In vitro estimates of power output by epaxial muscle during feeding in largemouth bass

Recent work has employed video and sonometric analysis combined with hydrodynamic modeling to estimate power output by the feeding musculature of largemouth bass in feeding trials. The result was an estimate of approximately 69 W kg(-1) of power by the epaxial muscle during maximal feeding strikes. The present study employed in vitro measurements of force, work and power output by fast-twitch epaxial muscle bundles stimulated under activation conditions measured in vivo to evaluate the power output results of the feeding experiments. Isolated muscle bundles from the epaxial muscle, the sternohyoideus and the lateral red or slow-twitch muscle were tied into a muscle mechanics apparatus, and contractile properties during tetanic contractions and maximum shortening velocity (Vmax) were determined. For the epaxial muscles, work and power output during feeding events was determined by employing mean stimulation conditions derived from a select set of maximal feeding trials: 17% muscle shortening at 3.6 muscle lengths/s, with activation occurring 5 ms before the onset of shortening. Epaxial and sternohyoideus muscle displayed similar contractile properties, and both were considerably faster (Vmax approximately 11-13 ML s(-1)) than red muscle (Vmax approximately 5 ML s(-1)). Epaxial muscle stimulated under in vivo activation conditions generated approximately 60 W kg(-1) with a 17% strain and approximately 86 W kg(-1) with a 12% strain. These values are close to those estimated by hydrodynamic modeling. The short lag time (5 ms) between muscle activation and muscle shortening is apparently a limiting parameter during feeding strikes, with maximum power found at an offset of 15-20 ms. Further, feeding strikes employing a faster shortening velocity generated significantly higher power output. Power production during feeding strikes appears to be limited by the need for fast onset of movement and the hydrodynamic resistance to buccal expansion.     

The epaxial-hypaxial subdivision of the avian somite

In all jaw-bearing vertebrates, three-dimensional mobility relies on segregated, separately innervated epaxial and hypaxial skeletal muscles. In amniotes, these muscles form from the morphologically continuous dermomyotome and myotome, whose epaxial-hypaxial subdivision and hence the formation of distinct epaxial-hypaxial muscles is not understood. Here we show that En1 expression labels a central subdomain of the avian dermomyotome, medially abutting the expression domain of the lead-lateral or hypaxial marker Sim1. En1 expression is maintained when cells from the En1-positive dermomyotome enter the myotome and dermatome, thereby superimposing the En1-Sim1 expression boundary onto the developing musculature and dermis. En1 cells originate from the dorsomedial edge of the somite. Their development is under positive control by notochord and floor plate (Shh), dorsal neural tube (Wnt1) and surface ectoderm (Wnt1-like signalling activity) but negatively regulated by the lateral plate mesoderm (BMP4). This dependence on epaxial signals and suppression by hypaxial signals places En1 into the epaxial somitic programme. Consequently, the En1-Sim1 expression boundary marks the epaxial-hypaxial dermomyotomal or myotomal boundary. In cell aggregation assays, En1- and Sim1-expressing cells sort out, suggesting that the En1-Sim1 expression boundary may represent a true compartment boundary, foreshadowing the epaxial-hypaxial segregation of muscle.     

Functional anatomy of the trunk musculature in the slow loris (Nycticebus coucang)

Lorisid locomotor and postural behaviour exhibits a number of features that distinguish it clearly from other primates. The comparative myological study of the trunk in the slow loris (Nycticebus coucang) and the squirrel monkey (Saimiri sp.) presented here reveals differences that are related to unique aspects of lorisid positional behaviour. While quadrupedal running and leaping requires flexion and extension of the spine, slow climbing quadrupedalism in lorisids depends on spinal lateral flexion and rotation. The contrasting development of the epaxial musculature in the two species dissected reflects these different requirements. Bipedal suspension is a common posture in the lorisids during which rotation and dorsiflexion of the head is made possible by the robustly developed deep, dorsal, cervical musculature. The long lower lever arm in the M. rectus abdominis may play a significant role in the ventroflexion required to regain a quadrupedal stance. © 1995 Wiley-Liss, Inc.     

Hedgehog signaling regulates the amount of hypaxial muscle development during Xenopus myogenesis

Hedgehog (Hh) signaling is proposed to have different roles on differentiation of hypaxial myoblasts of amniotes. Within the somitic environment, Hh signals restrict hypaxial development and promote epaxial muscle formation. On the other hand, in the limb bud, Hh signaling represses hypaxial myoblast differentiation. This poses the question of whether differences in response to Hh signaling are due to variations in local environment or are intrinsic differences between pre- and post-migratory hypaxial myoblasts. We have approached this question by examining the role of Hh signaling on myoblast development in Xenopus laevis, which, due to its unique mode of hypaxial muscle development, allows us to examine myoblast development in vivo in the absence of the limb environment. Cyclopamine and sonic hedgehog (shh) mRNA overexpression were used to inhibit or activate the Hh pathway, respectively. We find that hypaxial myoblasts respond similarly to Hh manipulations regardless of their location, and that this response is the same for epaxial myoblasts. Overexpression of shh mRNA causes a premature differentiation of the dermomyotome, subsequently inhibiting all further growth of the epaxial and hypaxial myotome. Cyclopamine treatment has the opposite effect, causing an increase in dermomyotome and a shift in myoblast fate from epaxial to hypaxial, eventually leading to an excess of hypaxial body wall muscle. Cyclopamine treatment before stage 20 can rescue the effects of shh overexpression, indicating that early Hh signaling plays an essential role in maintaining the balance between epaxial and hypaxial muscle mass. After stage 20, the premature differentiation of the dermomyotome caused by shh overexpression cannot be rescued by cyclopamine, and no further embryonic muscle growth occurs.