Objective:To observe the influence of Bushen Yiqi Decoction and aerobic exercise on the expression of mitochondria biosynthesis related signaling molecules p38MAPK,CaMKⅡ,PGC-1α,MEF2C and COXⅣ in D - galactose-induced aging rats’ skeletal muscle. Methods40 male SD rats were randomly divided into five groups:normal group, model group, traditional Chinese medicine group, exercise and traditional Chinese medicine group and methandienone group. The rats were received a subcutaneous injection of 10% D-galactose solution(100 mg·kg-1,once a day)for 10 weeks to make the aging model except normal group rats. Bushen Yiqi Decoction, aerobic exercise and methandienone were used to the corresponding experimental groups to intervene for 10 weeks. β-Galase of blood serum were tested by ELISA; Calcium content of gastrocnemius mitochondria were tested by Methyl thyme phenol blue (MTB); The expression of mitochondrial biosynthesis related signal transduction molecules (p38MAPK,CaMKⅡ,PGC-1α,MEF2C and COXⅣ) were tested by Western blot respectively.  Results:Compared with normal group, model group rats’ aging biology markers β-Galase, calcium content in mitochondria increased significantly. The protein expression (protein) of model rats’ CaMKⅡ, MEF2C, PCG-1 alpha decreased obviously, and the protein expression of P38MAPK increased significantly. The Bushen Yiqi Decoction combined with aerobic exercise could obviously decrease calcium content, and increase the protein expression of CaMKⅡ, PGC-1α, MEF2C and COXⅣ of the model aging rats. The methandienone could obviously increase the protein expression of PCG-1α and COXIV of the model aging rats, decrease calcium content obviously.  Conclusion:The decline of aging model rats’ skeletal muscle function may related to expression changes of mitochondria biosynthesis related signal transduction pathways molecular CaMKⅡ, p38MAPK, PCG-1 alpha, MEF2C and energy metabolism related genes (COXIV). The Bushen Yiqi Decoction combined with aerobic exercise can delay age-related degradation of the skeletal muscle in some degree through improving the abnormal changes of the above index.