Muscles of a different 'color'

Abstract

The rules that govern many aspects of skeletal muscle structure and function are very different for the extraocular muscle allotype. The myoblast lineages present in the extraocular muscle primordia are permissive for generation of an unusually wide range of fiber types. The balance that is struck between genetic specification and activity dependent factors in shaping fiber phenotype to suit the demands of complex visuomotor systems is not yet well defined. Because skeletal muscle has high energy demands, diversity in fiber types is needed to maximize efficiency; greater diversity in fiber composition then indicates a more diverse functional repertoire. Together, the characteristics of small motor unit size, precise dependence of muscle force upon motor neuron discharge rate, high contractile speed but low tension development, and contractile protein heterogeneity contribute toward the high precision and diversity that is required for eye movements. Finally, the structural and functional characteristics and plasticity of the individual extraocular muscle fiber types play an important role in determining their response to disease or manipulation. The lack of uniform responses across the muscle allotypes in disease, or in response to pharmaceutical or surgical interventions, requires that we obtain a better understanding of the fundamental differences that exist between muscle groups.

Postnatal suppression of myomesin, muscle creatine kinase and the M-line in rat extraocular muscle

“…Myomesin 2 is initially present in slow-twitch (type I) myofibers but then is lost during postnatal maturation (Carlsson et al, 1990;Grove et al, 1985Grove et al, , 1987Grove et al, , 1989Grove and Thornell, 1988). This observation cannot, however, reconcile the postnatal loss of Myom1, Myom2 and a structural M-line from EOM, since 80-85% of its myofibers are fast-twitch (Porter and Baker, 1996;Porter et al, 1995;Spencer and Porter, 1988), a functional mode generally regarded as dependent upon an M-line and the associated muscle CK. Moreover, while myomesin 2 is lost from postnatal slow-twitch fibers, they still retain morphological M-lines ; myomesin 1 and CK-M may both contribute to the structural M-lines in the absence of myomesin 2.…”

“…During eye movements, there are demands for precision, speed and fatigue resistance that are experienced by few other skeletal muscles. Consequently, EOM is phenotypically unlike other skeletal muscles across a wide range of traits, including basic fiber type classification schemes, gene expression profiles and disease susceptibility (Cheng and Porter, 2002;Fischer et al, 2002;Kaminski et al, 2002;Porter, 2002;Porter and Baker, 1996;Porter et al, 1995Porter et al, , 2001aPorter et al, ,b, 1998. The absence of the M-line system is consistent with known cytoskeletal organization differences between extraocular and other skeletal musculature (Cheng and Porter, 2002;Porter et al, 2001a) and suggests that eye muscle may use novel mechanisms to transmit contractile force to the sarcolemma and tendon.…”

“…We have previously shown that extraocular muscle (EOM) is fundamentally different from other skeletal muscles (Cheng and Porter, 2002;Porter and Baker, 1996;Porter et al, 2001a). Here, we investigated the temporal expression patterns of the M-line and of myomesin and CK isoforms in rat EOMs in comparison with those in other striated muscles.…”

Fiber Types in Mammalian Skeletal Muscles

“…Their specific tension is lower than that developed by limb muscles (503), although some contrasting results have been reported (239). At variance with limb muscles, a very high speed of contraction (159,616) coexists with a relatively high resistance to fatigue (240) correlated with high SDH activity. Adult EOMs express most known striated muscle myosin isoforms, including MyHC-slow tonic, coded by the MYH7b (MYH14) gene (661), MyHC-EO coded by MYH13 and the developmental MyHC-emb and -neo isoforms.…”

Proteomic profiling of naturally protected extraocular muscles from the dystrophin-deficient mdx mouse

“…For example, intrinsic laryngeal and certain distal muscle fibers, as well as extraocular muscle (EOM), are protected from a severely degenerative phenotype in dystrophic organisms [5][6][7][8][9][10][11]. Although the contractile efficiency of EOM is weakened in various muscle-related pathologies, such as myasthenia gravis, myasthenic syndromes, botulism, and myotonia congenita [12][13][14], they are usually spared in DMD patients [15][16][17].…”