Why icing is good

All data were tested and confirmed as normally distributed using the Shapiro—Wilks formula. The false discovery rate was used to control for multiple comparisons between groups. The necrotic muscle fibers were identified by enlarged myofibers without nuclei. In the rats sacrificed at 3 d after injury, the necrosis had cleared almost entirely in the sham group, whereas several necrotic areas were still present within the icing group. Several macrophages were visible throughout the necrotic tissue in the sham group, but these cells were not as prominent in the icing group.

In the rats sacrificed at 7 d after injury, the necrosis had cleared, and several immature centrally nucleated muscle fibers were evident in muscle tissue from both the sham and icing groups. In the rats sacrificed at 28 d after injury, the inflammatory cell influx had resolved, and normal tissue structure was almost restored with the exception of large maturing myofibers. Representative cross sections of skeletal muscle tissue.

E Shows muscle tissue from an uninjured rat for comparison. Arrowheads indicate necrotic muscle fibers. Arrows indicate regenerating muscle fibers centrally placed nuclei. Representative images of immunohistochemistry staining of neutrophils. Skeletal muscle tissue was stained with HIS48 antibody to identify neutrophils. Sham A,C and icing B,D groups at 1 and 3 d after injury.

Representative images of immunohistochemistry staining of macrophages. Skeletal muscle tissue was stained with CD68 antibody to identify macrophages. Sham A—C and icing D—F groups at 1, 3, and 7 d after injury.

Arrows indicate macrophages. There were no neutrophils present in muscle in either group at 7 and 28 d after injury data not shown. Quantitative data for neutrophil A and macrophage B count in skeletal muscle tissue. Neutrophils and macrophages were not present in skeletal muscle tissue from uninjured control rats. CD34 staining was used to identify endothelial cells Wiik et al.

Staining for CD34 was quantified as the area of positive staining as a percentage of the total area of tissue within the field of view. Thereafter, the percentage of CDstained area was greater in muscle from the icing and sham groups than in the control group. Representative images of immunohistochemistry staining of endothelial cells.

Skeletal muscle tissue was stained with CD34 antibody to identify endothelial cells. Sham A—D and icing E—H groups at 1, 3, 7, and 28 d after injury. Arrows indicate vessels. The data are shown as a percentage relative to the total area of muscle tissue within the field of view.

In contrast to the staining for CD34 and consistent with other reports Qu et al. Staining for vWF was quantified as the area of positive staining as a percentage of the total area of tissue within the field of view.

Representative images of immunohistochemistry staining for vWF antibody to identify endothelial cells in muscle tissue. Sham A—C and icing D—F groups at 1, 3, 7, and 28 d after injury. Arrows indicate mature vessels. It was greater in muscle from the sham group vs. Representative images of immunohistochemistry staining with VEGF antibody. Muscle tissue was obtained from the sham A and icing B groups at 3 d after injury.

Arrows indicate vessels expressing VEGF. Arrowheads indicate positively stained macrophages. We used nestin to identify maturing endothelial cells Cizkova et al. Staining for nestin was quantified as the area of positive stain as a percentage of the total area of tissue within the field of view. Nestin was also detected in the sarcoplasm of immature myotubes and myofibers. At 28 d, few large muscle fibers expressed nestin. Representative images of immunohistochemistry staining.

Nestin antibody was used to identify endothelial cells in muscle tissue from the sham A—D and icing E—H groups at 1, 3, 7, and 28 d after injury. Arrows indicate positively stained endothelial cells. The vessel volume in muscle was determined by micro-CT. Quantitative data for vessel volume A and number of regenerating myofibers B in skeletal muscle tissue. At 7 d after injury, many centrally nucleated regenerating muscle fibers were present in the sham group, whereas only a few were present within the icing group.

The aim of this study was to examine the effects of icing soon after muscle contusion injury on subsequent inflammation, angiogenesis, revascularization, and myofiber regeneration. Despite these differences, capillary density and the cross-sectional area of myofibers did not differ significantly between the icing and sham groups.

