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.

There are indications that intrauterine crowding may cause intrauterine growth retardation with the possibility of an impaired myofiber hyperplasia. The aim of the study was to confirm this by generating large differences in uterine space using sows that were unilaterally hysterectomized-ovariectomized (HO; crowded) or unilaterally oviduct ligated (OL; non-crowded). In the study, seven HO and seven OL Swiss Large White third parity sows were used. At farrowing, litter size and litter birth weight were determined. Subsequently, within each litter two male and two female progenies each with the respectively lowest (L) and highest (H) birth weight were sacrificed. Internal organs and brain were weighed, and longissimus (LM) and semitendinosus muscle (SM) samples were collected. Histological analyses were performed in both muscles using mATPase staining after preincubation at pH 4.3 and 10.2. Myosin heavy chain (MyHC) polymorphism was determined in the LM by means of SDS-PAGE. The number of piglets born alive was similar in both sow groups, but litter size expressed per uterine horn was lower (P , 0.05) in OL than HO sows. Consequently, OL progeny were markedly heavier (P , 0.01). Regardless of gender, the organs, the brain and the SM were heavier (P , 0.001) in OL and H compared with HO and L offspring, respectively. Compared with HO pigs, the SM of OL offspring tended (P , 0.1) to have more myofibers, which were of larger (P , 0.05) size. However, myofiber density appeared to be lower (P , 0.1) in the SM of OL than HO pigs. The impact of birth weight on myofiber characteristics was limited to the lower (P , 0.05) myofiber density in the SM and the larger (P , 0.01) myofiber size in the light portion of the SM of H than L offspring, whereas myofiber hyperplasia did not differ between birth weight categories. The SM, but not the LM, of male offspring had a greater (P , 0.05) myofiber density. This did not affect total SM myofiber number. The relative abundance of fetal and type I MyHC in the LM was lower (P , 0.05) and that of type II MyHC was greater (P , 0.001) in OL than HO pigs. The current data suggest that regardless of birth weight and gender, in the LM and SM of individuals born from a crowded environment, not only hyperplasia but also hypertrophy of myofibers is impaired and their maturity seems delayed.