Alpine Rhodosin Exercise-induced Fatigue In Skeletal Muscle Mitochondrial Ca²⁺-ATP Enzyme And H⁺-ATPase Enzyme Activity And Its Metabolism Of Free Radicals

With the development of competitive sports is highly developed, the competitionis fiercer than ever, in addition to as much as possible to improve the level of training,coaches and athletes are also very much hope that through the improve athletic abilityauxiliary means, especially the application of certain non-prohibited drugingredientssubstances to enhance physical fitness, combat fatigue, give full play to thepotential for movement of the body, in order to get the best athletic performance. Thesame time, the modern social life, fitness have higher demand, but also hope that thesupplement can improve physical function, delaying fatigue special nutrition in orderto facilitate better physical exercise, good fitness effect.Rhodiola is a recently discovered an anti-fatigue effect of the drug is sedum, is anatural formulation precious medicinal plants, known as the "plateau ginseng andsnow-capped mountains immortality," said. Rhodiola no contraband medicines, willnot damage the athlete’s body, able to resist premature fatigue, as soon as possible sothat the body recover from the fatigue state and to improve the competitive level ofthe athletes. It is generally considered Fatigue mainly related to energy consumption,metabolic disorders, central nervous system and the endocrine system dysfunctionaspects, the Rhodiola through the regulation of body function, play a role inanti-fatigue. So research Rhodiola sports fatigue, athletes and fitness crowdhomeostasis in the body is important in the race and sports training.Experimental purposes: fatigue in rats skeletal muscle mitochondrial Ca²⁺-ATPenzyme and H⁺-ATPase activity changes, free radicals metabolism to determine theeffects produced by the principle of fatigue and Rhodiola fight fatiguefor research, soas to help athletes and fitness crowd, so to master the more scientific movementmeans and methods to improve athletic performance and enhance their physique.Therefore, the study of exercise-induced fatigue is to improve with the purpose ofrestoring function where.Experimental Methods:50healthy SD male rats to adapt to the end of thetraining, then remove10as normal control group, and the remaining40as exercise-induced fatigue model group. Related indicators of the reaction fatigue of thebody in the blood of rats after4weeks of training, test indicators show that if the testresults in the range of fatigue indicators judged to be successful modeling. Successfulmodeling selected32rats were randomly divided into exercise-induced fatigue quietgroup, exercise-induced fatigue medication group the sports fatigue exercise groupand exercise-induced fatigue movement medication group, n=8, cage feeding, theremaining large rat spare. On the sports fatigue medication group andexercise-induced fatigue Sports medication group fed daily alpine Rhodosin200mg/kg, exercise-induced fatigue exercise group and exercise-induced fatigueSports medication group continued surrounding active recovery movement, the timeincrements from10min to20min, the minimum intensity control15m/min, maximumintensity control at18m/min. Every other day movement. Rats enthusiasm recoveryafter exercise, five groups of rats were killed one by one, decapitated, blood, thenquickly skinned legs, remove the gastrocnemius, extracted mitochondrial weredetected skeletal muscle mitochondrial Ca²⁺-ATP enzyme and H⁺-ATPase activitychanges, as well as indicators of muscle tissue superoxide dismutase （SOD） andmalondialdehyde （MDA）.Results:（1） Skeletal Muscle Mitochondrial Ca²⁺-ATP enzyme: Compared withthe normal group, the quiet group significant difference （P <0.01）, decreased by60.85%. Quiet medication group had significant difference （P <0.05）, decreased by23.17%. The exercise group and a significant difference （P <0.05）, a decrease of29.8%. Exercise medication group had no significant difference. Compared with thequiet group, quiet medication group had significant difference （P <0.01）, increased by70.13%. The exercise group and a significant difference （P <0.01）, increased by66.4%. Sports medication group had significant difference （P <0.01） increased by132.8%. Compared with the exercise group, quiet no significant difference in themedication group, sports medication group had significant difference （P <0.05）,increased by39.9%. Quiet medication group and sports medication group significantdifference （P <0.05）, increased by21.76%.（2） in rat skeletal muscle mitochondrialH⁺-ATP enzyme: Compared with normal group, quiet group significant difference （P <0.01）, increased by36.49%. Quiet medication group had no significant difference.The exercise group and a significant difference （P <0.05）, increased by15.32%.Exercise medication group had no significant difference. Compared with the quietgroup, Lao Jing medication group, a significant difference （P <0.01）,23.69%. Theexercise group and a significant difference （P <0.05）,9.27%lower. Sports medicationgroup had significant difference （P <0.01）,26.42%. Compared with the exercisegroup, quiet medication group had significant difference （P <0.05）,10.72%. Sportsmedication group had significant difference （P <0.05）,18.45%. Quiet medicationgroup with the sport medication group showed no significant difference.（3） inskeletal muscle SOD: Compared with normal group, quiet group significant difference（P <0.01）, reduced by18.62%. Quiet medication group had significant difference （P<0.05）, and8.14%lower. The exercise group and a significant difference （P <0.05）,9.11%lower. Exercise medication group had no significant difference. Compared withthe quiet group, quiet medication group had significant difference （P <0.05）, increasedby12.79%. The exercise group and a significant difference （P <0.05）, increased by11.78%. Exercise medication group a significant difference （P <0.01）, increased by18.39%. Compared with the exercise group, quiet medication group and exercisemedication group had no significant difference. Quiet medication group with the sportmedication group showed no significant difference.（4） rat skeletal muscle MDA:Compared with normal group, a quiet group significant difference （P <0.01）,increased by54.97%. Quiet medication group had no significant difference. Theexercise group and a significant difference （P <0.05）, increased by22.03%. Exercisemedication group had no significant difference. Compared with the quiet group, quietmedication group had significant difference （P <0.01）,41.03%. Exercise group wassignificant difference different （P <0.05）,20.51%reduction. Sports medication grouphad significant difference （P <0.01）,30.76%. Compared with the exercise group, quietmedication group had significant difference （P <0.05）,26.71%. Exercise medicationgroup had no significant difference. Quiet medication group with the sport medicationgroup showed no significant difference.Experimental results:（1） experimental rat skeletal muscle mitochondrial Ca²⁺-ATPase activity decreased significantly after the Exercise Fatigue may be afactor in causing skeletal muscle fatigue. The Supplemental alpine Rhodosin makeSkeletal Muscle Mitochondrial Ca²⁺-ATPase activity recovered to near normal levelsof Rhodiola also make the organization intracellular Ca²⁺concentration to maintain asteady state, to avoid cell metabolism disorder, to ensure the cell membrane throughpermeability and integrity, thereby contributing to the recovery of exercise fatigue.（2） After exercise in skeletal muscle mitochondrial H⁺-ATPase activity increasedsignificantly, but can not be sure whether the mitochondrial membrane is complete,there is synthesis and decomposition of ATP are two possible. Alpine Rhodosin alsomake the H⁺-ATPase activity tends to the normal steady state, to maintain the integrityof the cell membrane, the possible conclusion is the alpine Rhodosin make H⁺-ATPaseactivity maintained at a relatively normal level, the synthesis of ATP the ability tomaintain stability, thereby avoiding the generation of fatigue.（3） The results show that: The alpine Rhodosin can enhance the SOD activity inrat skeletal muscle tissue, clear oxygen free radicals generated due toexercise-induced fatigue, improve the antioxidant capacity of skeletal muscle toreduce the content of MDA, thus delay fatigue occurs or accelerate the recovery fromfatigue.