Autophagy of osteoblasts (OB) regulating bone metabolism is a research hotspot in the field of life medicine. OB autophagy can regulate osteoporosis (OP) induced by aging, oxidative stress, estrogen deficiency and glucocorticoid (GCs) treatment by mediating RUBCN, SIRT1, OPG, etc. At the same time, OB autophagy can also regulate OP by activating Notch and FoxOs proteins, up-regulating the expression of osteogenic transcription factors (such as Runx2, Osterix) and mediating AMPK, mTOR, Wnt and JNK pathways to act on OB and osteoclast differentiation. Exercise is an important means to improve OP, and its molecular mechanism is closely related to the up-regulation of PI3K, AMP, TNF-α and SIRT1 expression by exercise. The above factors can activate key factors or pathways such as AMPK, mTOR, Wnt, PI3K/Akt/mTOR, and NF-κB, regulate the expression of downstream target genes (β-catenin, mTOR, FoxO3a, and Bcl-2) to up-regulate the expression of autophagy factors Beclin-1, ATG, and LC3, promote OB autophagy to restore dynamic balance in the body, thereby regulating bone formation and bone resorption, and improving OP. However, the current relationship between exercise, OB autophagy and OP has not been clarified, and there is a lack of systematic review analysis. Therefore, this article intends to review and analyze the mechanism of OB autophagy in the improvement of OP by exercise, and provide a new theoretical basis and research ideas for the prevention and treatment of OP.