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Molecular adaptations of cardiac and skeletal muscles to endurance training in a canine model of sudden death

Moustafa, Moustafa Bayoumi

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2005, Doctor of Philosophy, Ohio State University, Physical Activity and Educational Services.
The present study investigated the effects of 10-weeks of endurance training (progressive treadmill running) on the adaptation of cardiac and skeletal muscles in a canine model of sudden death. At the completion of the 10-weeks study period, dogs were euthanized and samples of skeletal muscles [diaphragm & extensor digitorum longus (EDL)], and heart were dissected, trimmed of visible fat and connective tissues, and then frozen in liquid nitrogen. SDS-PAGE gels were used to analyze myosin heavy chain isoforms and Western blotting was used to assay the protein expression of calcineurin A (CnA). An echocardiogram was used to measure left ventricular (LV) systolic wall thickness. The diaphragm muscle of ET animals showed a significant increase in MHC IIa (P<0.003) concomitant with a significant decrease in MHC I (P<0.03). The EDL muscle of ET animals showed a significant decrease in MHC I (P<0.009). There were no significant changes in either MHC IIa or MHC IId/x. CnA protein did not significantly change in either diaphragm or EDL. These data suggest that endurance training may induce a shift in MHC isoforms independent of changes in CnA protein expression. In the cardiac muscle, left ventricle (LV) citrate synthase activity was significantly lower (-40.3%) in the Susceptible/sedentary control (S/SC) compared to the resistant/sedentary control group (R/SC) (1103.8±221.6 vs. 1848.3±194.2 µmol/mg protein/min, p < 0.05). Endurance training increased (35.5%) LV CS activity in the susceptible dogs [susceptible/endurance trained (S/ET), 1711.3±138.5 vs. S/SC 1103.8±221.6 µmol/mg protein/min, p < 0.05] but did not alter this activity in the resistant/endurance trained (R/ET) dogs. Training also induced a significant (p < 0.025) increase in LV systolic wall thickness (S/ET, pre 10 ± 0.3, post 11.2 ± 0.5; R/ET pre 8.8 ± 0.5, post 9.8 ± 0.5 mm), but CnA protein expression in the LV did not change. These data suggest that CS activity is impaired in susceptible dogs and that this deficit can be corrected by endurance training. Furthermore, endurance training can elicit ventricular hypertrophy without increasing CnA protein expression.
Timothy Kirby (Advisor)

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Citations

  • Moustafa, M. B. (2005). Molecular adaptations of cardiac and skeletal muscles to endurance training in a canine model of sudden death [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1133375886

    APA Style (7th edition)

  • Moustafa, Moustafa. Molecular adaptations of cardiac and skeletal muscles to endurance training in a canine model of sudden death. 2005. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1133375886.

    MLA Style (8th edition)

  • Moustafa, Moustafa. "Molecular adaptations of cardiac and skeletal muscles to endurance training in a canine model of sudden death." Doctoral dissertation, Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1133375886

    Chicago Manual of Style (17th edition)