過去單靠骨質掃描往往不足以檢測出短時間內微小的骨質流失現象，若透過骨質生化指標或荷爾蒙指標之改變，可迅速地檢測骨質代謝之變化。由於運動強度與運動持續時間的差異，休閒性運動者與菁英運動員在從事單車運動後所產生的骨質代謝作用反應大相逕庭，在高強度單車運動刺激後，骨質代謝趨勢可能較偏向分解作用；長時間中等強度的運動則產生不一致的效果，反應不同可能肇因於運動刺激造成體內荷爾蒙濃度改變，並藉此調節骨保護素(Osteoprotegerin, OPG)與可溶性受體活化核因子kB配體蛋白(soluble Receptor Activate Nuclear Factor kappa B Ligand , sRANKL)之平衡，進而產生骨質代謝作用變化。有別於以往單車運動屬於非負重運動而亦導致骨質流失的傳統觀念，配合運動持續時間與運動強度的調整，以及適度鈣離子的補充，單車運動也可以是維護骨骼健康的休閒活動。

Due to the difference of intensity and duration, bicycling differently affect armature riders and professional cyclists on bone metabolism. High intensity and high capacity cycling training tend to decreased bone mineral density especially on none weight-bearing site. However, prolong moderate-intensity bicycle riding seems to alter bone metabolism and toward bone formation. Recent researches indicate that bicycling may not be detrimental to bone health and possibly provide some benefit effects. Monitor of bone biochemical markers provide a more practical way to early detect changes of bone metabolism in response to exercise stimuli. Among several biological and biochemical markers, Osteoprotegerin (OPG) and soluble receptor activator of nuclear factor κB ligand (sRANKL) act as key regulators of bone metabolism. Hormones and cytokines which might alter bone metabolism were mostly media through OPG/sRANKL pathway. Exercise dramatically affects OPG/sRANKL balance and the magnitudes of changes were correlated to both duration and intensity, but not level of weight-bearing. There seems to be a threshold that exercise affect bone metabolism which composed of exercise intensity and duration. In conclusion, with proper designed prescription and well calcium supplement, bicycling could be a benefit exercise for bone health.