J. Anim. Sci. 2006. 84:E113-E123
© 2006 American Society of Animal Science
Consequences of birth weight for postnatal growth performance and carcass quality in pigs as related to myogenesis1
C. Rehfeldt2 and
G. Kuhn
Research Unit Muscle Biology and Growth, Research Institute for the Biology of Farm Animals, D-18196 Dummerstorf, Germany
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Abstract
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In polytocous species such as the pig there is intralitter variation in birth weight and skeletal muscle fiber number. It is commonly recognized that low birth weight in piglets correlates with decreased survival and lower postnatal growth rates. In the majority of low birth weight piglets low numbers of muscle fibers differentiate during prenatal myogenesis, for genetic or maternal reasons, and those low birth weight piglets with reduced fiber numbers are unable to exhibit postnatal catch-up growth. Pigs of low birth weight show the lowest growth performance and the lowest lean percentage at slaughter. In addition, they tend to develop extremely large muscle fibers (giant fibers) and poor meat quality, which results in part from the inverse correlation between fiber number and fiber size. Prenatal growth and myogenesis are under the control of various genetic and environmental factors, which can be targeted for growth manipulation. Genetic selection is considered a suitable tool to improve fetal growth and myogenesis. Prenatal development is mainly dependent on a close interrelation between nutritional supply/use and regulation by hormones and growth factors. In particular, the maternal somatotropic axis plays a significant role in the control of myogenesis. Thus, treatment of sows with GH until mid-gestation was able to increase birth weight and the number of muscle fibers in the small littermates of the progeny that are disadvantaged by insufficient nutrient supply. Growth hormone treatment was associated with increased nutrient availability to the embryos and changes in regulatory proteins of the GH-IGF axis. Interactions between maternal nutrition and the somatotropic axis in determining prenatal growth and myogenesis are worthy of further investigation.
Key Words: birth weight • carcass quality • growth hormone • myogenesis • pig
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INTRODUCTION
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Birth weight is an important economic trait in pig production. It is commonly recognized that low birth weight in piglets correlates with decreased survival and lower postnatal growth rates (Pomeroy, 1960
; Widdowson, 1977; Pond et al., 1985; Pond and Mersmann, 1988; Ritter and Zschorlich, 1990; Milligan et al., 2002; Quiniou et al., 2002). Usually, so-called runts that fall short of a certain limit in birth weight are excluded from rearing. The phenotype of a newborn piglet is the result of its embryonic and fetal development, which is a very complex and highly integrated process. Prenatal growth is mainly dependent on the nutritional supply to the embryo/fetus and its ability to use the available substrates. In turn, nutritional partitioning and utilization are under the control of hormones and growth factors but, conversely, nutrition may also influence the hormonal status (Straus, 1994; Thissen et al., 1994; Brameld, 1997; Brameld et al., 1998; Breier, 1999; Robinson et al., 1999). Maternal features that are determined by genetic (breed, genotype) and environmental (e.g., feeding, housing) factors further modify these interactions.
The maternal diet controls fetal growth directly by providing glucose, amino acids, and other essential nutrients for the conceptus (Robinson et al., 1999). Another important factor in the pig is the competition for these nutrients among littermates in utero, because fetal and birth weight have been shown to correlate inversely with litter size (Milligan et al., 2002; Quiniou et al., 2002; Town et al., 2005). In addition, the position of the fetus within the uterus may play a role in causing differences in nutritional supply (McLaren et al., 1960; Perry and Rowell, 1969; Widdowson, 1977; Wigmore and Stickland, 1983a). Continuous inadequate nutrition may have serious consequences for fetal development. Furthermore, nutrition during fetal life may affect adult animal performance, which is also termed "fetal programming" according to previous research in humans (Barker, 1998). This seems to be especially important when fetal muscle development (myogenesis) is adversely affected (Handel and Stickland, 1987a,b; Dwyer et al., 1993; Kuhn et al., 2002). This brief review will therefore focus on the consequences of intrauterine growth retardation as related to myogenesis on postnatal growth and carcass quality in the pig and discuss possibilities to improve fetal (muscle) growth.
