The purpose of this study was to determine the effect of periodic low-intensity exercise during hindlimb suspension on the mass, relative weight, myofibrillar protein content in soleus, plantaris and gastrocnemius muscles. To examine the effectiveness of periodic low-intensity exercise on mass, and myofibrillar protein content of hindlimb muscles, adult female Wistar rats were suspended(HS) and half of these rats walked on a treadmill for 45min/day(15 min every 4h) at 5m/min and a $15^{\circ}$ grade(HS-EX). Soleus wet weight was 33.51% significantly smaller(p<0.005) and relative soleus weight of hindlimb suspended rats was 31.96% smaller(p<0.005) compared with those of control rats following seven days of hindlimb suspension. Plantaris wet weight was 7.5% smaller(p<0.01) and relative plantaris weight was 11.83% smaller(p<0.05) compared with those of control rats following seven days of hindlimb suspension. Gastrocnemius wet weight was 11.31% significantly smaller(p<0.005) and relative gastrocnemius weight was 17.13% significantly smaller(p<0.005) compared with those of control rats following seven days of hindlimb suspension. Soleus wet weight while increased by relative soleus weight increased by 25.13%, 27.59% each through periodic low intensity exercise during hindlimb suspension(p<0.05, p<0.05). Plantaris wet weight and relative plantaris weight increased by 1.04%, 10.98%(p<0.05) each, and gastrocnemius wet weight and relative gastrocnemius weight increased by 1.98%, 12.02%(p<0.05) each through periodic low intensity exercise during hindlimb suspension. Wet weight of soleus, plantaris and gastrocnemius in HS-EX rats did not recover to control level. Myofibrillar protein content of soleus, plantaris and gastrocnemius was 48.24%, 40.85% and 37.33% significantly smaller(p<0.005) respectively compared with those of control rats following seven days of hindlimb suspension. Myofibrillar protein content of soleus, plantaris and gastrocnemius increased by 40.68%, 25.07% and 17.93%(p<0.005) each through periodic low intensity exercise during hindlimb suspension. Myofibrillar protein content of soleus, plantaris, and gastrocnemius in HS-EX rats did not recover to control level. The results suggest that periodic low intensity exercise can attenuate hindlimb muscle atrophy induced by hindlimb suspension.
This study investigated how dietary fat affects muscle atrophy and lipid metabolism in various muscles during hindlimb immobilization in rats. Twenty-four male Sprague?Dawley rats had their left hindlimb immobilized and were divided into four groups by dietary fat content and composition. The contralateral hindlimb (control) was compared with the immobilized limb in all dietary groups. Rats (n = 6/group) were fed a 4% corn oil diet (CO), 2.6% corn oil + 1.4% fish oil diet (FO), 30% corn oil diet (HCO), or a 30% beef tallow diet (HBT)after their hind limbs were immobilized for 10 days. Data were collected for the gastrocnemius, plantaris and soleus muscles. Muscle atrophy was induced significantly after 10 days of hindlimb immobilization, resulting in significantly decreased muscle mass and total muscle protein content. The protein levels of peroxisome proliferator activated receptor ${\delta}$ (PPAR${\delta}$) in the plantaris, gastrocnemius, and soleus increased following hindlimb immobilization irrespective of dietary fat intake. Interestingly, the PPAR${\delta}$ mRNA level in the plantaris decreased significantly in all groups and that in the FO group was lower than that in the other groups. The soleus PPAR${\delta}$ mRNA level decreased significantly following hindlimb immobilization in the FO group only. Muscle carnitine palmitoyl transferase 1 (mCPT1) mRNA level was not affected by hindlimb immobilization. However, the mCPT1 mRNA level in the FO group was significantly lower in the plantaris but higher in the soleus than that in the other groups. The pyruvate dehydrogenase kinase 4 (PDK4) mRNA level in the plantaris decreased significantly, whereas that in the soleus increased significantly following hindlimb immobilization. The plantaris, but not soleus, PDK4 mRNA level was significantly higher in the FO group than that in the CO group. The increased PPAR${\delta}$ protein level following hindlimb immobilization may have suppressed triglyceride accumulation in muscles and different types of dietary fat may have differentially affected muscle atrophy according to muscle type. Our results suggest that ${\omega}$-3 polyunsaturated fatty acids may suppress muscle atrophy and lipid accumulation by positively affecting the expression level and activity of PPAR${\delta}$ and PPAR${\delta}$-related enzymes, which are supposed to play an important role in muscle lipid metabolism.
