The role of osteoblast (OB) autophagy in regulating bone metabolism is a research hotspot in the field of biomedicine. OB autophagy can regulate osteoporosis ( OP ) induced by aging, oxidative stress, estrogen deficiency, and glucocorticoids (GCs) by mediating factors such as run and cysteine rich domain containing Beclin-1 interacting protein (RUBCN), silent information regulator of transcription 1 (SIRT1), and osteoprotegerin (OPG).OB autophagy can also regulate OP by activating notch receptor ( Notch) and forkhead box protein O subfamily (FoxO), up-regulating the expression of osteogenic transcription factors (such as Runx2 and Osterix), and mediating the amp-activated protein kinase (AMPK), mammalian target of rapamycin complex (mTOR), Wnt, and c-Jun n terminal kinase (JNK) pathways to act on OB and osteoclast (OC) differentiation. Exercise is an important means of improving OP, and its molecular mechanism is closely related to the up-regulation of phosphatidylinositol 3 kinase (PI3K), adenosine monophosphate (AMP), tumor necrosis factor-alpha (TNF-α), and SIRT1 expression. These in turn activate key factors or pathways (including AMPK, mTOR, Wnt, PI3K/ protein kinase B (Akt) / mTOR, and nuclear transcription factor-κB (NF-κB) ), regulate the expression of downstream target genes (β-catenin, mTOR, FoxO3a and B cell lymphoma-2 (Bcl-2) ) to up-regulate the expression of autophagy factors (Beclin-1, autophagy related genes (ATG), and microtubule-associated protein 1 light chain 3 ( LC3) ), and promote OB autophagy to restore the dynamic balance in the body, thereby regulating bone formation and bone resorption and improving OP.The relationships among exercise, OB autophagy and OP, however, remain unclear and there is currently a lack of systematic reviews. Here we review and analyze the mechanism of OB autophagy in relation to exercise-induced improvements in OP, and provide a new theoretical basis and research ideas for the prevention and treatment of OP.