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PRINCIPLES OF MYOGENESIS AND POSTNATAL MUSCLE GROWTH
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As for fetal growth in general, prenatal skeletal muscle development (myogenesis) is determined by nutrient availability and is under the control of hormones and growth factors affecting changes in metabolism at the level of transcription and translation of regulatory and structurally important genes. They interact with a series of transcription factors such as the myogenic regulatory factors, which play a key role in controlling muscle-specific gene expression (for reviews see Weintraub, 1993; Olson and Klein, 1994; Rawls and Olson, 1997; Arnold and Braun, 2000).
Skeletal myogenesis and its control have been the subject of a number of comprehensive reviews (Miller et al., 1993; Florini et al., 1996; Brameld et al., 1998; Buckingham, 2001; Maltin et al., 2001; Picard et al., 2002; Wigmore and Evans, 2002). The elementary events of myogenesis are stem cell commitment, proliferation and apoptosis of myoblasts, differentiation and fusion of myoblasts, and finally, maturation of muscle fibers. These events determine the number of muscle fibers that are formed prenatally. Another population of myoblasts, termed satellite cells (Mauro, 1961), does not form fibers but stays close to the myofibers. Satellite cells are able to divide and serve as the source of new myonuclei during postnatal growth (Moss and Leblond, 1971; Schultz, 1974). They contribute to growth of fiber size and also participate in regeneration processes, whereas myonuclei themselves remain mitotically quiescent. In most mammalian skeletal muscles, prenatal development (time shortly after birth in rodents) ends with a given number of fibers that does not further increase. Thereafter, the increase in skeletal muscle mass results mainly from an increase in muscle fiber size (hypertrophy), which is, in turn, limited by genetic and physiological factors (see Rehfeldt et al., 2000; Figure 1).
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Figure 1. Postnatal development of fiber diameter and total fiber number per cross section in the semitendinosus muscle of German Landrace pigs (Rehfeldt et al., 1987).
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An important phenomenon is that the number of prenatally formed muscle fibers determines, at least in part, the rate of postnatal fiber hypertrophy. During postnatal development, the individual muscle fibers generally grow more slowly when the number of fibers is high, and conversely, fibers grow rapidly when the number of fibers is low (summarized by Rehfeldt et al., 2000). This has been shown for several species such as mouse (Rehfeldt et al., 1988), chicken (Locniskar et al., 1985), pig (Staun, 1972; Fiedler et al., 1997; Larzul et al., 1997), and cattle (Osterc, 1974) by negative phenotypic and genetic correlation coefficients ranging from –0.3 to –0.8. On the other hand, both fiber number and fiber thickness are positively correlated with muscle cross-sectional area. An example for the pig longissimus muscle is given in Figure 2. Large loin areas can be associated with high fiber numbers at low fiber size and vice versa. The largest loin areas, however, are achieved with an optimal combination of fiber number and fiber size.
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Figure 2. Contour plot of the phenotypic correlation (r) between longissimus muscle fiber number and fiber cross sectional area with different levels of loin area in German Landrace pigs at market weight (n = 260; Rehfeldt et al., 2004a). The areas of intensity from white to black include all points of combination of fiber number and fiber cross-sectional area that occur at a certain loin area.
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INTRAUTERINE GROWTH RETARDATION IS ASSOCIATED WITH LOW NUMBERS OF MUSCLE FIBERS AND MYONUCLEI
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Effects of prenatal undernutrition on fetal growth and myogenesis in the pig have been demonstrated both by the naturally occurring variations in birth weight within litters and in response to maternal undernutrition during pregnancy. The influence of prenatal and maternal nutrition on muscle development has recently been reviewed by Stickland et al. (2004) and Rehfeldt et al. (2004a).