Purpose: The purpose of this study was to determine the effect of DHEA on hindlimb muscles(soleus, plantaris and gastrocnemius) in a focal brain ischemia model rat. Method: Twenty-seven male Sprague-Dawley rats were randomly divided into three groups: CINS(cerebral ischemia + normal saline), CIDH(cerebral ischemia + DHEA), or SHNS(sham + normal saline). Both the CINS and CIDH groups underwent a transient right middle cerebral artery occlusion operation. In the SHNS group, a sham operation was done. 0.34mmol/kg DHEA was administered daily by an intraperitoneal injection for 7days. Results: The muscle weight, muscle fiber cross-sectional area of the Type I muscle fiber of soleus and Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of gastrocnemius, and muscle strength in the CINS group decreased compared with the SHNS group. The muscle weight, muscle fiber cross-sectional area of the Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of soleus, and muscle strength in the CIDH group increased compared with the CINS group. Conclusion: It was identified that muscle atrophy could be induced during 7 days after a cerebral infarction, and DHEA administration during the early stages of a cerebral infarction might attenuate muscle atrophy.
This experimental study was designed to investigate the effects of Cibotii Rhizoma on the muscle atrophy induced by hindlimb suspension in rats. The measurement has been performed on the activity of CK, aldolase, LDH, AST, ALT and quantity of creatine in serum of hindlimb suspension rats. The results were as ; 1. Cibotii Rhizoma significantly inhibited the increase of the activity of CK in serum. 2. Cibotii Rhizoma significantly inhibited the increase of the quantity of creatine in serum. 3. Cibotii Rhizoma significantly inhibited the increase of the activity of aldolase in serum. 4. Cibotii Rhizoma significantly inhibited the increase of the activity of LDH in serum. 5. Cibotii Rhizoma significantly inhibited the increase of the activity of AST in serum. 6. Cibotii Rhizoma significantly inhibited the increase of the activity of ALT in serum.
Purpose: The purpose of this study was to examine the effects of cerebral ischemia on Type I(soleus) and Type II(plantaris, gastrocnemius) muscles, and to determine the effects of isometric contraction training by electro- stimulation on Type I and II muscles in cerebral ischemia model rats. Method: Twenty-five male Sprague-Dawley rats were randomly divided into four groups: ST(stroke), STES(stroke+electrostimulation), SH(sham) and SHES (sham+electrostimulation). The ST and STES groups received a transient right middle cerebral artery occlusion operation. The SH and SHES groups received a sham operation. The STES and SHES groups had daily isometric contraction training by electrostimulation(100Hz, 45mA, 7.5V) on hindlimb muscles for 7days. Result: Plantaris and gastrocenmius muscle weight, myofibrillar protein contents of soleus and gastrocnemius, and the muscle fiber cross-sectional area of gastrocnemius in the ST group significantly decreased compared with the SH group. Soleus, plantaris, gastrocnemius muscle weight, myofibrillar protein contents of soleus and gastrocnemius, and the Type I muscle fiber cross-sectional area of soleus and the Type II muscle fiber cross-sectional area of gastrocnemius in the STES group significantly increased compared with the 57 group. Conclusion: Hindlimb muscle atrophy occurs after acute stroke and isometric contraction training by electrostimulation during early stages of a stroke attenuates muscle atrophy of Type I and Type II muscles.
Objective: This study was conducted to confirm the effect of physiotherapy on the balance and walking in dog with sciatic nerve injury and degenerative arthritis of stifle joints. Design: Single case study Methods: The dog walked abnormally for six months and was administrated in S animal hospital. The dog's right hindlimb was operated for cranial cruciate ligament repair and the dog had been taking a nonsteroidal anti-inflammatory analgesic before being refered. There was severe degenerated osteoarthritis in the right hindlimb. During stance and walking, the right hindlimb was often shown partial weight bearing. The dog's left hindlimb was shown plantigrade stance and walking. The radiograph was shown an intact calcaneal tendon in the left hindlimb. In the neurologic examination, sciatic nerve injury in the left hindlimb was confirmed. The dog was treated using muscle strengthening, proprioceptive exercise, underwater treadmill and Laser therapy two, or three times a week for 3 months. At the 10th and 17th treatment, it was evaluated through stance and gait analyzer system to measure dog's balance and walking. Results: 3 months following physiotherapy, the dog's balance was improved in center of pressure(COP). And peak vertical force(PVF), vertical impulse(VI) was increased in right hindlimb and double stance was decreased. Conclusions: Physiotherapy may have improved the prognosis in this dog with severe osteoarthritis and sciatic nerve injury. This study suggested that animal physiotherapy is a valuable way to improve balance and walking.
Purpose: The purpose of this study was to examine effects of decreased locomotor activity on mass, Type I and II fiber cross-sectional areas of ipsilateral and contralateral hindlimb muscles 21 days after establishing the Parkinson's disease rat model. Methods: The rat model was established by direct injection of 6-hydroxydopamine (6-OHDA, 50 ${mu}g$) into the left substantia nigra after stereotaxic surgery. Adult male Sprague-Dawley rats were assigned to one of two groups; the Parkinson's disease group (PD; n=17) and a sham group (S; n=8). Locomotor activity was assessed before and 21 days after the experiment. At 22 days after establishing the rat model, all rats were anesthetized and soleus and plantaris muscles were dissected from both ipsilateral and contralateral sides. The brain was dissected to identify dopaminergic neuronal death of substantia nigra in the PD group. Results: The PD group at 21 days after establishing the Parkinson's disease rat model showed significant decrease in locomotor activity compared with the S group. Weights and Type I and II fiber cross-sectional areas of the contralateral soleus muscle of the PD group were significantly lower than those of the S group. Conclusion: Contralateral soleus muscle atrophy occurs 21 days after establishing the Parkinson's disease rat model.
The purpose of this study was to determine the effect of regular exercise during dexamethasone injection on the body weight, weight of hindlimb muscles and adrenal gland in Young rats. 80-100g Wistar rats were divided into control, exercise, dexamethasone injection(dexa), and exercise during dexamethasone injection(D+E) group. The dexa group received daily subcutaneous injection of dexamethasone at a dose of 5mg/kg body weight for 10 days. The exercise group ran on a treadmill for 60min /day(20 minutes every 4 hour) at l0m/min and a 10$^{\circ}$ grade. The control group received daily subcutaneous injection of normal saline at a dose of 5mg /kg body weight for 10 days. The D+E group ran on a treadmill for 60min /day (20 minutes every 4 hour) at 10m/min and a 10$^{\circ}$ grade. Body weight of both control and exercise group increased significantly until 10 days, that of both dexa and D+E group decreased significantly, resulting in 79.47 and 78.75% decrease respectively compared to the first day of experiment. Body weight and muscle weight of the soleus, plantaris and gastrocnemius decreased significantly with dexamethasone injection. Relative weight of the plantaris and gastrocnemius of the dexa group decreased significantly compared to that of the control group. Body weight and muscle weight of the gastrocnemius of the exercise group increased significantly, and the muscle weight of the soleus and plantaris tended to increase. The Relative weight of the plantaris was comparable to the control group and that of the soleus and gastrocnemius tended to increase in the exercise group. Body weight and muscle weight of the soleus and plantaris of the D+E group showed a tendency to increase, and muscle weight of the gastrocnemius increased significantly compared to the dexa group. The Relative weight of the soleus and gastrocnemius tended to increase, and that of the plantaris of the D+E group increased significantly compared to the dexa group. Body weight, muscle weight and relative weight of the soleus, plantaris and gastrocnemius of the D+E group did not recover to that of the control group. Adrenal gland weight of the dexa and D+E group tended to increase, and that of the exercise group increased significantly. From these results, it can be suggested that regular exercise during dexamethasone injection might attenuate the decrease of body weight and hindlimb muscle weight induced by the dexamethasone injection.
Purpose: The purpose of this study was to examine the effects of daily exercise before steroid treatment on mass, the type I and II fiber cross-sectional area, and myofibrillar protein content of hindlimb muscles in a rat model. Method: Adult male Sprague-Dawley rats were randomly assigned to one of three groups: a control group(n=10) that had a normal saline injection for 7days, a steroid group(n=10) that had a steroid injection for 7days, and an exercise-steroid group(n=10) that ran on the treadmill for 7days before a steroid treatment. Body weight and food intake were measured every day. At 15 days all rats were anesthetized and the soleus, plantaris and gastrocnemius muscles were dissected. Result: The exercise-steroid group showed significant increases as compared with the steroid group in body weight, muscle weight of the soleus and gastrocnemius, type II muscle fiber cross-sectional area of plantaris, and myofibrillar protein content of the soleus, plantaris, and gastrocnemius. As compared with the control group, the steroid group showed significant decreases in body weight and diet intake, muscle weight, the type II fiber cross-sectional area and myofibrillar protein content of the soleus, plantaris, and gastrocnemius muscles. Conclusion: Daily exercise before steroid treatment attenuates hindlimb muscle atrophy, with type II muscle changes more apparent than type I muscle changes.
Purpose: This study was to evaluate the effect of ${\alpha}-lipoic$ acid, a potent free radical scavenger, on the expression of active form of extracellular signal-regulated kinase (pERK1/2) proteins from hindlimb muscles of rats following ischemia-reperfusion injury. Material and methods: 64 health, $280{\sim}350\;g$ weighted Sprague-Dawley male rats were used. In order to make a muscle flap, the gastrocnemius (GC) and soleus (SOL) muscles were dissected and elevated. The popliteal artery was occluded for 4hours and reperfused for 10 minutes, 30 minutes, 1 hour, 2 hours and 4 hours, respectively. Results: The ischemia by occlusion of the popliteal artery itself caused a minimal change in expression of phosphorylated form of proteins observed in hindlimb muscle. In contrast, after 4 hours of ischemia, immunoreactivity for pERK1/2 in the GC muscle showed dual peaks at 10 minutes and 4 hours after reperfusion. In ${\alpha}-lipoic$ acid treated group, the expression of pERK1/2 was increased significantly compared to I/R-only group. Conclusion: These results suggest that ${\alpha}-lipoic$ acid may protect I/R injury of the skeletal muscle through free radical scavening and activation of intracellular pERK1/2 expression.
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