There is increasing evidence that load-bearing is an important, if not the most important, functional influence on bone mass and architecture. Load-bearing most probably exerts its influence through the dynamic strains engendered in the bone tissue. Mechanically adaptive bone modeling and remodeling can be regarded as a homeostatic mechanism regulating functional bone strains at each location throughout the skeleton. Because most long bones are loaded in a certain amount of bending normal function, strains vary across the bones' cross-section. Both the longitudinal curvature and cross-sectional shape of a number of bones engender strains during functional loading rather than reduce them. Bone's adaptive response to load-bearing therefore results in functional strains which are neither uniform in distribution nor minimal in magnitude. Not all aspects of bone's strain environment are equally effective as influences on bone architecture. Unusual strain distributions, high strains, and high strain rates seem to be particularly osteogenic. The osteogenic response which follows exposure to such strains appears to saturate after only a few loading cycles. This is consistent with adaptive bone (re)modeling being sensitive to strain "errors," which are not repeated frequently, rather than the repetitious strain cycles engendered during normal predominant activities. Exercise regimens designed to control bone architecture can usefully capitalize on this feature of the adaptive (re)modeling response. Each exercise session need not be prolonged but should include as many novel strain distributions as possible, preferably involving high peak strains and strain rates. To maintain any level of bone mass requires a continued, loading-related osteoregulatory stimulus. Exposure to appropriate load-bearing exercise needs therefore to be repeated, probably at daily or alternate-daily intervals. In short-term experiments in rat bones, estrogen amplifies the osteogenic response to a single period of loading. The features of postmenopausal bone loss are consistent with the etiology of the condition being primarily withdrawal of estrogen's contribution to bone's mechanically adaptive response.