Skip to Main Content
 

Global Search Box

 
 
 
 

Files

File List


osu1095372379.pdf (507.33 KB)

ETD Abstract Container

Abstract Header

Exercise-induced mechanisms of muscle adaptation in mdx mice

Lekan, Jaimy Marie
http://rave.ohiolink.edu/etdc/view?acc_num=osu1095372379

Abstract Details

2004, Doctor of Philosophy, Ohio State University, Educational Studies: Hums, Science, Tech and Voc.
Duchenne Muscular Dystrophy (DMD) is a genetic disease that results from absence of the dystrophin protein, affects 1 in 3,500 male births, and leads to death by late teens to early twenties. Absence of the dystrophin protein leads to muscle wasting and cardiomyopathy due to compromised plasma membrane structure and impaired force transduction. Endurance exercise training involving cardiovascular overload may aid in maintenance and function of muscle. Hypotheses were tested to determine if endurance exercise training altered: a.) skeletal muscle fiber type composition; b.) regeneration and collagen accumulation in skeletal muscle; and c.) cardiomyopathic features in the mdx and delta-cys/mdx animals. Methods: Six groups of nine animals were studied: C57/BL10 (C57) sedentary, C57 swim, mdx-sedentary, mdx –swim, delta-cys/mdx-sedentary, and delta-cys/mdx-swim. Mice were progressively swim-trained five days/week for 10 weeks, while forelimb grip strength measurements were taken weekly and swim time to exhaustion was recorded at each session. Following training, soleus, extensor digitorum longus, quadriceps, diaphragm, and cardiac muscles were excised. Myosin heavy chain isoform composition, regeneration of myofibers and collagen content were examined. Cardiac tissue cross sections were examined for evidence of cardiomyopathy. Results: Exercise training led to an increase in forelimb grip strength in mdx, delta-cys/mdx, and C57 mice compared with non-swim trained mice. Swimming resulted in increases of type IIa and decreases of type IIx myosin heavy chain proportions in diaphragm muscles of mdx mice. Swim training did not cause increased damage in any skeletal muscle examined from mdx, delta-cys/mdx, or C57 animals. Furthermore, swimming did not cause significant increases in parameters of cardiomyopathy in dystrophic animals. Conclusion: The swim training protocol used in the present investigation resulted in training adaptations in mdx and delta-cys/mdx mice, and did not cause any additional damage to skeletal or cardiac muscles of the animals. Further examination is needed to determine if the training adaptations lead to functional improvements in these dystrophic animals. Analysis: Comparisons of dependent variables between groups were made using an ANOVA. Bonferroni and Dunnett’s T3 post-hoc tests were used to determine where differences existed. Alpha level was set a priori at p < 0.05.
Steven Devor (Advisor)
77 p.
dystrophin; swim training; Duchenne muscular dystrophy

Recommended Citations

Citations

  • Lekan, J. M. (2004). Exercise-induced mechanisms of muscle adaptation in mdx mice [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1095372379

    APA Style (7th edition)

  • Lekan, Jaimy. Exercise-induced mechanisms of muscle adaptation in mdx mice. 2004. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1095372379.

    MLA Style (8th edition)

  • Lekan, Jaimy. "Exercise-induced mechanisms of muscle adaptation in mdx mice." Doctoral dissertation, Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1095372379

    Chicago Manual of Style (17th edition)

osu1095372379
1,278
© 2004, all rights reserved.
This open access ETD is published by The Ohio State University and OhioLINK.