期刊
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
卷 279, 期 4, 页码 C1290-C1294出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.2000.279.4.C1290
关键词
dystrophin; force deficit; sarcolemma; myofibrils; strain
资金
- NIAMS NIH HHS [AR40864] Funding Source: Medline
- NIA NIH HHS [AG15434] Funding Source: Medline
Muscle fibers of mdx mice that lack dystrophin are more susceptible to contraction-induced injury, particularly when stretched. In contrast, transgenic mdx (tg-mdx) mice, which overexpress dystrophin, show no morphological or functional signs of dystrophy. Permeabilization disrupts the sarcolemma of fibers from muscles of mdx, tg-mdx, and control mice. We tested the null hypothesis stating that, after single stretches of maximally activated single permeabilized fibers, force deficits do not differ among fibers from extensor digitorum longus muscles of mdx, tg-mdx, or control mice. Fibers were maximally activated by Ca2+ (pCa 4.5) and then stretched through strains of 10%, 20%, or 30% of fiber length (L-f) at a velocity of 0.5 L-f/s. Immediately after each strain, the force deficits were not different for fibers from each of the three groups of mice. When collated with studies of membrane-intact fibers in whole muscles of mdx, tg-mdx, and control mice, these results indicate that dystrophic symptoms do not arise from factors within myofibrils but, rather, from disruption of the sarcolemmal integrity that normally provides protection from contraction-induced injury.
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