Natural Variations in Birth Weight
Comparison of small- with large-weight piglets within litters indicates that prenatal undernutrition in pigs is related to lower muscle fiber numbers, myonuclear numbers, or muscle DNA content (e.g., Wigmore and Stickland, 1983a,b; Handel and Stickland, 1987a,b; Dwyer and Stickland, 1991; Rehfeldt et al., 2001a). Wigmore and Stickland (1983b) showed that large fetuses within porcine litters generally exhibited higher muscle fiber numbers in complete sections of the semitendinosus muscle than did small fetuses. They concluded that most of the variation was due to a difference in the number of secondary myofibers that formed around each primary. The diameter of the primary myofibers was greater in the larger fetuses and the larger primaries appeared to support more developing secondaries. Dwyer and Stickland (1991) reported that intralitter variation could be attributed to both primary fiber number and secondary to primary fiber ratio. The larger fetuses also contained more DNA in their muscles than the small fetuses (Wigmore and Stickland, 1983a). The variations in muscle fiber number between littermates is very important, because only piglets with high fiber number were able to exhibit postnatal catch-up growth (Handel and Stickland, 1988). On average, postnatal growth and feed conversion efficiency, from 25 kg to slaughter, were positively correlated with muscle fiber number (Dwyer et al., 1993). Besides the variation within litters, the number of competing fetuses affects the result of fetal myogenesis. When the number of conceptuses in utero was reduced by unilateral oviduct ligation, fetal weight, semitendinosus muscle weight, and fiber number were clearly increased (Town et al., 2004).
Influence of Maternal Undernutrition
Fetal growth retardation can also be induced by maternal undernutrition during pregnancy. Thus, birth weight of offspring from sows fed a low-energy diet has been found to be lower than the birth weight of offspring from sows fed a high-energy diet throughout gestation (Pond, 1973; Buitrago et al., 1974; Bee, 2004). Likewise, maternal protein restriction has detrimental effects on fetal growth when either applied transitionally or throughout gestation (Pond et al., 1969, 1987)
Restrictive maternal feeding has been reported to cause decreases in muscle fiber number and myonuclear number in rats (e.g., Bedi et al., 1982; Glore and Layman, 1983) and in guinea pigs (Ward and Stickland, 1991; Dwyer and Stickland, 1992; Dwyer et al., 1995). When sows were fed either a high- or a low-energy level (8 vs. 2.2 Mcal of DE/d) during gestation, significant differences in total weight and total DNA and protein content of the gastrocnemius muscle at birth have been reported (Buitrago et al., 1974). Likewise, lower muscle weights (triceps, semitendinosus), and lower muscular DNA, RNA, and protein contents have been found up to 100 d of age in offspring from sows fed 50% of the requirements throughout gestation (Robinson, 1969). Whether these differences in muscle weight and DNA content were caused by differences in the number of muscle fibers or in the area of the individual fibers was not investigated. In contrast, Bee (2004) observed a difference in birth weight (P = 0.08) when feeding sows at either a low (40% below control), average, or high (40% above control) level during the first 50 d of gestation, but did not find any difference in muscle weights, muscle area, or muscle fiber area in the progeny at market weight. However, the percentage of adipose tissue was higher in pigs born to the restrictively fed sows. Ezekwe and Opoku (1988) showed that pregnant gilts fasted for 2 wk before parturition gave birth to piglets with reduced DNA content in the gastrocnemius muscle, but this was not maintained at 49 d postnatal; other traits such as muscle weight, RNA content, and protein content remained unchanged. In summary, the effects of maternal feeding on fetal growth may be similar to the effects of prenatal undernutrition caused by maternal constraints in utero, although the effect on fiber formation and resulting number of fibers remains to be investigated. It seems however, that transitional feed restriction has no permanent effect, whereas severely restricted feed intake throughout gestation shows lasting detrimental effects on postnatal (muscle) growth.
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RELATIONSHIPS AMONG MYOGENESIS, BIRTH WEIGHT, GROWTH, AND CARCASS QUALITY
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Recent Experiments
To elucidate the influence of fetal growth retardation we examined the influence of low birth weight/low fiber number on postnatal growth and carcass composition in pigs of market weight (Kuhn et al., 2002; Rehfeldt, 2005). In this experiment, piglets of 16 sows of German Landrace were assigned to 3 birth weight groups: 25% to low weight (LW, <1.20 kg), 50% to middle weight (MW); and 25% to heavy weight (HW, >1.62 kg). Three neonates with the lowest, middle, and highest birth weight were selected from each litter for the analysis of body composition and muscle fiber characteristics (runts <800 g were excluded). The remaining piglets were reared until slaughter.
