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为进一步研究改善贫血状况和采用恢复手段促进骨骼肌的快速恢复打下基础。方法:将20只Wistar大鼠随机分为安静对照组(n=10)和运动组(n=10)。采用7周递增负荷跑台运动建立运动性低血色素大鼠模型,建模成功后第二天宰杀大鼠,取骨骼肌和肝脏测定肌糖原、肝糖原含量,并测定骨骼肌的SDH活性和UCP3mRNA表达。结果:1)7周递增负荷跑台运动导致了运动大鼠红细胞计数、血红蛋白、红细胞压积显著降低(P<0.05),建模成功;2)运动性低血色素并未影响大鼠肌糖原和肝糖原的恢复(P>0.05);3)运动性低血色素大鼠骨骼肌SDH活性非常显著降低(P<0.01),使得UCP3mRNA表达非常显著增多(P<0.01)。结论:运动性低血色素不影响肌糖元和肝糖原的恢复速度,但是可以显著降低骨骼肌琥珀酸脱氢酶的活性,提示运动性低血色素状态可能使骨骼肌有氧氧化能力降低;运动性低血色素大鼠骨骼肌UCP3mRNA表达显著增加,可能与UCP发挥运动抗氧化的快速应答有关。
Lay the foundation for further research on improving anemia status and using recovery methods to promote the rapid recovery of skeletal muscle. Methods: Twenty Wistar rats were randomly divided into control group (n = 10) and exercise group (n = 10). The rat model of exercise-induced hypochromia was established by increasing treadmill exercise at 7 weeks. The rats were sacrificed on the second day after successful modeling. Muscle glycogen and hepatic glycogen were determined in skeletal muscle and liver, and the SDH activity of skeletal muscle And UCP3 mRNA expression. The results showed that: 1) After 7 weeks of incremental load, treadmill exercise resulted in red blood cell count, hemoglobin and hematocrit in exercise rats decreased significantly (P <0.05), and the model was established successfully; 2) Exercise hypochrome did not affect rat muscle glycogen (P> 0.05). 3) The SDH activity of skeletal muscle of exercise hypochromic rats was significantly decreased (P <0.01), and the expression of UCP3 mRNA was significantly increased (P <0.01). Conclusion: Exercise hypoglycemia does not affect the recovery rate of muscle glycogen and glycogen, but can significantly reduce the activity of succinate dehydrogenase in skeletal muscle, suggesting that exercise hypoglycemic state may reduce the ability of skeletal muscle aerobic oxidation; exercise The expression of UCP3mRNA in skeletal muscle of hypoglycemic rats increased significantly, which may be related to the rapid response of UCP to exert anti-oxidative activity.