| Aim:Exercise-induced fatigue(EF)was first mentioned in the 19th century by Mosso.It was properly defined only in 1982,after more than a hundred years.In the understanding its pathophysiology,many theories have been proposed.Yet these theories can only offer explanation for a fraction of its pathophysiology,while the complete picture of it remains unsolved.As the quality of life improves,exercise is becoming a more popular option to keep fit and maintain a healthy lifestyle.Due to the lack of proper guidance for exercise,the incidences of exercise-induced fatigue have been on the rise.To relieve exercise-induced fatigue,recent studies and traditional chinese medicine have proposed several relief methods.The more common methods include rest,energy supplements,mental regulation,physiotherapy,hyperbaric oxygenation,hydrotherapy,oral herbal decoctions,acupuncture etc.With regards to the mechanisms by which these treatment methods work,many different theories had been proposed and proven through extensive research.It was reported that Tuina Therapy can effectively provide relief for EF.However its underlying mechanism has been little researched and remained unknown.5'adenosine monophosphate-activated protein kinase(AMPK)is the energy regulator of the human body and plays an important role in exercise metabolism.More researchers are increasingly interested in how AMPK is involved in the metabolism of nutrients such as glucose,proteins,cholesterol etc since it provides a hope of alternative cure for endocrine diseases.This study aims to investigate the mechanism by which Tuina Therapy relieves symptoms of EF,particularly by studying the changes in the levels of AMPK.Methods:60 10-week-old healthy male Wistar mice underwent running test to select mice that are good to run.Of the 60 mice tested,30 mice were filtered out for poor running ability while 30 good mice were separated into 3 groups randomly;control group,model group and tuina group.Mice in model group and tuina group underwent running session daily for 28 days.Mice in tuina group were administered tuina therapy treatment after every running session.After 28 days of running sessions,the mice were tested for lactin(LAC),urea nitrogen(BUN),creatinine kinase(CK),malondialdehyde(MDA),superoxide dismutase(SOD),adenosine monophosphate(AMP),adenosine triphosphate(ATP),adenosine monophosphate-activated protein kinase(AMPKa2).Results:1)Mice in both tuina and model groups have higher levels of LAC,BUN and CK compared to the mice in control group.The differences are statistically significant(P<0.01)which is an indication that the model of EF was successfully established.2)Levels of LAC,BUN and CK were lower in tuina group when compared with model group and the difference is statistically significant(P<0.05);marker for cell damage,MDA levels were also lower for mice of tuina group when compared with mice in model group(P<0.05);marker for cell antioxidant,SOD levels were higher in mice of tuina group than that of model group(P<0.05).3)Markers for cellular energy,ATP and AMPKa2,were of higher levels in mice of tuina group than that of model group.The difference is statistically significant(P<0.01).Mice in tuina group have lower levels of AMP than that of model group(P<0.05).4)The relationship between levels of BUN,LAC,CK,SOD,MDA and AMPKa2 proteins were statistically insignificant(P>0.05).5)The differences in the levels of Na-K+-ATP enzymes and Ca2+-ATP enzymes between mice in tuina group and model group are statistically insignificant.Conclusion:1)Tuina therapy can reduce the cumulative toxicity of metabolites.2)Tuina therapy can increase levels of AMPKa2 through AMP/ATP-AMPK pathway.3)Further research is required to study to confirm if the cumulative toxicity of metabolites are reduced through AMP/ATP-AMPK pathway.4)It has not been statistically proven that Tuina can protect the activity of Na-K+-ATP enzymes and Ca2+-ATP enzymes,however it remains hopeful that Tuina can sustain the activity of these enzymes. |
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