| Sarcopenia is a general syndrome that is characterized by a progressive loss of skeletal muscle mass (quantity and size) and strength, especially the type II muscle fiber. It can cause the decline of body function, and even loss of life. Although this syndrome is common in older people, and have a serious threat to the health and quality of life of older persons, its mechanism is not very clear. One of the important reasons that cause sarcopenia is the imbalance in protein metabolism. Several studies revealed that skeletal muscle protein synthesis is declined and on the contrary, the skeletal muscle protein degradation is increased in the elderly people. These altered the protein composition of skeletal muscle subsequently caused the decline in muscle mass (quantity and size) and finally made the muscle strength declined. Another important mechanism is the occurrence of apoptosis in senescent skeletal muscle cells which may lead to a reduction in skeletal muscle cells, and result in skeletal muscle atrophy. In which mitochondria-mediated caspase-dependent apoptosis is considered to be the main factor. But in recent years the type II programmed cell death---autophagy---has been showed that there is a key role in the development of sarcopenia. Autophagy as an important intracellular protein degradation pathway, its role in sarcopenia is not only limited to cause the cell death directly, but also can lead to rapid protein degradation. Both excessive activation and/or inactivation of autophagy, will affect the protein content of cells, and stimulate a number of columns chain reaction. So this provide us a new inspiration for the prevention and treatment of sarcopenia that if we can regulate the autophagy flux by some interventions to control the occurrence of sarcopenia. As we all know, sports, in particular resistance exercise, can promote physiological hypertrophy, which provides feasible ideas for the prevention and treatment of sarcopenia.Objective:this article is designed to determine the alterations of autophagy in 20-months C57BL/6 skeletal muscle with sarcopenia, and to observe the effect of a life-long endurance and resistance exercise on the autophagy related genes'expression. So as to provide some effective ways that can counterwork sarcopenia for skeletal muscle.Methods:54 C57BL/6 mice were randomly divided into young control group (YC), aged control group (OC), life-long treadmill group (LE), life-long ladder group (LR), old treadmill group (OE), old age Ladder group (OR),9 for each group. The age of YC group mice are 3 months and other groups are raised naturally to 20 months. LE group and the LR group were engaged in a treadmill and ladder-climbing training for 17 months respectively, OE group and OR group engaged in a treadmill and ladder-climbing training only for 2 months respectively. The exercise performed once a day and three days a week. After that Q-PCR was used to detect the biological autophagy related genes LC3, Beclinl, LAMP-2 and Bnip3 mRNA expression.Results:1)With the aging growing, skeletal muscle mass decreased significantly in natural aging C57BL/6 mice, and the sarcopenia is occurred in these mice.2) Compared with the YC group, LC3b, LAMP-2b and Bnip3 mRNA expression was significantly increased in OC group, and LAMP-2a mRNA expression was no significant difference.3) Compared with the OC group, lifelong endurance training can significantly increase the ratio of LC3a/LC3b, and increase Beclinl, LAMP-2a, LAMP-2b mRNA expression significantly, but Bnip3 mRNA expression was significantly reduced.4) Compared with the OC group, lifelong resistance training can decrease LC3a, Beclinl, LAMP-2a mRNA expression, but no significant difference; and can decrease LC3b, Bnip3 mRNA expression significantly.5) Compared with the LE, Beclinl, LAMP-2a, LAMP-2b expression was increased, and has a very significant difference.Conclusion:1) 20 months old C57BL/6 mice can be used as the model animal of sarcopenia.2) With the aging growing, the autophagy flux was increased, and this increasing may be excessive that can cause the increasing of protein degradation, and reduce the skeletal muscle mass, lead to sarcopenia in 20 months old C57BL/6 mice.3) Lifelong endurance training can control the body weight in young mice, and can effectively inhibit excessive autophagy, thus easing sarcopenia symptoms.4) Lifelong resistance training can effectively control the body weight of mice up to the old age, and can reduce autophagic activity and protein degradation in a certain range to prevent the development of sarcopenia.5) Compared with the LE group, Beclinl, LAMP-2a, LAMP-2b mRNA expression was increased significantly in LR group, suggesting that life-long endurance training had a better effect on the control of excessive autophagy than the life-long resistance training.
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