Abstract
We investigated the effects of single and repeated exposures to whole-body cryotherapy on biomarkers of bone remodeling and osteo-immune crosstalk: sclerostin, osteocalcin (OC), C-terminal cross-linked telopeptide of type I collagen (CTx-I), osteoprotegerin (OPG) and free soluble receptor activator for nuclear factor κ B ligand (sRANKL). The study included 22 healthy males, grouped in high physical fitness level (HPhL) and low physical fitness level (LPhL), all undergone 10 consecutive sessions in a cryogenic chamber (− 110 °C). We observed a significant time-effect on sclerostin (p < 0.05), OC (p < 0.01), CTx-I (p < 0.001), OC/CTx-I (p < 0.05), and significant differences in sRANKL between the groups (p < 0.05) after the 1st cryostimulation; a significant time-effect on OC (p < 0.001) and OC/CTx-I (p < 0.001) after the 10th cryostimulation, and a significant time-effect on CTx-I (p < 0.001) and OC/CTx-I (p < 0.01) after 10 sessions of WBC. In conclusion, in young men, the first exposure to extreme cold induced significant changes in serum sclerostin. The changes in sRANKL, between groups, suggest that fitness level may modify the body's response to cold. The effects of the first stimulus and the whole session are not identical, probably due to the physiological development of habituation to cold.
Highlights
Whole body cryotherapy (WBC), referred to as whole-body c ryostimulation[1], is a procedure based on short exposures (1–3 min) to extremely cold air (− 110 °C) in a controlled chamber[2]
An overview of baseline characteristics in high physical fitness level (HPhL) and low physical fitness level (LPhL) group are given in Tables 1 and 2
The effects of the acute cold stimulation at either the beginning (1st session) or the end (10th session) of the WBC treatment on blood concentration of sclerostin, OC, CTx-I, OC/CTx-I ratio, OPG, sRANKL, OPG/sRANKL ratio are presented in Figs. 1 and 2
Summary
Whole body cryotherapy (WBC), referred to as whole-body c ryostimulation[1], is a procedure based on short exposures (1–3 min) to extremely cold air (− 110 °C) in a controlled chamber[2]. A way by which bone interacts with energy metabolism, is attributed to osteocalcin (OC) which acts on pancreatic cells and adipocytes, at least in rodents and in vitro models[12] According to this new vision, glucose homeostasis, fat metabolism, adipose tissue metabolism, and bone remodeling are closely linked and regulate one the other in order to maintain the energy h omeostasis[14,15]. Sclerostin, a Wnt signaling pathway antagonist[18], is a glycoprotein primarily secreted by osteocytes[19] This osteokine downregulates bone formation and promotes bone resorption by increasing expression and release of receptor activator of nuclear factor κB ligand (RANKL) from o steoblasts[20]. The RANKL/RANK/OPG system, a key homeostatic axis linking bone metabolism and immune function, participates in the regulation of bone resorption. Because sclerostin antagonizes the Wnt/β-catenin signal pathway, changes in sclerostin expression can modulate resorption by regulating OPG25
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