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

摘要

Endurance training provokes structural and regulatory adaptation in both healthy and diseased mammalian hearts that can protect against lethal arrhythmias. 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. The purpose of the skeletal muscle study was to assess the effect of 10-weeks endurance training (progressive treadmill run) on myosin heavy chain (MHC) isoforms protein expression in canine skeletal muscles. Nineteen purpose-bred female mongrel dogs were randomly assigned to either endurance trained (ET) (n = 10) or sedentary control (SC) (n = 9) (cage rest) groups. A progressive aerobic training protocol was used to train the exercise group for 10-weeks. At the completion of the 10-weeks study period, dogs were euthanized and samples of skeletal muscles [diaphragm & extensor digitorum longus (EDL)] 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).; In the cardiac muscle, we tested the effects of 10-weeks of endurance training (progressive treadmill running) on the cardiac oxidative capacity, left ventricular wall thickness, and CnA protein expression in dogs either susceptible (n = 12) or resistant (n = 10) to ventricular fibrillation. The animals were randomly assigned into four groups [susceptible/endurance trained (S/ET), n = 6 - susceptible/sedentary control (S/SC) n = 6, - resistant/endurance trained (R/ET), n = 4 - resistant/sedentary control (R/SC), n = 6]. At the completion of the 10-week training or 10-week control period, citrate synthase (CS) activity was assayed for each heart chamber. 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. (Abstract shortened by UMI.)