Vol 69, No 2 (2018)
Original paper
Published online: 2017-12-20

open access

Page views 4230
Article views/downloads 1945
Get Citation

Connect on Social Media

Connect on Social Media

Effects of physical activity on sclerostin concentrations

Małgorzata Janik1, Michał Stuss12, Marta Michalska-Kasiczak1, Anna Jegier3, Ewa Sewerynek12
Pubmed: 29465155
Endokrynol Pol 2018;69(2):142-149.


Osteoporosis is a serious medical and socioeconomic problem of the 21st century. Mechanical load is a key regulator which controls bone formation and remodelling, with participation of osteocytes. Sclerostin is produced and released by mature osteocytes into bone surface, where it inhibits the conveyance of osteoblast proliferation and differentiation activating signals from mesenchymal cells, thus suppressing new bone formation. The goal of the study was an evaluation of the effects of a 12-week physical training programme on the levels of bone turnover markers [Sclerostin, Osteocalcin (OC), C-terminal telopeptide of type I collagen (β-CTX)] in blood serum of women with osteopenia. Materials & Methods: The study included 50 women of the Regional Menopause and Osteoporosis Centre of the WAM Teaching Hospital, at the age of 50-75 years with the diagnosis of osteopenia, obtained on the basis of hip and/or lumbar spine densitometry (T-score from -1.0 to -2.5 SD). During the initial 12 weeks (between point 1 and 2), the patients maintained their previous, normal level of physical activity. During subsequent 12 weeks (between point 2 and 3), a programme of exercise was implemented. The programme included the interval training on a bicycle ergometer, three times a week for 36 minutes. During the entire study duration, all the patients received a supplementation of calcium (500 mg) and vit. D3 (1800 IU) once daily. Serum levels of OC, alkaline phosphatase (ALP), β-CTX and sclerostin were assayed at 3 time points. Results: After the course of the exercise cycle, the OC concentration was increased, sclerostin levels decreased, while no statistical differences were observed in β-CTX levels vs. the period of physical inactivity. No correlations were found between sclerostin level changes and osteocalcin level changes during the training time, because of too small groups. Neither statistically significant were the differences in alkaline phosphatase, calcium and phosphorus levels. Conclusions: The obtained results emphasise the role of physical training as an effective stimulation method of bone formation processes in women with osteopenia. Sclerostin can be a marker of physical activity. < /p > < p >

