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Circulating sclerostin is not suppressed following a single bout of exercise in young men.

Katelyn I GuerriereJulie M HughesErin Gaffney-StombergJeffery S StaabRonald W Matheny
Published in: Physiological reports (2019)
The aim of this study was to determine whether an acute bout of exercise reduces serum sclerostin under diet-controlled conditions that stabilize the parathyroid hormone (PTH)-1,alpha-hydroxylase axis. Fourteen male volunteers (age, 22.1 years ± 4.05; BMI, 27.3 kg/m2  ± 3.8) completed a randomized crossover study in which they performed 10 sets of 10 repetitions of plyometric jumps at 40% of their estimated one-repetition maximum leg press or a nonexercise control period. A calcium-controlled diet (1000 mg/day) was implemented prior to, and throughout each study period. Blood was drawn for analysis of serum sclerostin, Dickkopf-1, markers of bone metabolism (PTH, calcium), markers of bone formation (bone alkaline phosphatase, BAP; osteocalcin, OCN), and markers of bone resorption (tartrate-resistant acid phosphatase 5b, TRAP5b; C-telopeptide cross-links of type I collagen, CTX) at baseline and 12, 24, 48, and 72 h following exercise or rest. Changes in serum concentrations were expressed as percentage change from individual baselines. Data were analyzed using a repeated measured linear mixed model to assess effects of time, physical activity status (rest or exercise condition), and the time by activity status interaction. There was a significant effect of exercise on OCN (P = 0.005) and a significant interaction effect for CTX (P = 0.001). There was no effect of exercise on any other biochemical marker of bone metabolism. A single bout of plyometric exercise did not induce demonstrable changes in biochemical markers of bone metabolism under conditions where dietary effects on PTH were controlled.
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