Literature DB >> 9066912

Myonuclear loss in atrophied soleus muscle fibers.

R S Hikida1, S Van Nostran, J D Murray, R S Staron, S E Gordon, W J Kraemer.   

Abstract

BACKGROUND: A skeletal muscle fiber consists of many successive "territories," each controlled by the nucleus residing in that territory. Because nuclei appear to control a specific amount of territory (nuclear domain), nuclei must be added to accommodate an increase in fiber size. Because growth and hypertrophy require the addition of nuclei to fibers, it is of interest to determine whether atrophy causes a decrease in myonuclear number. This study compared the myonuclear population in the soleus muscles of rats that had undergone atrophy due to 10 days of spaceflight in the space shuttle, Endeavour, with muscles of ground-based control animals (10 rats each).
METHODS: Myofibrillar ATPase activity was used to determine the major skeletal muscle fiber types in control rats and those having spent 10 days in space, and dystrophin antibodies were used to label the sarcolemma to identify underlying myonuclei.
RESULTS: Type I and II fibers were atrophied after the flight, but type I fibers were atrophied twice as much as type II. Myonuclei were counted in identified and measured fibers, and the distribution normalized to number per millimeter of fiber circumference; this was significantly greater in type II than in type I fibers in both groups of rats. However, although the muscle fibers from flight animals were significantly atrophied, the normalized number of nuclei were identical between control and flight animals, indicating that nuclei decreased in numbers as the fibers atrophied.
CONCLUSION: The nuclear domain is under strict control, and a decrease in the domain, as induced by atrophy, will cause nuclear degeneration and loss, which maintains a relatively constant size of the nuclear domain.

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Year:  1997        PMID: 9066912     DOI: 10.1002/(SICI)1097-0185(199703)247:3<350::AID-AR6>3.0.CO;2-Y

Source DB:  PubMed          Journal:  Anat Rec        ISSN: 0003-276X


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