| The muscle atrophy generally occurred after spinal cord injury distal to the site of injury .muscle mass and myofiber across-sectional area( CSA ) with different fiber types decreased .but the major muscles consisted of type I fibers ,which are postural muscles ,atrophy to the most extent .skeletal atrophy usually is combined with the loss of myofibers nuclei and may be caused by spinal transection, spinal cord isolation ,space flight , hindlimb disuse and denervation .most of studies mainly focused on the solues because of postural muscles and composing of 85-90% type I myofibers ,which is susceptible to atrophy .there has been much dispute over the loss of myofiber nuclei occurring in all fibers types, but it was obvious that the type I myofiber atrophy was excessive to type II .in addition .there have been some evidence to support the loss of myofibers nuclei associated with apoptotic nuclie .Although there is some controversy on the plantaris atrophy whether it is related to the loss of myofiber nuclei ,the hypertrophy of plantaris is combined with an increase in the number of myofiber nuclei . Other studies have showed that the muscles hypertrophy has to be associated with the proliferation of satellite cells .The previous tests supported that the exercise beginning soon after spinal cord injury may be decreased in the extent of muscles atrophy by involvement of satellite cells .The results showed that number of solues nuclei can't be restored by exercise after SCI ,although CSAof myofibers increased .It indicated that the increase in muscles size may occur without addition of myofibers nuclei ,and there is much plasticity in the domain of muscles nuclear .Insulin-growth factor (IGF) is involved in satellite cells proliferation and division .It is expressed with muscles damage or degeneration, which is very essential to the muscles regeneration , because the neutralizing antibodies to IGF inhibits this process .In addition , it has been proved that IGF-I is involved in the muscles hypertrophy process. The levels of IGF-I mRNA and protein obviously increased under hypertrophic conditions .Myofibers hypertrophy in transgenic rats was associated with IGF-I overexpression. Local injection in adult rats may result to muscles hypertrophy. Otherwise there is some controversy on IGF-I involved in attenuation of muscles atrophy.Whether transplantations of fetal spinal cord tissue and cycling exercise have effects on the changes of myosin heavy chain and fibers size after spinal cord transection at low thoracic cord in rats .Muscles disuse model may lead to a cascade changes of fibers size ,metabolic activity and function .The characteristic changes of muscles are decreasing in mass .fibers atrophy ,expression of myosin heavy chain after SCI, for example increase in expressing in type II isoforms . These changes occurred shortly after SCI ,and interruption of delivering information through spinal cord resulted the loss of muscles extension and endurance .The rapid shifting of muscles phenotypes from slow type to fast type supported that the proper neural activities are very important for keeping the expression of slow myosin heavy chain .The muscles are not damaged directly by spinal cord transection .The denervation of muscles isn't muscles physical damage ,and itmay be a change caused by the interruption of delivering information through motoneuron .The motoneurons distal to the lesion site absent of dominating from higher-up neurons will affect its' stimulation and phase activation , subsequently affect muscles contraction and metabolism .The cross domination of muscles further explained that motoneurons have effect on muscles construction and function ,but whether it is only one regulating factor on MHC expression , for example hormone especially thyroid hormones may regulate positively the fast fibers changes independent of denervation .A means of restoring spinal cord injury is neural tissue transplantation .The impaired neurons can be replaced by fetal spinal tissue ,it was proved that axonal integration will occur between host spinal cord and transplants by directly growing into and through transplants, or by axonal connecting between host and transplants . Fetal spinal tissue and peripheral nerve transplants may support axonal growing through the lesion site , leading to axonal activation and electric spreading by transplants , also these meliorated locamotion , until recently there were less notices about possible effect of transplants on hidlimb muscles .The possible effects of transplanted neurons on hindlimb muscles can be shown by serotonergic neurons transplanted distal to the lesion site after spinal cord transection.In this study, an exercise program and fetal spinal cord transplantation were utilized to restore descending spinal pathways and determine whether this mean can regulate the influence of spinal cord injury on hindlimb muscles. The recovery of hindlimb function requires innervation, maintaince of contractile strength and endurance of hindlimb muscles . The second is to investigate the exercise effect of hindlimb on muscles changes after spinalcord injury. In human there are many ways of endurance exercise to increase the oxidative capacity and decrease the fatigability of muscles, although the ability to convert myofibers from type II MHC to type I MHC is controversial. Methods: Rats were divided into five groups (n=5 per group): control, nontransected;spinal cord transected at T10 , transplants were made simultaneously in TxTp and TxExTp groups.daily cycling exercise was initiated 5 days after surgery in TxEx and TxExTp, with all animals being sacrificed 60 days after surgery. The soleus and plantaris muscle and spinal cord were dissected , which were used as analysis of immunohistochemistry and Northenblorts and spinal cord morphology. Results: muscles is normally composed of myofibers expressing either type I (90%) or type Ila (10%) MHC. Following a spinal transection, expression of type I MHC isoform decreased (18% of myofibers), type Ila MHC expression increased (65% of myofibers). Most myofibers coexpressed multiple MHC isoforms. there was a decrease in the number of myofibers expressing type I or Ila isoforms but little change in expression of IIx MHC. Transection resulted in atrophy of type I myofibers to approximately 50% of normal size, whereas myofibers were significantly larger after TxEx (74% of control) and in TxTp (77% of control). Type Ila myofibers also were significantly larger in TxTp compared with the Tx only group. Furthermore, myofiber nuclear number of soleus was decreased by 40% in Tx and was not affected in TxEx or TxTp but was restored in TxExTp. A strong correlation (r = 0.85) between myofiber cross-sectional area and myofiber nuclear number was observed in soleus, but not in plantaris muscle, in which myonuclear number did not change with any of the experimental manipulations. 5'-Bromo-2'-deoxyuridine-positive nuclei inside the myofibermembrane were observed in Tx- ExTp soleus muscles, indicating that satellite cells had divided and subsequently fused into myofibers, contributing to the increase in myonuclear number. The increase in satellite cell activity did not appear to be controlled by the insulin-like growth factors (IGF), as IGF-I and IGF-II mRNA abundance was decreased in Tx soleus and plantaris, and was not restored with the interventions. The composition of the transplant tissue resembled that of normal, mature spinal cord tissue, except for the lack of distinct areas of gray and white matter. Small and medium-sized neurons surrounded by numerous glial cells were dispersed throughout the transplant .there were larger changes in transplants sizes and the extent of integration with host among animals. Conclusion: the mean myofiber size was significantly greater after TxEx and TxTp compared with myofibers in Tx only animals. Thus, although neither strategy shifted the MHC profile towards the control, both interventions influenced the extent of atrophy observed after spinalization. These data suggest that palliative strategies can be developed to modulate some of the changes in hind limb muscles that occur following a spinal cord injury.
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