Contusion injury caused extensive necrosis in skeletal muscle during the first 3 d after injury. Icing appeared to prolong the clearance of necrotic tissue, possibly by preventing or delaying the infiltration of neutrophils and macrophages into the damaged muscle Teixeira et al. The decline or delay in infiltration of inflammatory cells is consistent with the results of other studies that have treated muscle injuries with ice Carvalho et al.

This is the first study to investigate whether icing influences angiogenesis and vessel volume in regenerating muscle. Contusion injury induced a sustained increase in the expression of vWF in muscle that lasted at least 28 d. Conversely, contusion injury appeared to suppress CD34 expression in muscle in the first 7 d after injury.

Icing reduced the expression of vWF and CD34 to a lesser extent between 3 and 7 d after injury. Nevertheless, we were able to quantify the area of positive staining for CD34, vWF, and VEGF as percentages of the total area of tissue within the field of view. However, it is possible that capillary density differed between these groups at 3 and 7 d after injury. As such, we cannot attribute the VEGF staining exclusively to angiogenesis.

These differences in staining for vWF and VEGF between the icing and sham groups were accompanied by smaller vessel volume at 3 and 7 d after injury, as measured by contrast-enhanced micro-CT Figure 13A.

Because we could not assess capillary density at these time points, it is difficult to compare the time courses of angiogenesis and collateral vessel growth, as assessed by vessel volume. Others have reported differences in the time course of angiogenesis and collateral vessel growth in skeletal muscle following hind limb ischemia Ito et al.

It is possible that icing exerted a greater effect on vessel volume than on angiogenesis. Our results are not directly comparable with this other research because we assessed static measures of angiogenesis, whereas Schaser et al. Their assessment was also restricted to 1 d after injury. Icing may induce different effects on microcirculatory dynamics in muscle in the days and weeks after injury.

Icing delays satellite cell proliferation in damaged muscle Takagi et al. Evidence for this notion is that proliferating and differentiating satellite cells stimulate human vascular endothelial cells to form tubular-like structures in vitro Christov et al. Skeletal muscle expresses cold shock domain protein A Saito et al. These effects appear to be linked to lower cellular metabolism Coassin et al. When amputated, ischemic limbs of cats are exposed to hypothermia, ATP and phosphocreatine depletion and tissue acidosis are attenuated Osterman et al.

The effects of hypothermia on the production of reactive oxygen species ROS are variable Rauen and de Groot, ; Alva et al. Some research demonstrates that when applied in isolation, hypothermia increases the production of ROS by adenocarcinomic alveolar basal epithelial A cells Sun et al.

Conversely, many studies have reported that when applied following injury, hypothermia reduces the formation of ROS in neuronal cells Gao et al.

In injured rat skeletal muscle, icing decreases the formation of superoxide anions, lipid peroxidation, and activity of the antioxidant enzyme catalase Merrick et al. These findings contrast with other evidence that hypoxia stimulates ROS production in skeletal muscle fibers Zuo and Clanton, ; Zuo et al. Evidence also exists that hypothermia increases angiogenesis in the spinal cord Kao et al. More research is therefore needed to understand the effects of icing on ROS production and angiogenesis in skeletal muscle following injury.

We measured the expression of nestin as a marker of revascularization in skeletal muscle Cizkova et al. Nestin has been detected in endothelial cells Mokry et al. Consistent with other research Vaittinen et al. Pericytes also express nestin, colocalize with endothelial cells and capillaries in skeletal muscle, and contribute to angiogenesis Birbrair et al.

We found that icing attenuated or delayed upregulation of nestin expression in regenerating muscle. Considering that nestin is involved in the differentiation of endothelial cells Cizkova et al. We did not double-stain the muscle tissue for nestin and another marker of endothelial cells e. Nor did we stain the muscle for myotubes, Schwann cells, or axons, which also express nestin Cizkova et al. Accordingly, we cannot establish definitively whether the nestin staining that we observed solely represents revascularization.

We found that icing did not alter myofiber cross-sectional area at 7 or 28 d after injury. However, it did appear to delay myofiber maturation, as indicated by a greater number of immature myofibers with centrally located nuclei at 28 d after injury Figure 13B. Our findings contrast with those of Takagi et al, who reported that icing resulted in more immature myofibers at 14 d but not at 28 d and smaller myofiber cross-sectional area at 28 d after injury Takagi et al.

These differences may be explained by the use of younger rats 8 weeks old and induction of injury by crushing the extensor digitorum longus muscle with forceps for 30 s in the study by Takagi et al. In conclusion, icing attenuated or delayed the infiltration of inflammatory cells, the expression of proangiogenic factors, and change in vessel volume in muscle following injury.

However, these effects were not sufficient to reduce capillary density or prevent effective muscle regeneration. We applied ice treatment at only one time point soon after muscle injury. It is possible that more frequent icing may have produced different effects on inflammation, angiogenesis, and myofiber regeneration. We also used only male rats. Icing may have produced different effects in female rats because of the effects of estrogen on the time course and dynamics of muscle regeneration Enns and Tiidus, Future research could systematically examine whether the duration, timing, or frequency of icing treatment influence inflammation, angiogenesis, and muscle tissue regeneration after injury.

DS, ZB, MW, TP, RS, and JP agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

National Center for Biotechnology Information , U. Journal List Front Physiol v. Front Physiol. Published online Mar 7. Daniel P. The main benefit of icing an injury is to help control or reduce pain.

That may seem like a good thing. However, Dr. Mirkin says that icing for any more than 5 minutes is detrimental to tissue repair, and can also reduce strength, flexibility, and endurance. If you use ice for pain management, use it no more than 5 minutes, and remove it for a minimum of 20 minutes before reapplying.

According to Dr. Mirkin, there is no reason or benefit to apply ice to an injury more than six hours after the initial incident. Other physical therapists agree, at least that the main benefit of ice is pain relief, and that ice should be applied immediately after an injury and for a short period of time only.

There is limited research on the effectiveness of both heat and cold therapy. One small study found no difference in outcomes in patients with ankle injury who received no ice, or ice and compression, or ice without compression. Researchers continue to study the best way to deal with soft tissue injuries and the jury is still out on the most effective treatments. Compression and elevation of an injury may still be appropriate and helpful. Neither action completely stops the release of IGF-1, so the immune response is still able to do its job, yet compression can help manage excessive swelling, which is often one culprit in causing pain.

Still, many experts advise that treatment should be tailored to the athlete. Functional rehab and balance training may be more effective than immobilization, particularly when in managing grade I and II ankle sprains.

As an athlete, it's important to pay attention to any warning signs your body sends, and avoid injury if you can. Preventive measures such as exercising within your physical limits and using protective gear are crucial. If you do sustain a sports injury, it's important to stop playing and have a medical evaluation to determine the extent of the injury and begin the rehab process quickly. Get exercise tips to make your workouts less work and more fun. Does cryotherapy improve outcomes with soft tissue injury?

J Athl Train. Effect of local cold-pack application on systemic anabolic and inflammatory response to sprint-interval training: A prospective comparative trial. Eur J Appl Physiol. Mechanisms and efficacy of heat and cold therapies for musculoskeletal injury. Postgrad Med. Comparative immediate functional outcomes among cryotherapeutic interventions at the ankle.

Ice packs can help minimize swelling around the injury, reduce bleeding into the tissues, and reduce muscle spasm and pain. Ice packs are often used after injuries like ankle sprains have occurred. Applying an ice pack early and often for the first 48 hours will help minimize swelling, and decreasing swelling around an injury will help to control the pain. Ice treatments may also be used for chronic conditions, such as overuse injuries in athletes. In this case, ice the injured area after activity to help control inflammation.

Never ice a chronic injury before activity. You can make ice packs with ice cubes in a plastic bag or wet tea towel; a pack of frozen peas is also ideal and can go in and out of the freezer.

Never place ice directly on an injury; keep the pack moving to avoid ice burns. Never treat with ice for more than 30 minutes, and remove the pack immediately if the injury appears bright pink or red. Heat treatments should be used for chronic conditions to help relax and loosen tissues and to stimulate blood flow to the area.

Use heat treatments for conditions such as overuse injuries before participating in activities.