Piglets of low birth weight grew slower compared with piglets of high birth weight as seen by daily gains, which were 582, 619, and 641 g/d from birth to d 175 in LW, MW, and HW pigs, respectively. The ranking in weight was the same at birth and at slaughter, although the differences between MW and HW were no longer significant (Figure 3). Already at birth, significant differences in the body composition were found (Table 1). Low-weight piglets exhibited higher percentages of internal organs, bones, and skin, whereas the percentage of muscle tissue was smaller than in HW piglets. By chemical analysis of the whole body, the LW piglets contained less fat and protein and more water, indicating their relative immaturity. Correspondingly, significant differences were observed in the weight, cross-sectional area, and length of the semitendinosus muscle that were used to determine muscle fiber characteristics. The LW piglets had formed a significantly lower number of muscle fibers (P < 0.05) during fetal development (Figure 4). This resulted mainly from lower numbers of secondary fibers (P = 0.08). The linear correlation coefficients of birth weight with the semitendinosus (Figure 5) and psoas major muscle fiber number in an extended data set (62 piglets born to 23 sows) were r = 0.5 and r = 0.7, respectively, in this breed, indicating that in the majority of LW piglets, low numbers of muscle fibers differentiate during myogenesis and that muscle fiber number is important in determining birth weight.
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Figure 3. Birth weights (n = 180) and live weights 1 wk before slaughter (n = 58; d 175) of pigs divided by birth weight groups (LW = low, MW = middle, HW = heavy). Within age group, least squares means without a common superscript differ between the birth weight groups (P < 0.05).
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Figure 4. Total and secondary muscle fiber numbers of semitendinosus muscle in different birth weight groups (LW = low, MW = middle, HW = heavy) of newborn piglets (n = 47). Within total or secondary fiber number, least squares means without a common superscript differ between the birth weight groups (P < 0.05).
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Figure 5. Relationships of birth weight with semitendinosus muscle fiber number by phenotypic correlation (r) estimated from data of 62 piglets born to 23 German Landrace sows (P < 0.0001).
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Muscular protein concentration was lowest in LW piglets and the activity of creatine kinase (CK) as a marker of muscular differentiation was also markedly lower than in HW piglets (Table 2). The DNA concentration was highest in LW piglets, but total DNA content was lowest as well. Consequently, in LW piglets, prenatal cell proliferation, differentiation, and protein accretion in skeletal muscle were far below average. In addition, LW piglets tended to exhibit the lowest blood glucose concentration (P = 0.12; 77% of HW; correlation with BW was r = 0.40), indicating that they were not adequately supplied with nutrients in utero.
Based on the principles of muscle fiber growth (see Figures 1
and 2), we would expect faster fiber growth in low birth weight pigs, and expect the plateau of fiber growth to be attained earlier than in pigs of high birth weight. Indeed, we found the largest fibers in slaughter pigs of low birth weight (LW) both in the semitendinosus and in the longissimus muscle. The ranking of fiber number was found to be the same as at birth, with low fiber numbers in LW and high numbers in HW pigs (Figure 6). No differences were observed in the frequencies of different fiber types such as slow twitch oxidative, fast twitch oxidative, and fast twitch glycolytic fibers (data not shown), suggesting that postnatal fiber type differentiation is not dependent on birth weight. What we observed instead were differences in the percentage of giant fibers in both semitendinosus (HW = 0%; LW = 0.07%; P = 0.06) and longissimus (HW = 0.07%; LW = 0.44%; P < 0.05) muscles. These are structurally abnormal fibers of extreme size that appear in postmortem muscle and are considered to arise from hypercontraction. Extreme fiber size and higher frequencies of giant fibers have been shown to be associated with poor meat quality in pigs and poultry (Klosowska et al., 1979; Fiedler et al., 1999). Close genetic relationships between the frequency of hypercontracted giant fibers and various meat quality characteristics have been found in pigs (Fiedler et al., 2004). The genetic correlation coefficients were rg = 0.8 for drip loss and brightness and rg = –0.8 for pH at 45 min postmortem in longissimus muscle. Probably, the muscles of LW pigs contained more fibers of extreme size, which would likely be incompatible with normal fiber function.
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Figure 6. Fiber number and fiber cross sectional area of semitendinosus muscle in slaughter pigs (d 182; n = 58) of different birth weight groups (LW = low, MW = middle, HW = heavy). Within fiber number or cross-sectional area, least squares means without a common superscript differ between the birth weight groups (P < 0.05).
