Acute molecular responses of skeletal muscle to resistance exercise in able-bodied and spinal cord-injured subjects

Abstract

. Acute molecular responses of skeletal muscle to resistance exercise in ablebodied and spinal cord-injured subjects. J Appl Physiol 94: 2255-2262. First published February 28, 2003 10.1152/japplphysiol.00014.2003.-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. mechano-growth factor; insulin-like growth factor I; insulinlike growth factor binding protein; myogenin INACTIVITY CAN LEAD TO A LOSS of muscle mass and function. Complete spinal cord injury (SCI) leads to inactivation and profound muscle unloading. The muscles of SCI patients are characterized by severe atrophy, as well as extensively altered metabolic and contractile protein profiles (6,19,40). For example, within several months of SCI, muscles and their constituent myofibers can be reduced to ϳ41% of the size of those of able-bodied (AB) individuals (16, 15). The loss in muscle mass and function can contribute to a number of health problems, such as decreased cardiorespiratory fitness, impaired glucose tolerance, and osteoporosis (37, 39).Recognition of potential benefits to be garnered by maintaining or increasing muscle mass in SCI patients has lead to a number of studies aimed at using electromyostimulation (EMS) to induce contractile activity in the muscles of these patients. In AB subjects, EMSinduced resistance exercise has been shown to result in increases in muscle size and performance (13,14,41). Studies have also shown...

Electrical Stimulation During Gait Promotes Increase of Muscle Cross-sectional Area in Quadriplegics: A Preliminary Study

“…The 15% increase in quadriceps CSA confirms previous studies that showed muscle increase in chronic spinal cord-injured patients using NMES in other modalities of therapy [3,19]. Two studies suggest NMES does not reverse muscle atrophy in chronic spinal cord-injured patients [1,16] but can promote moderate increases after muscle contractions against some external load [20,21].…”

“…The inability to find increases in muscle CSA after gait training without NMES was possibly the result of insufficient mechanical load imposed on paralyzed muscles (reduction of 30%-50% of body weight during gait) associated with severity of the spinal cord lesion (complete and extensive lesions). Although the data at the beginning of gait training with and without NMES tended to be different, it has been reported that muscles of subjects with chronic spinal cord injuries can improve after exercise [3,14,19,22]. This fact was observed in subjects with low CSA values in the gait group, who also benefited from the training.…”

“…Decrease in average muscle cross-sectional area (CSA) [8], replacement of Type I muscle fibers by Type II fibers [4], infiltration of adipose tissue inside muscles, reduction in the oxidative enzyme level, mitochondria concentration, and number of capillaries are observed in muscles located below the injury level [3,18,21].…”

Plasma iron levels appraised 15 days after spinal cord injury in a limb movement animal model

“…This provides a possible explanation for muscle atrophy in SCI rats because SCI hinders the rat 0 s movements and leads to diminished locomotor activity. 15,16 A possible limitation of this is that, because of technical problems, ferritin levels were not determined. Such an analysis would be extremely important because ferritin is an endothelial reticulum protein responsible for storing iron, and there is a relationship between serum ferritin levels and the amount of iron stored.…”

“…Compared with CTRL1, the SCI1 (1 day after SCI) and the SHAM1 group showed significantly reduced levels of plasma iron (F (2,15) ¼ 12.008, P ¼ 0.00077; ANOVA) and transferrin (F (2,15) ¼ 25.688, P ¼ 0.00001; ANOVA) ( Figure 1a).…”