Cycling Duration and Bone Markers in in Active Young Adults

Plain-language summary

Exercise is an important factor in bone health. Sclerostin is one of the key molecules involved in bone response to mechanical loading. In particular, sclerostin decreases bone formation directly through the inhibition of Wnt/ β-catenin signaling and increases bone resorption indirectly via upregulation of the RANK/RANKL. The Wnt pathway is an anabolic signaling pathway, which leads to the activation of osteoblasts. OPG is another osteokine secreted by osteoblasts and osteogenic stomal cells that has a protective osteogenic role in humans by inhibiting the binding of RANKL to its receptor RANK. The RANK/RANKL pathway is a catabolic signaling pathway controlling osteoclast differentiation. Only a few studies have examined the effects of one single bout of high impact exercise on serum sclerostin levels in adults, most of which are from the investigators' lab. However, not many studies have examined the acute effects of moderate intensity, low-impact exercise on osteokines of the Wnt signaling. Previous studies have only investigated the impact of high intensity cycling on sclerostin, OPG and RANKL, however, no research has been done to investigate the response of osteokines to moderate intensity continuous cycling. This study aims to investigate differences in osteokines and markers of bone turnover following three moderate intensity cycling trials of different duration (30, 60 and 120 min) in an energy replete state. The question we aim to answer is whether there is a threshold of time where continued stimulus from moderate strain on the bone fails to elicit an additional metabolic response in bone or even becomes osteocatabolic, when athletes are in an energy replete state. Additional biochemical responses to the exercise will also be examined including inflammatory markers, glucose, anabolic/hormonal markers and oxidative stress.

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