An attempt to improve Ferreira-Junior model concerning the anti-inflammatory action of whole-body cryotherapy after exercise induced muscular damage (EIMD)

Recently, an interesting model trying to explain the anti-inflammatory action of whole body cryotherapy (WBC) after exercise induced muscular damage (EIMD) was published by Ferreira Junior et al. in Frontiers in Physiology (Ferreira-Junior et al., 2014). The authors have suggested that soluble intercellular adhesion molecule-1 (sICAM-1) could be one of the main influencing compounds that could regulate the cryotherapy antiinflammatory response. According to the authors, after EIMD sarcomeres are disrupted leukocytes (neutrophils, monocytes, and lymphocytes) are mobilized to the injured tissue via sICAM-1. Afterward, pro-inflammatory cytokines and reactive oxygen species are produced in muscle by leukocytes. Together, leukocytes, pro-inflammatory cytokines, and reactive oxygen species cause intramuscular degradation, which amplifies the initial muscle damage. The authors suggested that a drop in core temperature induced by WBC would likely cause constriction of local arterioles and venules and lower the amount of leukocytes arriving to the exercise-induced muscular inflammation. Moreover, WBC may hasten the recovery from EIMD by reducing sICAM-1 and therefore limiting the migration of leukocytes from blood circulation to the damaged tissues. The first part of the explanation concerning the WBC-induced vasoconstriction is understandable though a drop in core temperature is not always clear (no changes in core temperature has been observed after 2 min exposure at −110◦C Westerlund et al., 2003). However, concerning the second part of the explanation dealing with a lower concentration of circulating sICAM-1. I would argue that an increase in the blood concentration of this analyte might paradoxically occur. Intercellular adhesion molecule-1 is a widely distributed adhesion factor present on the surfaces of endothelial cells and leukocytes. This protein mediates adhesion and transmigration of leukocytes through the endothelium. Surface expressed ICAM-1 is apparently shed from the cells and then circulates as soluble ICAM-1 (sICAM-1) although the full mechanism is not clear. Therefore, blood sICAM-1 concentration increase may be due to several mechanisms: