• Journal of Korean Academy of Nursing
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• v.32 no.4
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• pp.550-559
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• 2002

This study was conducted to determine whether low intensity regular exercise following dexamethasone treatment could attenuate steroid-induced muscle atrophy. Method: 36 Wistar-rats(90-110g) were divided into six groups: control group(C), dexamethasone treatment group(D), sedentary group after normal sedentary period(C+S), sedentary group after dexamethasone treatment period(D+S), exercise group after normal sedentary period(C+E), and excercise group after dexamethasone treatment period(D+E). D, D+S, and D+E groups received dexamethasone injection(5mg/Kg) for seven days whereas C, C+S, and C+E groups received normal saline injection. Both C+E and D+E groups ran on a treadmill for 60 minutes/day(20minutes/4hours) at 15m/min and a 10$^{\circ}$grade for seven recovery days. Result: Post-weight(body weight before muscle dissection) of D group significantly decreased by 16.03%, and that of D+E group significantly increased by 15.51% compared with pre-weight(body weight before steroid treatment). TypeII muscle(plantaris and gastrocnemius) weights of D group were significantly lower than those of C group. Myofibrillar protein contents of typeII muscles of D group tended to decrease comparing with C group. In D+E groups, body weights and relative weights of typeII muscles(muscle weight(mg)/post-weight(g)) tended to increase comparing with D+S group. Conclusion: It is suggested that steroid- induced muscle atrophy can be ameliorated through low intensity regular exercise after dexamethasone treatment.

• Journal of Yeungnam Medical Science
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• v.16 no.1
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• pp.34-42
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• 1999

The effects of hyperglycemia and hyperlipidemia on utilization of muscle glycogen during 45 minute Session of treadmill running(26 m/min, 8% grade) were evaluated using Sprague Dawley rats, and the characteristics of the 4 different type of muscles, I.e., soleus, white and red gastrocnemius, and plantaris, on glycogen utilization were simultaneously investigated. Hyperglycemia was induced by 145-165 mg/dL of oral glucose administration, and hyperlipidemia was induced by combined treatment of intraperitoneal heparine injection of 444 uEq/L and 10 % intralipose oral adminstration. During the hyperglycemic trial, the glycogen utilization of plantaris muscle was decreased by 13 % in 45 minute session of treadmill running compared to the control trial(p<0.05), and the glycogen utilization of white gastrocnemius was also decreased. The sparing tendency of glycogen was observed in soleus and red gastrocnemius by 5-13 % during 30 and 45 minute session of treadmill running in hyperglycemic trial. There was no glycogen sparing effect of hyperlipidemia in soleus, red gastrocnemius and plantaris muscle subjected in this experiment during exercise. However, only a slight sparing tendency of white gastrocnemius muscle was observed. In summary, the glycogen sparing effect of hyperglycemia during exercise was observed in plantaris and white gastrocnemius muscles in rats. However, there was no glycogen sparing effect of hyperlipidemia in the 4 hindlimb muscles. It was observed that the glycogen sparing effect of hyperglycemia is more prominent in fast glycolytic muscle fibers.