Intrauterine crowding impairs formation and growth of secondary myofibers in pigs

Abstract

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.

Impact of dietary l-arginine supply during early gestation on myofiber development in newborn pigs exposed to intra-uterine crowding

“…One approach to enhance hyperplasia is by supplementing l -arginine to the sows during early gestation, shown to be leading to increased formation of P myofibers, which serve as a scaffold for the development of the S myofibers [13]. To alter the intra-uterine environment, either unilateral ovary-hysterectomy or unilateral oviduct ligation of sows can be applied, where sows subjected to the latter procedure have shown to display minimal crowding and adequate placental development [18]. Thus, compared with intact natural crowded sows as used in the current study, OL sows with average prolificacy are suitable models for investigating the consequences of IUC and IUGR in newborn piglets.…”

“…It involved five OL sows originating from a previous experiment of Pardo et al [18] and five prolific IN sows. The five IN sows were siblings to the five OL sows.…”

Exposure to ergot alkaloids during gestation reduces fetal growth in sheep

“…Intrauterine growth restriction of the fetus during the second trimester of gestation reduces the formation of secondary muscle fibers. The ratio of secondary to primary muscle fibers is reduced with intrauterine crowding in pigs (i.e., runt pig, Aberle, 1984; Pardo et al, 2013) and maternal under-nutrition from d 28 to 78 in sheep (Zhu et al, 2004). Cross-sectional area was also reduced ( P < 0.05) in slow and fast-MHC myofibers of the LT and ST muscles in E+ compared to E− (Figure 5).…”

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

“…Ward and Stickland (1991) concluded that in pigs myofibre hyperplasia is completed by day 90 of gestation, whereas recent data suggest that naturally or due to dietary interventions a certain increase in myofibre number occur within the first weeks of life (Lösel et al, 2009;Bérard et al, 2011). Nevertheless, the available data unequivocally show that at birth low birth weight pigs have fewer myofibres but of greater size compared with their higher birth weight littermates (Pardo et al, 2013). In this study, mean myofibre size was 15 and 10% greater in the LM and STM dark , respectively, in L barrows but no morphometric changes in muscle characteristics were observed.…”