This study was carried out to determine effects of electrical stimulation on the soleus, target muscle of the sciatic newt, of white rat normal muscles. The biometric, histochemical, ultrastructural observations were made. The following results were obtained. A daily electrical stimulation of the skeletal muscle of the normally-functioning rat caused an increase of girth and weight of the muscle fibers for 2 weeks. No noticeable change was observed afterwards. More specifically, the density of volume of the red muscle fiber increased. whereas the density of the white muscle fiber decreased. The electrical stimulation group(experimental group) showed hypertrophy of the muscle fibers and narrowing of the space between perimysium and endomysium. Normally, glycogen granules are accumulated regardless of classification of muscle fibers. In addition, the NADH-TR reaction results were in agreement with the biometric findings, in that the red muscle fibers significantly increased. The ultrastructural observations revealed that mitochondria was formed in the red muscle fiber parallel to the muscle fibers of normal muscle, while mitochondria was observed in the sarcomere region of the white muscle fiber. However, activation of mitochondria took place in the sarcolemma region of the muscle fiber, and generation of mitochondria was observed in the sarcomere region of the white muscle fiber.
The aim of this study was to compare features of muscle atrophy induced by cast fixation. denervation and suspension of rat hindimb. Muscle mass and glycogen of the soleus and plantaris muscles were studied after 3, 7, or 14 days of cast fixation, denervation and suspension. The results as follows: 1. Body weight of rats decreased significantly after 3 days and showed gradually increase after 7 and 14 days of hindlimb cast fixation, denervation and suspension. Particularly hindlimb suspended rats showed a rapid decrease after 3 days in body weight. 2. Relative weight of soleus and plantaris musclcs decreased significantly by hindlimb cast fixation, denervation and suspension, particularly after 7 days. The decrease rate was the lowest in suspended rats. 3. Glycogen content of soleus muscle decreased significantly after 14 days of hindlimb cast fixation, denervation and suspension. Also glycogen content of plantaris muscle decreased significantly after 14 days of hindlimb cast fixation and denervation, but not significantly after hindlimb suspension. These results indicate that suspension of hindlimb muscles causes less atropy than cast fixation or denervation, likely due to maintainment a few activities during hindlimb suspension. We concluded that the decrease in mechanical strains imposed on the muscle during inactivity was the main factor for the development of atrophy. These basic data suggest that some experimental conditions such as electrostimulation or stretching, participate in countermeasure programmes.
An, Gyeong-Ju;Lee, Yoon-Kyong;Im, Ji-Hae;Choi, S-Mi;Choe, Myoung-Ae
Journal of Korean Biological Nursing Science
/
v.2
no.2
/
pp.67-80
/
2000
The purpose of this study was to identify hindlimb muscle atrophy in stroke induced rat and determine the effect of endurance exercise on body weight, weight of hindlimb muscle during 7 days after stroke induction. Thirty four male Sprague-Dawley rats with 200-270g body weight were divided into four groups : control, control+exercise(Con+Ex), stroke, and exercise after stroke(St+Ex) group. The control group and Con+Ex group received sham operation and the stroke group and St+Ex group received right MCA occlusion operation by using silicon-coated probe. The Con+Ex and St+Ex groups ran on a treadmill for 20min/day at 10m/min and $10^{\circ}grade$. Daily body weight and diet intake were measured every morning for 7 days. Cerebral infarction of stroke and St+Ex groups were identified by staining with TCC for 30minutes. The data were analyzed by Kruskal-Wallis test and Mann-Whitney U test using the SPSSWIN 9.0 program. Body weight of the control group at the 7th day increased by 18.3% significantly from the first day of experiment, that of the stroke group at the 7th day decreased by 6.7% significantly compared to the day of receiving right MCA occlusion operation. Body weight of the Con+Ex group at the 7th day increased by 10.3% significantly form the first day of experiment, that of St+Ex group at the 7th day also increased by 13.4% significantly compared to the day of receiving right MCA occlusion operation. The total amount of diet in stroke group decreased significantly compared to that of St+Ex and that of control group. In stroke group the wet weight of both sides of soleus, plantaris, and gastrocnemius muscles decreased significantly compared to that of control group. The relative