ECTS Abstracts (2015) 1 P254

Changes in Markers of Bone Turnover and Sclerostin during Arduous Military Training

Rachel Izard1, William Fraser2 & Julie Greeves1

1HQ Army Recruiting and Training Division, Upavon, Wiltshire, UK; 2Norwich Medical School, University of East Anglia, Norwich, Norfolk, UK.

Background: Increased mineralisation and periosteal expansion of the tibia following short-term military training suggests changes in bone turnover, favouring formation. Sclerostin, which has anti-anabolic effects and is inhibited by mechanical loading, has recently been identified as a key regulatory marker in mechanotransduction of bone. The aim of this study was to examine the effects of 10 weeks arduous military training on markers of bone turnover and sclerostin.

Methods: Male Army recruits (n=82) undertaking initial Infantry training volunteered to participate. Early morning blood samples (0500 – 0545h) were collected at Baseline, Mid and End (weeks 1, 5 and 10) of training following an overnight fast and analysed for markers of bone formation (P1NP and OC), resorption (βCTX), sclerostin, regulatory markers of calcium metabolism (intact PTH, albumin adjusted Ca and PO4) and vitamin D (total 25(OH)D). Data were analysed using repeated measured ANOVA (SPSS v19); statistical significance was set a-priori at P<0.05.

Results: P1NP increased from Baseline to Mid, returning to Baseline values at End (112.5±67.6, 126.3±69.2, 111.2±62.3 μg/l). OC decreased from Baseline at Mid and End (50.2±28.3, 43.9±22.2, 40.0±20.5 ng/ml). βCTX decreased from Baseline to Mid, returning to Baseline values at End (1.08±0.49, 0.90±0.49, 1.03±0.45 ng/ml). Sclerostin decreased from Baseline at Mid returning to Baseline values at End (42.45±16.9, 37.1±13.4, 40.1±13.1 pmol/l). 25(OH)D decreased from Baseline to End (72.1±21.3, 41.8±15.6 nmol/l) and increases in Ca and PO4 were observed. iPTH remained unchanged.

Conclusions: These findings suggest an early, transient and orchestrated change of bone markers to increase bone density and alter bone structure in response to mechanical loading. These findings strongly support in vivo a role of sclerostin in mechanotransduction.

Disclosure: The authors declared no competing interests. This work was sponsored by the UK Ministry of Defence (Army).

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