influence of Genetic Selection on Muscle Growth. The number of muscle fibers is related to changes during growth and development and fast-growing animals have more muscle fibers than slow-growing animals (Dransfield and Sosnicki, 1999). Within a strain, the number of muscle fibers increases with increasing average daily gain and gain to feed ratio (Stickland, 1995). In avian species, muscle fiber diameter increases with age and genetic potential for breast meat. Geese selected for meat yield had larger fibers than birds selected for egg production, and that fast-growing lines had larger diameter fibers than slow growing lines (Klosowska et al. 1993). This increase is also associated with an increase in the number of giant fibers, which typically have cross-sectional areas that are three to five times larger than normal muscle fibers (Dransfield and Sosnicki, 1999; Remignon et al., 2000). Remignon et al. (2000) reported that the incidence of giant fibers was higher in turkey lines selected for rapidgrowth when compared to unselected, slow-growing lines. They suggested that giant fibers result from defects in the developing muscle fibers leading to structural and metabolic abnormalities within the fibers. Effects on Vascular Structure. Postnatal growth and development of skeletal muscle is mainly due to hypertrophy of the existing muscle fibers (Bechtel, 1986). Muscle growth results in a concomitant decrease in capillary density because, as the fibers increase in length and diameter, the capillaries surrounding the fibers are displaced (Kurnoth et al., 1994). To compensate for the loss of capillary density there is a parallel increase in the number of capillaries around the fibers. Furthermore, normal muscle growth is accompanied with a linear increase in capillary to fiber ratio with increased fiber area. The fiber type present in the muscle is also known to influence capillary density and capillary to fiber ratio. Fibers in which there is a high level of oxidative metabolism (red) have been reported to have a higher number of capillaries around the fibers than those that surround fast glycolytic fibers (white) (Romanul, 1965; Kurnoth et al., 1994). Evidence of vascular defects in turkey muscles was reported by Sosnicki et al. (1991) who investigated the capillary to fiber relationship of normal and myopathic pectoralis and bicep femoris muscles of turkeys. Myopathic muscles had a lower capillary density, fewer capillaries surrounding a single fiber, and a lower capillary to fiber ratio and a greater intercapillary distance than those of normal muscles. However, 2

3 whether the capillary morphometry of myopathic muscles resembles the muscles from fast-growing birds remains to be determined. Growth Rate and Muscle Degeneration. The incidence of muscle degeneration has been associated with rapid growth and increased muscling of turkeys. Because muscle damage is difficult to detect in living animals, the use of circulating plasma levels of creatine kinase (CK) has been used as an indirect indicator of muscle damage (Hollands et al., 1980; Mitchell and Sandercock, 1995). Wilson et al. (1990) studied the relationship between body weight, muscle histopathology and plasma CK in three lines of turkeys selected for rapid growth and one slow growing line. The three selected lines exhibited significantly higher levels of CK when compared to the unimproved line. They observed a positive correlation between the levels of plasma CK, age and growth rate with the incidence of damaged muscle. The older the birds and the faster their growth, the greater the muscle damage, and the higher the plasma CK levels. Histopathological evaluation of skeletal muscle showed degenerative changes that included scattered and focal necrosis, hypercontraction of muscle fibers, proliferation of connective and fat tissue in the endomysium and perimysium, and infiltration of necrotic areas by mononuclear cells. They concluded that selection for rapid growth has created muscles that outgrow their life support systems, which thus brings about muscle damage. Deep Pectoral Myopathy. Deep pectoral myopathy (DPM) is a polygenic abnormality of the supracoracoideus muscle of broilers and turkeys (Dickinson et al., 1968; Harper et al., 1971). The condition is characterized by a necrotic lesion that is limited to the deep pectoral muscle on one or both sides. The necrotic muscles usually have a dehydrated wood-like texture, a gross edematous appearance and a discoloration ranging from pale yellow to dark purple. Eventually the lesion develops a characteristic green color. The cranial part of the muscle is often normal, and the part caudal to the necrotic portion is pale and distinctly atrophied. The condition affects mainly adult birds with an incidence of around 15%, although incidences as high as 43% have been reported (Wight and Siller, 1980; Hollands et al., 1981). Susceptibility however is not confined to adult birds, because it has been observed in 7-week-old broiler chickens (Richardson et al., 1980). The condition has been reported to occur exclusively in birds genetically selected for increased musculature, particularly for breast meat yield. Evidence that this condition is the direct result of intense genetic selection has been shown in studies with wild turkeys and less intensely selected older commercial strains. These birds did not exhibit the condition naturally or after experimental induction and are apparently not susceptible to DPM. Hollands et al. (1981) and Grunder et al. (1984) evaluated the condition in commercial meat-type chicken strains and found an incidence of up to 43%, whereas in commercial strains representing broiler strains of 15 to 20 years ago, there was no incidence of DPM. Anatomical and histopathological studies have revealed that selection for increased muscle size altered the vascular structure in relation to the muscle or skeleton, thus affecting blood circulation in the deep pectoral muscle. Martindale et al 3

4 (1979) and Siller and Wight (1979) reported that the exercise-stimulated deep pectoral muscle of heavy-type strains increase in pressure within the fascial compartment by one-fifth more than light-type strains. These findings agree with studies of the vascular structure of the muscle that established that the myopathy is the result of ischemia brought about by an increase in internal pressure in the muscle that occludes the cranial and pectoral arteries resulting in a loss of blood supply and leading to a necrotic lesion. In all types of poultry, the muscle increases in weight by about 20% during activity, but because of its anatomical compartment, the size increase from muscular activity is so marked in the heavy-type breeds that the muscle becomes strangulated and ischemic (Siller, 1985). The same phenomenon does not occur in light-type breeds because there is enough space available to accommodate the swelled muscle. It is unknown why the compartment in birds selected for increased musculature has not also enlarged enough to allow for the normal function of the muscle. IMPLICATIONS As genetic selection for increased BW is expected to continue in the future, muscle abnormalities and meat quality problems will become more evident. The increased incidence of muscle related problems might be seen as a warning of more problems to arise if selection for rapid growth is continued without modification. The current selection criterion to maximize growth performance may no longer be the best breeding program. Breeding programs that take into consideration the biochemical and morphological alterations resulting from genetic selection may improve muscle structure and potentially diminish or prevent muscle abnormalities. LITERATURE CITED Anthony, N.B., A review of genetic parameters in poultry: Efforts to improve meat quality. J. Muscle Foods. 9: Bechtel, P.J., Muscle development and contractile proteins. Pages 2-35 in: Muscle as Food. P. J. Bechtel, ed. Academic Press, New York, NY. Dickinson, E.M., J.O. Stevens, and D.H. Helfer, A degenerative myopathy in turkeys. Page 6 in Proc. 17 th West.Poult. Dis. Conf., University of California, Davis, CA. Dransfield, E., and A.A. Sosnicki, Relationship between muscle growth and poultry meat quality. Poultry Sci. 78: Dunnington, A.E., Pages 5-12 in Proceedings of the 4 th Genetics Applied to Livestock Production. Edinburg, Scotland. World Congress on Ewart, J., Evolution of genetic selection techniques and their application in the next decade. Gordon Memorial Lecture. Br. Poultry Sci. 34:

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