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Pigs of different birth weight differed in final carcass quality determined at slaughter (182 d of age). Carcass weights, meat percentages, and loin muscle areas were lower (P = 0.02 to 0.09) in LW than in HW pigs, as was the weight of the heart (P = 0.01; Table 3). On the other hand, the internal fat percentage was higher in LW pigs than in HW pigs. Likewise, the fat percentage by chemical analysis was numerically highest in LW pigs. Drip loss, an indicator of poor meat quality, was highest in LW and lowest in HW piglets. In summary, pigs having the largest fibers and the lowest fiber numbers exhibited the lowest meat percentage. Meat quality, on the other hand, was poorest in those pigs that had the largest fibers and the highest percentage of giant fibers.
Related Results of Research
Our results are in agreement with studies from Gondret et al. (2005) who compared the carcass quality of pigs of low and heavy birth weight. The muscle fiber number was 19% lower and myofiber cross-sectional area was 14% higher in semitendinosus and longissimus muscles from LW pigs. The LW pigs exhibited a lower feed conversion ratio, lower lean meat content, and a higher proportion of subcutaneous fat. In addition, LW pigs showed a lower score for loin meat tenderness that was negatively correlated with fiber size (r = –0.34). Bee (2004) found larger muscle fibers and an increased percentage of adipose tissue in slaughter pigs of low birth weight. Likewise, Hegarty and Allen (1978) and Powell and Aberle (1981) have observed lower muscle mass, higher fiber diameters for selected muscles, and increased amounts of intramuscular fat and perirenal fat, respectively, in LW pigs. Collectively, the data indicate that pigs of low birth weight develop lower carcass and meat quality and that this is related to low numbers of muscle fibers that undergo accelerated hypertrophy during postnatal growth.
Finally, a model of postnatal fiber growth is shown to explain the correlation of fiber number with lean growth and meat quality based on the assumption that a certain plateau is not exceeded (Figure 7). The middle curve represents the average fiber growth. In LW pigs, the increase in fiber size is faster because of the low fiber number, and the plateau of fiber growth is therefore attained earlier (see arrows). Consequently, nutritional energy can no longer be used for muscle accretion, but is mainly used to deposit fat. In contrast, pigs with high muscle fiber number (HW) attain this plateau later and may, therefore, have a higher potential of muscle accretion. In addition, LW pigs develop more fibers of extreme size because they are probably closer to the plateau of fiber growth at slaughter, whereas the MW and HW pigs are slaughtered before the fibers can grow to extreme size. This may be one of the reasons that LW pigs tend to develop poor meat quality.
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Figure 7. Model of the dependence of muscle fiber growth in size on birth weight (LW = low, MW = middle, HW = heavy). The dotted line indicates the probable age at slaughter; the arrows mark the transition to the plateau of the growth curve.
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Signs of obesity have also been observed in the primiparous sheep in response to maternal feed restriction or at low birth weights (Greenwood et al., 1998; Bispham et al., 2003; Symonds et al., 2003). Although muscle fiber number was not affected, muscle DNA content was clearly lower (Greenwood et al., 2000), as has been observed in the studies with pigs. In addition to the number of muscle fibers, the pool of satellite cells that are essential for postnatal muscle fiber growth and repair may be a limiting factor for postnatal muscle growth.
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IMPROVEMENT OF FETAL (MUSCLE) GROWTH
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If muscle cellularity is so important in determining birth weight and subsequent postnatal growth and carcass quality, successful strategies to influence fetal myogenesis are of interest.
Genetic Selection
Genetic selection is one instrument of choice to reduce variation in birth weight and to find an optimum balance of litter size and birth weight. Town et al. (2004) have demonstrated that fetal weight and semitendinosus muscle weight and fiber number increased when the number of fetuses was reduced by unilateral oviduct ligation. Furthermore, it has been shown by estimations of heritability coefficients, genetic correlations, and results of selection, that muscle fiber number and other muscle characteristics, such as the percentage of giant fibers, can be changed by selection and used in addition to traditional selection criteria for improving lean meat accretion and meat quality in pigs (Rehfeldt et al., 2000, 2004a; Fiedler et al., 2004). In future, the incorporation of marker-assisted selection by QTL or candidate gene approaches into new selection strategies may contribute to overcome the consequences of prenatal undernutrition (Wimmers et al., 2004).