Article available in PDF format

View PDF Download PDF file


  1. Schwab P, Scalapino K. Exercise for bone health: rationale and prescription. Curr Opin Rheumatol. 2011; 23(2): 137–141.
  2. Kohrt WM, Barry DW, Schwartz RS. Muscle forces or gravity: what predominates mechanical loading on bone? Med Sci Sports Exerc. 2009; 41(11): 2050–2055.
  3. Czarkowska-Paczek B, Wesołowska K, Przybylski J. [Physical exercise prevents osteoporosis]. Przegl Lek. 2011; 68(2): 103–106.
  4. Taylor AF, Saunders MM, Shingle DL, et al. Mechanically stimulated osteocytes regulate osteoblastic activity via gap junctions. Am J Physiol Cell Physiol. 2007; 292(1): C545–C552.
  5. Liu C, Zhao Y, Cheung WY, et al. Effects of cyclic hydraulic pressure on osteocytes. Bone. 2010; 46(5): 1449–1456.
  6. Gombos GC, Bajsz V, Pék E, et al. Direct effects of physical training on markers of bone metabolism and serum sclerostin concentrations in older adults with low bone mass. BMC Musculoskelet Disord. 2016; 17: 254.
  7. Marcus R. Mechanisms of Exercise Effects on Bone. In: Bilezikian JP, Raisz LG, Rodan GA. ed. Principles of bone biology 2nd. Academic Press, San Diego 2002: 1477–1488.
  8. Garnero P. New developments in biological markers of bone metabolism in osteoporosis. Bone. 2014; 66: 46–55.
  9. Pawlak-Buś K, Leszczyński P. Sklerostyna – nowy cel terapii anabolicznej niskiej masy kostnej. Reumatologia. 2010; 48: 183–187.
  10. van Bezooijen RL, ten Dijke P, Papapoulos SE, et al. SOST/sclerostin, an osteocyte-derived negative regulator of bone formation. Cytokine Growth Factor Rev. 2005; 16(3): 319–327.
  11. Sutherland MK, Geoghegan JC, Yu C, et al. Sclerostin promotes the apoptosis of human osteoblastic cells: a novel regulation of bone formation. Bone. 2004; 35(4): 828–835.
  12. Aguirre JI, Plotkin LI, Stewart SA, et al. Osteocyte apoptosis is induced by weightlessness in mice and precedes osteoclast recruitment and bone loss. J Bone Miner Res. 2006; 21(4): 605–615.
  13. Leblanc AD, Schneider VS, Evans HJ, et al. Bone mineral loss and recovery after 17 weeks of bed rest. J Bone Miner Res. 1990; 5(8): 843–850.
  14. Choi HY, Dieckmann M, Herz J, et al. Lrp4, a novel receptor for Dickkopf 1 and sclerostin, is expressed by osteoblasts and regulates bone growth and turnover in vivo. PLoS One. 2009; 4(11): e7930.
  15. Ott SM. Sclerostin and Wnt signaling--the pathway to bone strength. J Clin Endocrinol Metab. 2005; 90(12): 6741–6743.
  16. Lee NaK, Sowa H, Hinoi E, et al. Endocrine regulation of energy metabolism by the skeleton. Cell. 2007; 130(3): 456–469.
  17. Szulc P. The role of bone turnover markers in monitoring treatment in postmenopausal osteoporosis. Clin Biochem. 2012; 45(12): 907–919.
  18. Matsuo K. Cross-talk among bone cells. Curr Opin Nephrol Hypertens. 2009; 18(4): 292–297.
  19. Rubin C, Turner AS, Bain S, et al. Anabolism. Low mechanical signals strengthen long bones. Nature. 2001; 412(6847): 603–604.
  20. Questionnaire of Physical Activity, Polish version. Http://www.academia.edu/19229070/Mi%C4%99dzynarodowy IPAQ.
  21. Stuss M, Sewerynek E, Król I, et al. Assessment of OPG, RANKL, bone turnover markers serum levels and BMD after treatment with strontium ranelate and ibandronate in patients with postmenopausal osteoporosis. Endokrynol Pol. 2016; 67(2): 174–184.
  22. Zalecenia postępowania diagnostycznego i leczniczego w osteoporozie. Medycyna Praktyczna 2013.
  23. Ostrowska Z, Ziora K, Oświęcimska J, et al. Vaspin and selected indices of bone status in girls with anorexia nervosa. Endokrynol Pol. 2016; 67(6): 599–606.
  24. Ostrowska Z, Ziora K, Oświęcimska J, et al. TGF-β1, bone metabolism, osteoprotegerin, and soluble receptor activator of nuclear factor-kB ligand in girls with anorexia nervosa. Endokrynol Pol. 2016; 67(5): 493–500.
  25. Gołąbek K, Ostrowska Z, Ziora K, et al. Association between omentin-1, bone metabolism markers, and cytokines of the RANKL/RANK/OPG system in girls with anorexia nervosa. Endokrynol Pol. 2015; 66(6): 514–520.
  26. Deogenov VA, Zorbas YG, Kakuris KK, et al. The impact of physical exercise on calcium balance in healthy subjects during prolonged hypokinesia. Nutrition. 2009; 25(10): 1029–1034.
  27. Adami S, Gatti D, Viapiana O, et al. BONTURNO Study Group. Physical activity and bone turnover markers: a cross-sectional and a longitudinal study. Calcif Tissue Int. 2008; 83(6): 388–392.
  28. Pernambuco CS, Borba-Pinheiro CJ, Vale RG, et al. Functional autonomy, bone mineral density (BMD) and serum osteocalcin levels in older female participants of an aquatic exercise program (AAG). Arch Gerontol Geriatr. 2013; 56(3): 466–471.
  29. Ardawi MSM, Rouzi AA, Qari MH. Physical activity in relation to serum sclerostin, insulin-like growth factor-1, and bone turnover markers in healthy premenopausal women: a cross-sectional and a longitudinal study. J Clin Endocrinol Metab. 2012; 97(10): 3691–3699.
  30. Huovinen V, Ivaska KK, Kiviranta R, et al. Bone mineral density is increased after a 16-week resistance training intervention in elderly women with decreased muscle strength. Eur J Endocrinol. 2016; 175(6): 571–582.
  31. Ahn N, Kim K. Effects of 12-week exercise training on osteocalcin, high-sensitivity C-reactive protein concentrations, and insulin resistance in elderly females with osteoporosis. J Phys Ther Sci. 2016; 28(8): 2227–2231.
  32. Lombardi G, Lanteri P, Graziani R, et al. Bone and energy metabolism parameters in professional cyclists during the Giro d'Italia 3-weeks stage race. PLoS One. 2012; 7(7): e42077.
  33. Wen HJ, Huang TH, Li TL, et al. Effects of short-term step aerobics exercise on bone metabolism and functional fitness in postmenopausal women with low bone mass. Osteoporos Int. 2017; 28(2): 539–547.
  34. Mohr M, Helge EW, Petersen LF, et al. Effects of soccer vs swim training on bone formation in sedentary middle-aged women. Eur J Appl Physiol. 2015; 115(12): 2671–2679.
  35. Kaczmarek A, Nowak A, Leszczynski P. Bone Mineral Density and Biochemical Markers of Bone Metabolism in Women Engaging in Recreational Horseback Riding. J Phys Act Health. 2016; 13(5): 520–524.
  36. Clarke BL, Drake MT. Clinical utility of serum sclerostin measurements. Bonekey Rep. 2013; 2: 361.
  37. Bergström I, Parini P, Gustafsson SA, et al. Physical training increases osteoprotegerin in postmenopausal women. J Bone Miner Metab. 2012; 30(2): 202–207.
  38. Gaudio A, Pennisi P, Bratengeier C, et al. Increased sclerostin serum levels associated with bone formation and resorption markers in patients with immobilization-induced bone loss. J Clin Endocrinol Metab. 2010; 95(5): 2248–2253.
  39. Zagrodna A, Jóźków P, Mędraś M, et al. Sclerostin as a novel marker of bone turnover in athletes. Biol Sport. 2016; 33(1): 83–87.
  40. Lombardi G, Lanteri P, Colombini A, et al. Sclerostin concentrations in athletes: role of load and gender. J Biol Regul Homeost Agents. 2012; 26(1): 157–163.
  41. Allen MR, Iwata K, Phipps R, et al. Alterations in canine vertebral bone turnover, microdamage accumulation, and biomechanical properties following 1-year treatment with clinical treatment doses of risedronate or alendronate. Bone. 2006; 39(4): 872–879.
  42. Beck TJ, Kohlmeier LA, Petit MA, et al. Confounders in the association between exercise and femur bone in postmenopausal women. Med Sci Sports Exerc. 2011; 43(1): 80–89.