Effects of Topical Icing on Inflammation, Angiogenesis, Revascularization, and Myofiber Regeneration in Skeletal Muscle Following Contusion Injury

Abstract

Contusion injuries in skeletal muscle commonly occur in contact sport and vehicular and industrial workplace accidents. Icing has traditionally been used to treat such injuries under the premise that it alleviates pain, reduces tissue metabolism, and modifies vascular responses to decrease swelling. Previous research has examined the effects of icing on inflammation and microcirculatory dynamics following muscle injury. However, whether icing influences angiogenesis, collateral vessel growth, or myofiber regeneration remains unknown. We compared the effects of icing vs. a sham treatment on the presence of neutrophils and macrophages; expression of CD34, von Willebrands factor (vWF), vascular endothelial growth factor (VEGF), and nestin; vessel volume; capillary density; and myofiber regeneration in skeletal after muscle contusion injury in rats. Muscle tissue was collected 1, 3, 7, and 28 d after injury. Compared with uninjured rats, muscles in rats that sustained the contusion injury exhibited major necrosis, inflammation, and increased expression of CD34, vWF, VEGF, and nestin. Compared with the sham treatment, icing attenuated and/or delayed neutrophil and macrophage infiltration; the expression of vWF, VEGF, and nestin; and the change in vessel volume within muscle in the first 7 d after injury (P < 0.05). By contrast, icing did not influence capillary density in muscle 28 d after injury (P = 0.59). The percentage of immature myofibers relative to the total number of fibers was greater in the icing group than in the sham group 28 d after injury (P = 0.026), but myofiber cross-sectional area did not differ between groups after 7 d (P = 0.35) and 28 d (P = 0.30). In conclusion, although icing disrupted inflammation and some aspects of angiogenesis/revascularization, these effects did not result in substantial differences in capillary density or muscle growth.

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise

“…It has already been shown that cryotherapy can weaken or delay the infiltration of inflammatory cells (8,33), which could be explained by vasoconstriction caused by exposure to the cold. This causes the reductionof cellular permeability, and lymphatic and capillary vessels, and consequently reduces fluid propagation into the interstitial space (34).…”

Icing treatment in rats with crush syndrome can improve survival through reduction of potassium concentration and mitochondrial function disorder effect

“…Furthermore, low tissue temperature is the most powerful intervention towards limiting ischemia reperfusion injury (IRI), which may subsequently prevent mitochondrial damage and, therefore, reduce the severity of IRI (9). Basic animal studies have proved the positive effect of icing treatment over contusion injury (10) and crush injury in rats (11) in the early stages of attenuated inflammation (during migration of inflammatory cells); however, these effects were not sufficient to prevent effective muscle regeneration at later stages. Furthermore, such studies did not investigate and clarify the efficacy of icing intervention in improving survival, electrolyte balance, vital signs, and inflammation at early stages within 24 h.…”

Impact of heat therapy on recovery after eccentric exercise in humans

“…For example, cryotherapy, one widely popular postexercise recovery modality, appears to delay rather than improve recovery after a bout of eccentric exercise of the elbow flexors (50) as well as arm cycling exercise (8). In animal models of muscle injury, topical icing has been shown to delay the infiltration of inflammatory cells into the damaged muscle (45,47) and attenuate the expression of proangiogenic factors (45).…”