Acute effect of impact and resistance exercise on Wnt signaling modulators, bone and cartilage metabolism.

Impact and resistance exercise have potent osteogenic effects and may positively affect cartilage through tissue deformation. These effects may be mediated through inhibitors of Wnt signaling such as sclerostin and Dickkopf WNT signaling pathway inhibitor 1 (DKK1), which may also play a role in cartilage metabolism. This study evaluated the effect of acute bouts of impact and resistance exercise on biomarkers of bone turnover, signaling, and cartilage metabolism. Healthy young men completed impact or resistance exercise and a control trial in random order. Impact exercise involved 120 maximum-effort multidirectional jumps and hops. Resistance exercise involved 120 high load lower limb lifts. Jumps and lifts were interspersed with 1-3 s pauses. In control trial, participants rested in a supine position for same duration as exercise trial. Blood samples were taken pre, immediately and 24 h post exercise/rest and analyzed for sclerostin, DKK1, C-terminal telopeptide of type I collagen (CTX-I), procollagen I N-terminal propeptide (PINP), procollagen II C-terminal propeptide (PIICP) and cartilage oligomeric matrix protein (COMP). Repeated measures ANOVA compared time points, trials and their interaction. Participants were 26 men, mean (SD) age 23.4 (2.9) years. Impact exercise increased PINP immediately post exercise (by mean [95%CI] +10.8[4.8,17.2]%, p = .002) and 24 h later (+7.4[0.0,15.3]%, p = .05) whereas resistance exercise had no effect. A transient increase in sclerostin immediately post exercise occurred in the impact exercise trial only (+36.3[24.6,49.3]%, p < .001). Both exercise modes transiently increased DKK1 immediately post exercise (impact +32.4[23.1,42.4]%, p < .001; resistance +30.3[22.8,38.4]%, p < .001). COMP increased immediately after resistance exercise only (+36.2[16.0,59.8]%, p < .001). Neither form of exercise affected CTX-I. Impact and resistance exercise transiently increased Wnt signaling inhibitors. Resistance exercise increased a marker of cartilage turnover but did not affect markers of bone turnover. Impact exercise did not affect cartilage turnover markers. Increases in bone formation but not resorption markers may reflect positive adaptation to impact loading.