weight of affected(left) plantaris and gastrocnemius muscles decreased significantly compared to that of the control group. The difference between the weight of affected and unaffected soleus, plantaris, and gastrocnemius muscles were not significant in stroke group. The wet weight of right gastrocnemius muscles in Con+Ex group increased compared to that of control group. The relative weight of right gastrocnemius muscle increased significantly compared to that of the control group. The wet weight of St+Ex group increased significantly compared to that of the stroke group in both sides of soleus, plantaris, and gastrocnemius muscles. The relative weight of affected plantaris muscle increased significantly compared to that of the stroke group. The difference between the weight of affected and unaffected soleus, plantaris, and gastrocnemius muscles were not significant in St+Ex group. Body weight and wet weight of soleus, plantaris, and gastrocnemius muscles in the St+Ex group did not recover to the values of control group. Based on these results, it can be suggested that endurance exercise during acute stage of stroke can reduce muscle atrophy related to denervation, inactivity and undernutrition.
The aim of this study was to identify the effect of suspension unloading (SU) and electrical stimulation upon the development of neonatal muscular system. For this study, the neonatal rats were randomly divided into three groups: a control group, an experimental group I, and an experimental group II. The SU for experimental group I and II was applied from postnatal day (PD) 5 to PD 30. The electrical stimulation for soleus muscle of experimental group IIwas applied from PD 16 to PD 30 using neuromuscular electrical stimulation (NMES), which gave isometric contraction with 10 pps for 30 minutes twice a day. In order to observe the effect of SU and ES, this study observed myocyte enhancer factor 2C (MEF2C) and vascular endothelial growth factor (VEGF) immunoreactivity in the soleus muscles at PD 15 and PD 30. In addition, the motor behavior test was performed through footprint analysis at PD 30. The following is the result. At PD 15, the soleus muscles of experimental group Iand II had significantly lower MEF2C, VEGF immunoreactivity than the control group. It proved that microgravity conditions restricted the development of the skeletal muscle cells at PD 15. At PD 30, soleus muscles of the control group and experimental group II had significantly higher MEF2C, VEGF, immunoreactivity than experimental group I. It proved that the NMES facilitated the development of the skeletal muscle cells. At PD 30, it showed that SU caused the decrease in stride length of parameter of gait analysis and an increase in toe-out angle, and that the NMES decreased these variations. These results suggest that weight bearing during neonatal developmental period is essential for muscular development. They also reveal that NMES can encourage the development of muscular systems by fully supplementing the effect of weight bearing, which is an essential factor in the neonatal developmental process.
Background: It is doubtful that aging causes deteriorated glucose metabolism and insulin resistance of skeletal muscle. Some researchers had different results about it. So we have studied the mechanism responsible for the abnormal glucose tolerance associated with aging in rapidly growing and matured rats. Materials and Methods: Animals were used S.D. rats. Growing rats were 7 weeks old (BW: 160-190 gm) and matured rats were 28 weeks old (BW: 420-525 gm). Results: Fasting blood glucose and plasma insulin levels were significantly elevated in matured rat compared with growing rats. And during oral glucose tolerance test the glucose level was also significantly elevated in matured rats. These results confirmed an insulin resistant state of aging. Insulin levels at 30 minutes of oral glucose tolerance test was significantly elevated in growing rat. But at 120 minutes it was maintained at higher level in matured rats than in growing rats. It suggested the possibility of increased insulin secretion by initial stimulation of beta-cells in growing rats, and increased secretion and decreased catabolic rate of insulin in matured rats. Glucose uptake rate of soleus muscle in matured rats was lower than that of growing rats, but the difference was not statistically significant. The dose(insulin)-responsive(glucose uptake) curve of soleus muscle was only slightly deviated to the right side. Conclusion: Glucose metabolism of rat skeletal muscle was worsened by aging. The data of glucose uptake experiments suggested the possibility of insulin resistance of skeletal muscle in matured rats. but the mechanism of insulin resistance of skeletal muscle need further studies.
