Allometric scaling of maximal enzyme activities in the axial musculature of striped bass, Morone saxatilis (Walbaum).

It had been suggested that the activity of anaerobic enzymes in the white muscle of fish increases exponentially with body size to meet the increasing hydrodynamic costs of burst swimming. We tested whether this relationship holds across a very large size range of striped bass, spanning a nearly 3,000-fold range in body mass. We examined the scaling of marker enzymes of anaerobic (lactate dehydrogenase and pyruvate kinase) and aerobic (citrate synthase and malate dehydrogenase) metabolism in the red and white locomotor muscles. In white muscle, we found positive scaling of anaerobic enzymes only in smaller fishes. Positive scaling of anaerobic enzymes was not found among the samples that included fishes >1,000 g despite having a sufficiently large sample size to detect such scaling. The absence of positive scaling in the white muscles of large bass suggests that they are unable to generate sufficient power to sustain relative burst swimming performance. Enzymes from aerobic pathways had activities that were mass independent in both red and white muscle. Red and white muscles were metabolically distinct except among the smallest fishes. Among young of the year, the anaerobic capacity of red muscle approached that of white muscle and also showed positive scaling. This unusual pattern suggests that red muscle might augment white muscle during burst swimming and add to the total power generated by these small fish. Maximizing burst swimming performance may be critical for small fishes vulnerable to predation but unimportant for large fishes.

Variable expression of myoglobin among the hemoglobinless Antarctic icefishes.

The important intracellular oxygen-binding protein, myoglobin (Mb), is thought to be absent from oxidative muscle tissues of the family of hemoglobinless Antarctic icefishes, Channichthyidae. Within this family of fishes, which is endemic to the Southern Ocean surrounding Antarctica, there exist 15 known species and 11 genera. To date, we have examined eight species of icefish (representing seven genera) using immunoblot analyses. Results indicate that Mb is present in heart ventricles from five of these species of icefish. Mb is absent from heart auricle and oxidative skeletal muscle of all species. We have identified a 0.9-kb mRNA in Mb-expressing species that hybridizes with a Mb cDNA probe from the closely related red-blooded Antarctic nototheniid fish, Notothenia coriiceps. In confirmation that the 0.9-kb mRNA encodes Mb, we report the full-length Mb cDNA sequence of the ocellated icefish, Chionodraco rastrospinosus. Of the eight icefish species examined, three lack Mb polypeptide in heart ventricle, although one of these expresses the Mb mRNA. All species of icefish retain the Mb gene in their genomic DNA. Based on phylogeny of the icefishes, loss of Mb expression has occurred independently at least three times and by at least two distinct molecular mechanisms during speciation of the family.

Perinatal changes in avian muscle: implications from ultrastructure for the development of endothermy.

Endothermic heat production and the capacity to shiver develop soon after hatching in birds, permitting chicks to regulate their body temperature. Physiological studies have not clearly identified the developmental events causing this change in function. Here, we use electron microscopy to examine the development of structures involved in muscle activation, contraction, and metabolism coincident with the development of shivering thermogenesis. A stereological study was used to compare the ultrastructure of chicken iliofibularis before endothermic heat production was present (24 h before hatching) and 120 h later, when the iliofibularis had substantial capacity for shivering. Profound increases were found in the t-tubule system and terminal cisternae, mitochondrial cristae, and lipids. The number of triadic profiles increased 3.8-fold (7.6 +/- 1.31/100 microns 2 to 28.5 +/- 2.90/100 microns 2 fiber area). The surface area of cristae per mitochondrial volume doubled (12.0 +/- 1.50 microns 2/microns 3 to 25.7 +/- 1.84 microns 2/microns 3). Lipid droplets were rare in the iliofibularis of embryos about to hatch, but accounted for 4.4% of the muscle fiber volume in day 4 birds. We suggest that these ultrastructural changes more fully activate the iliofibularis, allow it to produce more heat both from calcium pumping and from contraction, and increase its endurance, thus permitting the muscle to be effective in thermogenesis.

A myogenic regulatory gene, qmf1, is expressed by adult myonuclei after injury.

Myogenic regulatory factors (MRFs) induce differentiation in developing muscle. We examined the role of MRFs in the repair of adult muscle using a model of stretch-induced injury in 5-wk-old chickens. The anterior latissimus dorsi muscle was stretched by loading the wing with 10% of body weight, while the contralateral muscle served as a control. At various intervals (0.5-72 h), chickens were killed by CO2 asphyxiation and the muscles were frozen. Slot hybridizations showed that the onset of high qmf1 expression occurred as early as 0.5 h, which was before regenerative processes involving satellite cell proliferation were observed. Maximal qmf1 expression varied among animals from 3 to 16 h and returned to control levels by 72 h. Within a muscle, in situ hybridization showed that maximal qmf1 expression varied spatially with > 60% of the nuclei within active fascicles being positive. We interpret this high percentage to mean that many of the nuclei of preexisting muscle fibers must be expressing qmf1. The expression of the protooncogene c-myc (presumably by proliferating cells such as satellite cells, fibroblasts, and capillary epithelial cells) and the MRF qmf1 (by myoblasts and adult muscle nuclei) are among the early molecular responses of injured muscle. We conclude that myogenic regulatory factors are not permanently repressed after embryonic development and that derepression plays a role in the repair of terminally differentiated myofibers.