title: Acute molecular responses of skeletal muscle to resistance exercise in able-bodied and spinal cord-injured subjects.
abstract: Spinal cord injury (SCI) results in muscle atrophy, which contributes to a number of health problems, such as cardiovascular deconditioning, metabolic derangement, and osteoporosis. Electromyostimulation (EMS) holds the promise of ameliorating SCI-related muscle atrophy and, therefore, improving general health. To date, EMS training of long-term SCI subjects has resulted in some muscle hypertrophy but has fallen short of normalizing muscle mass. The aim of this study was to compare the molecular responses of vastus lateralis muscles from able-bodied (AB) and SCI subjects after acute bouts of EMS-induced resistance exercise to determine whether SCI muscles displayed some impairment in response. Analysis included mRNA markers known to be responsive to increased loading in rodent muscles. Muscles of AB and SCI subjects were subjected to EMS-stimulated exercise in two 30-min bouts, separated by a 48-h rest. Needle biopsy samples were obtained 24 h after the second exercise bout. In both the AB and SCI muscles, significant changes were seen in insulin-like growth factor binding proteins 4 and 5, cyclin-dependent kinase inhibitor p21, and myogenin mRNA levels. In AB subjects, the mRNA for mechano-growth factor was also increased. Before exercise, the total RNA concentration of the SCI muscles was less than that of the AB subjects but not different postexercise. The results of this study indicate that acute bouts of resistance exercise stimulate molecular responses in the skeletal muscles of both AB and SCI subjects. The responses seen in the SCI muscles indicate that the systems that regulate these molecular responses are intact, even after extended periods of muscle unloading.
authors.affiliation: Department of Exercise Science, University of Georgia, Athens, Georgia 30602, USA.
authors.forename: C Scott
authors.initials: CS
authors.lastname: Bickel
authors.forename: Jill M
authors.initials: JM
authors.lastname: Slade
authors.forename: Fadia
authors.initials: F
authors.lastname: Haddad
authors.forename: Gregory R
authors.initials: GR
authors.lastname: Adams
authors.forename: Gary A
authors.initials: GA
authors.lastname: Dudley
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000235:genetics; D004558:Electric Stimulation; D005260:Female; D006801:Humans; D018974:Insulin-Like Growth Factor Binding Protein 4 / Q000235:genetics; D018975:Insulin-Like Growth Factor Binding Protein 5 / Q000235:genetics; D007866:Leg; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D018008:Myogenin / Q000235:genetics; D009994:Osmolar Concentration; D012333:RNA, Messenger / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D014891:Weight Lifting
chemical_list: C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D018974:Insulin-Like Growth Factor Binding Protein 4; D018975:Insulin-Like Growth Factor Binding Protein 5; C503799:MYOG protein, human; D018008:Myogenin; D012333:RNA, Messenger