Pattern of muscle fiber type formation in the pig

Abstract

The aim of this study was to analyze the temporal sequence of expression of the myosin isoforms in the populations of muscle fibers in the pig and to bring more information on the origin of the strikingly different pattern of fiber composition and distribution between the deep medial red (oxido-glycolytic) and superficial white (glycolytic) portions of semitendinosus (ST) muscle. Muscle samples were taken from 49-, 55-, 75-, 90-, 103-, and 113-(birth) day-old fetuses, from 6-, 11-, 21-, 35-, 50-, and 80-day-old piglets, and from a 3-year-old pig. Our results confirm the sequential formation of primary and secondary generation fibers. The use of immunohistochemistry and heterologous monoclonal antibodies (mAb) directed against specific myosin heavy chain (MHC) isoforms revealed a different pattern of gene expression between the two portions of the ST muscle for both generations of fibers. By 75 days of gestation (dg), primary myotubes from the deep medial portion stained positively for the anti-slow MHC mAb and negatively for the adult anti-fast MHC, whereas the opposite was observed in the superficial portion. Secondary fibers never expressed slow MHC until late gestation. Instead, they expressed an adult fast MHC isoform as soon as they formed in the deep medial portion and later on in the superficial portion. From late gestation to the first 3 postnatal weeks, slow MHC began to be expressed in a subpopulation of secondary fibers. These fibers were in the direct vicinity of primary myotubes in the deep medial portion, whereas their location could not be established in the superficial portion. The remaining secondary fibers matured to type IIA in the direct vicinity of these type I fibers and to type IIB at the periphery of the islets. In both portions of the muscle, a subpopulation of secondary fibers, the first ones to express slow MHC, also transitorily expressed a MHC that was identical or closely related to the a-cardiac MHC during the early postnatal period. A third generation of small diameter fibers was observed shortly after birth and reacted with the anti-fetal MHC mAb; their destiny remains to be established. The present work reveals a remarkable pattern of MHC gene expression in the pig and raises many questions on the real nature of these isoforms. In order to answer these questions, we have undertaken to make a cDNA library of pig skeletal muscle and to screen 0 1995 WILEY-LISS, INC.this library with the same mAbs used in the present study. o 1995 Wiley-Liss, Inc.

Intrauterine crowding impairs formation and growth of secondary myofibers in pigs

“…In addition, primary myofibers can be differentiated by size from the secondary myofibers. This was possible in the LM and the SM dark , whereas, in accordance to observations of Lefaucheur et al (1995), primary and secondary myofibers were not distinguishable in the SM light of newborn pigs using this mATPase histochemistry assay. To determine the cross-sectional area of the total SM, SM dark and SM light , cross-sections of the muscles were stained using anti-slow myosin heavy chain (MyHC) monoclonal antibodies (Novocastra lyophilized mouse monoclonal antibody myosin heavy chain (NCL-MHCs) diluted 1 : 20 in ultrapure water; Novocastra, Newcastle, UK).…”

Effects of l-carnitine supplementation to suckling piglets on carcass and meat quality at market age

“…An early-postnatal increase in total fibre number in pig muscle has been reported to occur in ST muscle cross sections at the mid-belly level (Rehfeldt et al, 2000 and2008b;Bé rard et al, 2011) and can be attributed to two mechanisms. On the one hand, the prenatal formation of primary and secondary myofibres (Wigmore and Stickland, 1983;Lefaucheur et al, 1995) is followed by a third wave of myofibre hyperplasia after birth and gives rise to new fibres. The frequency of these short and thin tertiary fibres decreases within the first weeks after birth (Mascarello et al, 1992;Lefaucheur et al, 1995;Bé rard et al, 2011).…”

“…On the one hand, the prenatal formation of primary and secondary myofibres (Wigmore and Stickland, 1983;Lefaucheur et al, 1995) is followed by a third wave of myofibre hyperplasia after birth and gives rise to new fibres. The frequency of these short and thin tertiary fibres decreases within the first weeks after birth (Mascarello et al, 1992;Lefaucheur et al, 1995;Bé rard et al, 2011). The second mechanism is related to the elongation of intrafascicularly terminating myofibres that already exist at birth.…”

“…This increase could be associated with the early-postnatal appearance of a third generation of fibres (Mascarello et al, 1992;Lefaucheur et al, 1995) or elongation of existing short fibres (Bérard et al, 2011).…”

Advances in research on the prenatal development of skeletal muscle in animals in relation to the quality of muscle-based food. I. Regulation of myogenesis and environmental impact

“…In large mammals (e.g. sheep and pigs), tertiary fibres have also been described developing between the secondaries (Lefaucheur et al, 1995), although this is hotly debated at times. In mammals, formation of new muscle fibres takes place in utero, with the numbers of muscle fibres within each muscle thought to be set around the time of birth (see reviews by Maltin et al, 2001;Picard et al, 2002;Brameld et al, 2003;Chang, 2007;Brameld and Daniel, 2008).…”