Objective:To observe any effect supplementing treadmill training with external application of relaxation cream on skeletal muscle cell apoptosis and IGF-1/PI3K/Akt signaling.Methods:Eight Wistar rats formed a healthy control group (the healthy group) and muscle atrophy was induced in the left hind limbs of another 32. Those 32 rats were randomly divided into a model control group (model group), a treadmill training group (treadmill group), a relaxation cream group (TCM group), and a group which received both treadmill training and the relaxation cream (combined group). After 6 weeks of the intervention, terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) was used to detect any apoptosis of skeletal muscle cells. Western blotting was employed to detect the protein expression levels of insulin-like growth factor 1 (IGF-1), phosphorylated PI3K (p-PI3K), phosphorylated Akt (p-Akt), B-cell lymphomato-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in the skeletal muscles.Results:The number of apoptotic cells in the skeletal muscles of the treadmill, TCM and combined groups was significantly less, on average, then in the model group. The difference in the combined group was significantly greater than in the other two groups. The expression of Bcl-2 protein in the model group was significantly lower than in the healthy group, while that of Bax protein had increased significantly. Compared with the model group, a significant increase in Bcl-2 protein expression and a significant decrease in Bax protein expression were observed in both the TCM and combined groups. Compared with the model group, the expression of IGF-1, p-PI3K and p-Akt proteins had increased significantly in both the TCM and combined groups, with significantly greater increases in the combined group, on average.Conclusion:Combining treadmill training with relaxation cream can inhibit the apoptosis of skeletal muscle cells, at least in DMA rats. The mechanism may be related to activation of the IGF-1/PI3K/Akt signaling pathway, up-regulation of Bcl-2 and down-regulation of Bax.