Stroke-prone spontaneously hypertensive rats (SHRSP) induce spontaneous osteoporosis. To elucidate the specific characteristics of bone metabolism, the SHRSP was compared with age matched Wistar-Kyoto (WKY) rats. We investigated the effects of prolonged swimming exercise training on bone mineral density (BMD) and metabolism in the SHRSP. Seven-week-old male SHRSP and WKY were divided into three groups; the sedentary control WKY group (n=6, WKY), the sedentary control SHRSP group (n=6, SP) and the swimming exercise training SHRSP group (n=6, SWIM) (in pool with 60 min./day, 5 days/week for 12 weeks). The femoral BMD, bone mineral content (BMC), strength, Ca and P contents (%) of SHRSP were approximately 17, 27, 25, 20 and 9%, respectively, lower than that of WKY (p<0.001). Serum alkaline phosphatase (AlP) had not changed between both of SP and WKY, but tartrate-resistant acid phosphatase (TrAcP) of SP approximately 3-fold higher than that of WKY (p<0.05). Both serum calcium (Ca) and intact parathyroid hormone (i-PTH) were similar between SP and WKY. However, serum phosphate (P) of SP was approximately 180wer than that of WKY (N.S.). These results suggested that SHRSP induces osteopenia by the bone turnover of the promoted osteoclast activity with disturbed phosphate homeostasis. On the other hand, the femoral BMD and strength were approximately 7% and 20%, respectively, decreased in the SWIM (p<0.001), and femoral bone Ca and P contents (%) were also approximately 11% and 14%, respectively, lower than that of SP (p<0.001). There were no significant difference between SWIM and SP on serum Ca, but serum P of SWIM was significantly lower than that of SP (p<0.05). These results suggested that the prolonged swimming exercise training in the SHRSP induces more cruelly hypophosphatemia, and leading to osteopenia eventually. We conclude that SHRSP induces osteopenia with disturbance of phosphate homeostasis, and the prolonged swimming exercise in the SHRSP might deteriorate hypophosphatemia and osteopenia.