4.3 Article

Physical training increases osteoprotegerin in postmenopausal women

Journal

JOURNAL OF BONE AND MINERAL METABOLISM
Volume 30, Issue 2, Pages 202-207

Publisher

SPRINGER TOKYO
DOI: 10.1007/s00774-011-0304-6

Keywords

Physical training; Postmenopausal women; Osteoprotegerin; Receptor activator for nuclear factor kappa B ligand; Sclerostin

Funding

  1. Stockholm County Council (ALF)
  2. Swedish Research Council [VR-M K2009-52X-10363-17-3]

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The purpose of this study was to explore whether mechanical loading by exercise over a 1-year period in postmenopausal women had an effect on the receptor activator for nuclear factor kappa B ligand/osteoprotegerin (RANKL/OPG) system or the levels of the Wnt-signaling antagonist sclerostin. A total of 112 postmenopausal were randomized to either sedentary life (controls) or physical activity (training group). Ninety-two women fulfilled the study protocol. The training program consisted of three fast 30-min walks and one or two 1-h aerobic training sessions per week. The effect on the bone mineral density of the hip assessed with dual X-ray absorptiometry was positive as reported earlier. Blood samples were taken from participants at baseline and after 1 year and serum levels of OPG, RANKL and sclerostin were quantified together with the bone metabolism markers C-terminal telopeptide of collagen type I (CTX) and bone-specific alkaline phosphatase (BALP). The results were analyzed using an analysis of covariance model using baseline values as the covariate. The training group displayed a clear mean increase of OPG +7.55 pg/ml compared to controls (p = 0.007). The mean changes for RANKL +0.19 pg/ml (square-root transformed data) and sclerostin +0.62 pmol/l were non-significant (p = 0.13 and p = 0.34). The changes in bone turnover markers CTX and BALP showed a tendency to decrease in the training group versus controls but the changes were small and nonsignificant. Although our study is limited in number of participating women, we have been able to show an OPG-associated, and RANKL- and sclerostin-independent, training-induced inhibition of postmenopausal bone loss.

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