Intrauterine crowding decreases average birth weight and affects muscle fiber hyperplasia in piglets1

Abstract

High prolificacy of sows and increased fetal survival lead to greater incidence of intrauterine crowding (IUC), which may then affect pre- and postnatal development of the progeny. The aim of the study was to assess the impact of IUC, using unilaterally hysterectomized-ovariectomized gilts (UHO), on organ and muscle development of their progeny at birth. In the study, 7 UHO and 7 intact control (Con) Swiss Large White gilts were used. At farrowing, if available, 3 male and 3 female progeny with a low (>0.8 and <1.2 kg), medium (>1.2 and <1.4 kg), and high (>1.6 kg) birth weight (BtW) were killed. Internal organs and brain were weighed, and semitendinosus (STN), psoas major (PM), and rhomboideus (RH) muscles were collected. Histological analyses were performed in PM, RH, and STN (dark and light portion) using myofibrillar ATPase staining after preincubation at pH 10.3. Myosin heavy chain (MyHC) polymorphism was determined in the PM using SDS-PAGE gel electrophoresis. Despite that only one-half of the uterine space was available, litter size was smaller (P < 0.01) only by 35% in UHO compared with Con gilts. However, UHO progeny tended (P = 0.06) to be lighter than Con progeny. The average BtW of the selected piglets did not differ (P = 0.17) between the 2 sow groups, whereas PM and kidneys tended to be lighter (P < 0.07) in UHO than in Con progeny. Compared with Con progeny, the PM and the STN(dark) of UHO progeny had fewer (P ≤ 0.05) secondary and total myofibers as well as fewer (P = 0.10) primary myofibers in the PM. In the RH, the secondary-to-primary myofiber ratio was smaller (P < 0.01) in UHO than in Con progeny, whereas the total number of myofibers did not (P = 0.96) differ. The relative abundance of fetal MyHC was less (P = 0.02) and that of type I MyHC tended (P = 0.09) to be greater in UHO than in Con offspring. With increasing BtW, organ and brain weights increased (P < 0.01). Muscle cross-sectional area and total number of myofibers in the light portion of the STN were greater (P < 0.05) in high and medium than in low piglets. In conclusion, IUC reduced hyperplasia of secondary and total myofibers in the STN(dark) and PM. These effects were independent of the BtW and sex.

Delayed muscle development in small pig fetuses around birth cannot be rectified by maternal early feed restriction and subsequent overfeeding during gestation

“…Because the MyHC slow isotype is predominant in primary fibers, this suggests delayed formation of secondary myofibers rather than of primary fibers in the smallest fetuses. In support, a lower secondary/primary fiber number ratio has been reported in some muscles of piglets having suffered from intrauterine crowding compared with their normal progeny (Bérard et al, 2010). Early maternal diet deprivation followed by feed over-allowance during gestation did not modify expression levels of stem cell markers, developmental myogenic signals and MyHC isoforms (except MyHC I percentage) in fetal muscles.…”

“…The natural variation in birth weights within porcine litters, which results from uterine crowding limiting nutrient availability (Foxcroft et al, 2006), has been notably considered to clarify the effects of in utero nutrition on muscle development. Small for gestational age pigs exhibit a lower number of muscle fibers (Wigmore and Stickland, 1983), and a lower ratio of secondary to primary myofiber populations when compared with their normal weight littermates at birth (Bérard et al, 2010). However, the developmental time course of myosin heavy chain (MyHC) isoforms, that are important genes in myogenesis as they code for proteins of the contractile apparatus, were only slightly affected by variations in piglet birth weights (Bérard et al, 2010).…”

“…Small for gestational age pigs exhibit a lower number of muscle fibers (Wigmore and Stickland, 1983), and a lower ratio of secondary to primary myofiber populations when compared with their normal weight littermates at birth (Bérard et al, 2010). However, the developmental time course of myosin heavy chain (MyHC) isoforms, that are important genes in myogenesis as they code for proteins of the contractile apparatus, were only slightly affected by variations in piglet birth weights (Bérard et al, 2010). Altogether, the underlying regulatory mechanisms accounting for these changes remain then to be clarified.…”

Compensatory growth feeding strategy does not overcome negative effects on growth and carcass composition of low birth weight pigs

“…Improvement of the reproductive performance can only be realized with highly prolific sow lines. The consequence of increased litter size is reduced intrauterine space per foetus, also known as intrauterine crowding, resulting in intrauterine growth retardation and ultimately low birth weight (Bérard et al, 2010b). Lower birth weight of piglets is not only associated with reduced likelihood of pre-weaning and nursery survival (Fix et al, 2010) but also impaired growth efficiency and unfavourable carcass characteristics (Rehfeldt et al, 2004;Gondret et al, 2006;Bérard et al, 2008).…”

Effects of dietary enrichment with a marine oil-based n-3 LCPUFA supplement in sows with predicted birth weight phenotypes on birth litter quality and growth performance to weaning

“…As events in utero, like maternal malnutrition or intra-uterine crowding (IUC), can have effects on birth weight, muscle fibre numbers and postnatal growth performance to slaughter (Foxcroft et al, 2006;Rehfeldt and Kuhn, 2006;Bérard et al, 2010), it is worthwhile to explore management options for gestating and lactating sows to decrease the variation in BW in the grow-finish barn.…”