| Objective: The functional status of autophagy plays an important role in the regulation of muscle metabolism induced by appropriate exercise training through maintaining homeostasis and improving motor adaptation and motor ability.In this study,an experimental mouse model with different exercise modes at middle-level exercise intensity was established to explore the molecular mechanisms of skeletal and cardiac muscle to exercise,which will provide a theoretical basis for improving exercise performance,and preventing muscle damage or other chronic diseases,as well as establishing scientific guidance for future gene selection of talent athletes based on functional status of autophagy.Methods: Totally 90 Kunming mice with the age of 8 weeks were randomly divided into short-term exercise group with 50 mice and long-term exercise group with 40 mice.Long-term exercise group was randomly divided into 4 subgroups including control group,voluntary wheel running group,treadmill running group and swimming group with 10 mice in each group.After completing adaptive training,the mice from short-term exercise group were subjected to swimming for 0,0.5,1,1.5 and 2 h.In long-term exercise group,the mice treadmill running group were subjected to treadmill running at 15 m/min once a day,with a training period of 1 h.Similarly,the mice from swimming group were subjected to loading-free swimming training for 1 h once a day.In addition,the mice from voluntary wheel running group were subjected to voluntary wheel running during 2 months living in the cage with a wheel.At the end of the whole exercise period,the skeletal muscle and myocardium of the mice were harvested immediately to evaluate the expression level of autophagy-related proteins such as Beclin1,LC-3,AMPK-α and PGC-1α,apoptosis inhibitor Bcl-2,antioxidant factor NRF-2,and glucose transporter Glut4 by Western blot.Moreover,the functional status of autophagy in skeletal muscle and myocardium was evaluated by transmission electron microscope through the observation of autophagosomes.Results:1.After short-term exercise training,autophagy-related proteins such as PGC-1α,AMPK-α and Beclin1 were significantly up-regulated in skeletal muscle(P < 0.05),and the expression of Glut4 was significantly increased after 1.5 or 2 h exercise.2.After short-term exercise training,the expression of autophagy-related protein such as Beclin1 in myocardium revealed the highest level(P < 0.05)after 1 or 1.5 h exercise.Similarly,the expression of NRF-2 was enhanced after 0.5 and 1 h exercise,respectively.3.After long-term exercise training,autophagy-related proteins such as Beclin1 and LC-3 were significantly up-regulated in skeletal muscle(P < 0.05),while voluntary wheel running showed more significant increase in the expression of Glut4(P < 0.05).4.Different exercise modes after training can increase the expression of autophagy-related protein Beclin1 and antioxidant factor NRF-2 in myocardium(P < 0.05).In particular,treadmill running and swimming can result in more significant up-regulation of Beclin1(P < 0.05).5.Different from short-term exercise training,long-term exercise training can reduce the expression of Bcl-2,thus inhibiting apoptosis(P < 0.05).6.Long-term loading-free swimming training can lead to more expression of Bcl-2 than treadmill running and voluntary wheel running(P < 0.05).Conclusion: Exercise training at appropriate intensity can activate autophagy in skeletal muscle and cardiac muscle.Long-term exercise training can enhance the plasticity of autophagy,thus improving the stability of homeostasis and keeping the balance of energy metabolism and utilization,and,also plays a very important role in improving exercise capacity.At the same time,the activation of autophagy and the expression of glucose transporter Glut4 can strengthen the transport of glucose during exercise training;promote the maintenance of skeletal muscle mass,which are conducive to the prevention and treatment of chronic diseases such as diabetes or sarcopenia. |
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