Purpose: The purpose of this study was to determine the effect of dehydroepiandrosterone (DHEA) on recovery of muscle atrophy induced by Parkinson's disease. Methods: The rat model was established by direct injection of 6-hydroxydopamine (6-OHDA, 20 ${\mu}g$) into the left striatum using stereotaxic surgery. Rats were divided into two groups; the Parkinson's disease group with vehicle treatment (Vehicle; n=12) or DHEA treatment group (DHEA; n=22). DHEA or vehicle was administrated intraperitoneally daily at a dose of 0.34 mmol/kg for 21 days. At 22-days after DHEA treatment, soleus, plantaris, and striatum were dissected. Results: The DHEA group showed significant increase (p<.01) in the number of tyrosine hydroxylase (TH) positive neurons in the lesioned side substantia nigra compared to the vehicle group. Weights and Type I fiber cross-sectional areas of the contralateral soleus of the DHEA group were significantly greater than those of the vehicle group (p=.02, p=.00). Moreover, extracellular signal-regulated kinase (ERK) phosphorylation significantly decreased in the lesioned striatum, but was recovered with DHEA and also in the contralateral soleus muscle, Akt and ERK phosphorylation recovered significantly and the expression level of myosin heavy chain also recovered by DHEA treatment. Conclusion: Our results suggest that DHEA treatment recovers Parkinson's disease induced contralateral soleus muscle atrophy through Akt and ERK phosphorylation.
Purpose: The purpose of this study was to determine the effect of Dehydroepiandrosterone(DHEA) administration alone or exercise combined with DHEA before steroid treatment on rat hindlimb muscles. Methods: Male Sprague-Dawley rats were assigned to one of three groups: a steroid group(S, n=10) that had no treatment for 7 days before steroid treatment; a DHEA-steroid group(DS, n=8) that had 0.34 mmol/kg/day DHEA injection once a day for 7 days before steroid treatment and an exercise+DHEA-steroid group(EDS, n=9) that ran on the treadmill combined with 0.34 mmol/kg/day DHEA injection for 7 days before steroid treatment. At 15 days all rats were anesthetized and soleus, plantaris and gastrocnemius muscles were dissected. Body weight, food intake, muscle weight, myofibillar protein content and cross-sectional area of the dissected muscles were determined. Results: The DS group showed significant increases(p<.05) as compared to the steroid group in body weight, and muscle weight of gastrocnemius muscles. The EDS group showed significant increases(p<.05) as compared to the S group in body weight, muscle weight, myofibrillar protein content, and Type II fiber cross-sectional area of soleus, plantaris and gastrocnemius muscles. Conclusion: Exercise combined with DHEA administration before steroid treatment prevents steroid induced muscle atrophy, with exercise combined with DHEA administration being more effective than DHEA administration alone in preventing muscle atrophy.
Physical activity and exercise can promote sensorimotor recovery from central nerve injury. It has been suggested that the functional recovery promoted by exercise training after spinal cord injury might be associated with insulin-like growth factor-I in the inflicted muscle. To investigate morphological and biochemical change of the soleus muscle after spinal cord injury, all tissues were used for H&E, immunofluorescence staining and Western blot. Also, BBB-test was used to evaluate behavioral improvement after spinal cord contusion. Thirty male Sprague-Dawley rats ($230{\pm}10\;g$; 7week in age) were assigned equally to three different groups; Normal (n=10), SCI (n=10), SCI+TMT (n=10). Every rat in SCI and SCI+TMT groups underwent laminectomy at T9 level and then contusion on the exposed spinal cord site in anesthetized condition. After one week-recovery from contusion, every rat in the SCI+TMT group exercised on a motorized treadmill for 30min/d, 5d/wk for 7wks. TMT followed by injury increased IGF-I induction levels in the soleus muscle and inhibited muscle atrophy. Behavioral scales for 4 and 8 weeks after spinal cord injury were improved in the SCI+TMT group compared to the SCI group. These results suggest that treadmill exercise after spinal cord injury might promote functional recovery along with muscle regrowth through the up-regulation of IGF-1 in muscle tissue.
Chronic alcoholic myopathy is one of the most common skeletal muscle disorders. It is characterized by a reduction in the entire skeletal musculature, skeletal muscle weakness, and difficulties in gait. Patients with alcoholic hepatitis and cirrhosis have severe muscle loss that contributes to worsening outcome. Although the myopathy selectively affects Type II (fast twitch, glycolytic, anaerobic) skeletal muscle fibers, total skeletal musculature is reduced. The severity of the muscle atrophy is proportional to the duration and amount of alcohol consumed and leads to decreased muscle strength. The mechanisms for the myopathy are generally unknown but it is not due to overt nutritional deficiency, nor due to either neuropathy or severe liver disease. Skeletal muscle mass and protein content are maintained by a balance between protein synthesis and breakdown and in vivo animal models studies have shown that ethanol inhibits skeletal muscle protein synthesis. Daekumeumja is a traditional Korean medicine that is widely employed to treat various alcohol-induced diseases. Muscle diseases are often related to liver diseases and conditions. The main objective of this study was to assess that Daekumeumja extract could have protective effect against alcoholic myopathy in a Sprague-Dawley rat model. Rats were orally given 25% ethanol (5ml/kg, body weight) for 8 weeks. After 30 minutes, rats were administrated with Daekumeumja extract. Controls were similarly administrated with the vehicle alone. The weights of gastrocnemius, soleus and plantaris muscles were assessed and the morphologic changes of gastrocnemius and plantaris muscles were also assessed by hematoxylin and eosin staining. In results, The muscles from ethanol treated rats displayed a significant reduction in muscle weight and average cross section area compared to Normal group. Daekumeumja extract treated group showed increased muscle weight and muscle fiber compared to the ethanol treated group. It was concluded that Daekumeumja extract showed ameliorating effects on chronic alcohol myopathy in skeletal muscle.
The hypothesis of this study was that diabetes-induced desensitization of rat soleus (SOL) and extensor digitorum longus (EDL) to non-depolarizing muscle relaxants (NDMRs) depends on the stage of diabetes and on the kind of NDMRs. We tested the different magnitude of resistance to vecuronium, cisatracurium, and rocuronium at different stages of streptozotocin (STZ)-induced diabetes by the EDL sciatic nerve-muscle preparations, and the SOL sciatic nerve-muscle preparations from rats after 4 and 16 weeks of STZ treatment. The concentration-twitch tension curves were significantly shifted from those of the control group to the right in the diabetic groups. Concentration giving 50% of maximal inhibition ($IC_{50}$) was larger in the diabetic groups for all the NDMRs. For rocuronium and cisatracurium in both SOL and EDL, $IC_{50}$ was significantly larger in diabetic 16 weeks group than those in the diabetic 4 weeks group. For SOL/EDL, the $IC_{50}$ ratios were significantly largest in the diabetic 16 weeks group, second largest in the diabetic 4 weeks group, and smallest for the control group. Diabetes-induced desensitization to NDMRs depended on the stage of diabetes and on the different kind of muscles observed while was independent on different kind of NDMRs. The resistance to NDMRs was stronger in the later stage of diabetes (16 versus 4 weeks after STZ treatment). Additionally, when monitoring in SOL, diabetes attenuated the actions of neuromuscular blockade more intensely than that in EDL. Nonetheless, the hyposensitivity to NDMRs in diabetes was not relevant for the kind of NDMRs.
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