Maternal Nutrition Above Requirements
A number of studies have investigated the effects of maternal nutrition on fetal muscle development. Feeding sows 36% above control levels from d 25 to 50 of gestation resulted in an increased fiber number/mm2 at unchanged muscle cross-sectional area in the offspring, which may imply increases in total fiber number (Gatford et al., 2003). Dwyer et al. (1994), who fed sows 100% above standard requirements for pregnant sows in the same period, found no increases in average fiber numbers. However, the number of secondary fibers was increased and the number of piglets within the litter exhibiting extremely low fiber numbers was decreased. Nissen et al. (2003) did not find any effect of increased maternal feed intake (approximately 150% above control) between d 25 and 50 or d 25 and 70 on average muscle fiber numbers, fiber areas, or fiber type distribution in the offspring, when slaughtered at approximately 100 kg of live weight. Likewise, Bee (2004) did not detect any differences in muscle weights, muscle cross-sectional areas, or muscle fiber area between offspring from sows fed either an average or high (approximately 40% above control) feeding level during the first 50 d of gestation. Based on his findings, he concluded that muscle fiber number of the offspring was not affected by maternal treatments. In all studies mentioned above, birth weight was found to be unchanged or decreased after increased maternal feed allowance.
In summary, maternal overnutrition seems not to be effective in stimulating myogenesis and increasing birth weight of progeny. However, further investigation to determine whether small fetuses within litters would profit from additional maternal feed intake would be valuable and could be important in reducing intralitter variation. In addition, the effects of specific feed compounds could be of further interest. For example, supplementing the maternal diet with L-carnitine has been reported to increase birth weight and/or litter weight of the progeny (Musser et al., 1999; Eder et al., 2001; Ramanau et al., 2004).
Manipulation of Fetal Myogenesis by Maternal Growth Hormone
Pituitary growth hormone (GH) is the principal hormone involved in regulating growth and metabolism. Numerous studies have shown the efficacy of GH in stimulating lean growth and inhibiting adipose tissue growth in postnatal pigs. Furthermore, research in the last decade has shown that circulating maternal GH plays a role in the prenatal development of the progeny (for an overview, see Rehfeldt et al., 2004b). Exogenous porcine GH (pGH) given to pregnant sows in a sufficient dose affected their metabolic status by increasing maternal plasma concentrations of glucose and free fatty acids and providing an endocrine environment (increased IGF-I, insulin) that may stimulate placental and fetal growth (Kveragas et al., 1986; Kirkwood et al., 1993; Sterle et al., 1995; Schneider et al., 2002; Gatford et al., 2003). Growth hormone administered to sows during gestation stimulated placental growth and modified the expression of regulatory proteins of the GH–IGF axis in placental tissues (Kelley et al., 1995; Sterle et al., 1998; Freese et al., 2005). It also increased nutrient availability to the embryo/fetus and induced short- and long-term changes in serum IGF-I concentrations in the progeny (Kelley et al., 1995; Sterle et al., 1995; Rehfeldt et al., 1993, 2001b). Consequently, fetal growth has been shown to be accelerated by maternal GH treatment (Sterle et al., 1995, 1998).
Advantages in growth gained by GH treatment during early and mid-gestation were not maintained until birth, whereas GH treatment during late, or the greatest part of gestation resulted in heavier piglets (Rehfeldt et al., 1993; Gatford et al., 2004). Gatford et al. (2004) reported that maternal long-term treatment with pGH from d 25 to 100 of gestation increased progeny size at birth, with the effects being greatest in the largest litters, suggesting that maternal constraints of fetal growth were effectively reduced. Consistently, if maternal GH level was increased by treatment during early gestation, only littermates that were disadvantaged by maternal constraints were able to grow faster until birth and to improve their body composition toward leanness at birth and at slaughter, which resulted in more homogeneous litters (Rehfeldt et al., 2001a; Kuhn et al., 2004).
