Estrogen and calcium are two well described determinants of postmenopausal skeletal mass. In protecting the organism against bone erosion, the two factors interact in a reciprocally sparing fashion. This manifests in the fact, that correction of the deficiency of one of the factors, as in the case of estrogen replacement therapy, prevents further bone loss despite the persistence of unaltered calcium intakes. The obverse is also true. Large dietary calcium intakes lead to calcium balance, despite the unrelieved estrogen deficiency of the menopause. It is hypothesized that physical activity which functions as another bone mass determinant, may also exert a sparing effect, and thus lower the requirements for calcium intake and perhaps bypass the need for estrogen replacement in the menopause. Confirmation of this hypothesis could provide a method for a nonpharmacologic approach to the prevention of osteoporosis and perhaps even an effective therapy for the repletion of bone tissue in the depleted osteoporotic skeleton.