It has been shown that the effects of maternal GH during early gestation (d 10 to 24 or 27) were related to changes in fetal myogenesis (Rehfeldt et al., 1993, 2001a,Rehfeldt et al., b, 2002). Individual muscle weights and/or cross-sectional areas were not affected in fetuses, neonatal piglets, and pigs at weaning or slaughter. Summarizing the data from 2 experiments with 46 sows, maternal pGH treatment did not significantly change the average total muscle fiber number, but tended to increase the number of primary muscle fibers in semitendinosus muscle (Table 4). However, consistent with the findings for birth weight, an increase in total fiber number was observed in LW littermates (Figure 8). When the total fiber number was higher (LW piglets), the numbers of both primary and secondary muscle fibers were increased (P < 0.05 and P < 0.10, respectively). The increase in secondary fiber number occurred as late as the last trimester and was accompanied by a higher expression of the myogenic regulatory factors MyoD and Myf-5 indicating that the muscle contained a higher proportion of proliferating myoblasts. It remained unclear whether secondary fiber formation was induced by more effective placental IGF action and better placental supply or by an unknown mechanism triggered by the higher number of primary fibers.
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Table 4. Semitendinosus muscle cross-sectional area, total fiber number, and numbers and ratios of secondary and primary muscle fibers in newborn piglets in response to maternal treatment with porcine growth hormone (pGH; 6 mg/d) from d 10 to 27 of gestation (Rehfeldt et al., 2004b)1
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Figure 8. Total fiber number (least squares means) in semitendinosus muscle of neonatal piglets born to gilts treated with placebo (control; n = 64) or 6 mg of porcine growth hormone (pGH) per d (n = 69) from d 10 to 27 of gestation (Rehfeldt et al., 2004b). There was a pGH x birth weight group (LW = low, MW = middle, HW = heavy) interaction for total fiber number (P = 0.11); +P = 0.09 for differences between pGH and control.
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As seen for fiber number, a tendency for a pGH x birth weight group interaction (P = 0.11) was found for the average specific CK activity. Creatine kinase activity was increased in LW and MW piglets but decreased in HW piglets. In addition, average muscle DNA and protein concentrations were significantly elevated independently of birth weight group (P < 0.05). Increases in total muscle fiber number can also be concluded from another study (Gatford et al., 2003). The authors found increased semitendinosus muscle cross sectional areas at unchanged fiber density (fiber number per mm2) in 61-d-old female progeny of sows treated with pGH during the second quarter of gestation. The results of both studies suggest that increased maternal glucose at least partly mediates the effect of maternal pGH treatment on muscle growth.
Unlike the above findings, treatment with pGH during mid- and late gestation was not able to induce an increase in the cross-sectional area or total semitendinosus muscle fiber number in neonatal piglets (Rehfeldt et al., 1993). This suggests that increased birth weight in response to higher maternal GH in late gestation is not related to increased muscle fiber numbers. In this case, the increases in birth weight result mainly from higher percentages of total body lipid, which has been explained by the diabetogenic state of the dams (Kveragas et al., 1986; Etienne et al., 1992).
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CONCLUSIONS
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In pigs, fetal growth retardation resulting in low birth weight and low numbers of skeletal muscle fibers cannot be compensated for during postnatal growth. Pigs of low birth weight exhibit the lowest lean growth, highest fat deposition, and poorest meat quality at slaughter. The number of muscle fibers formed prenatally is positively correlated with birth weight and plays a significant role in the relationship of birth weight with lean accretion and meat quality. Piglets with sufficient numbers of muscle fibers are therefore ideal for efficient pig production. Genetic selection is a suitable instrument to improve fetal (muscle) growth. Maternal feeding above requirements seems not to be very effective in improving fetal growth, with the exception that small littermates could profit from the additional nutrient supply. Treatment of sows with growth hormone until mid-gestation is able to increase birth weight and the number of muscle fibers in the offspring by stimulating fetal myogenesis. This effect, which is associated with increases in lean percentage, is only pronounced in small littermates that are most severely disadvantaged by insufficient nutrient supply.
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Footnotes
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1 Invited review. Presented at the "Effects of Maternal Nutrition on Offspring Performance" symposium held at the American Society of Animal Science Annual Meeting, Cincinnati, OH, July 24–28, 2005. 
2 Corresponding author: rehfeldt{at}fbn-dummerstorf.de
Received for publication August 8, 2005.
Accepted for publication October 10, 2005.
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Abstract
INTRODUCTION
