During my last semester at UMD, I wrote a thesis titled, “Effects of anti-inflammatory modalities on muscle regeneration after acute muscle injury”. Through my research I found that recommendations by sports medicine practitioners to ice and take NSAID’s to treat musculoskeletal injuries are ubiquitous, but unfortunately quite erroneous. When doctors, physical therapists and chiropractor’s prescribe these treatments, the underlying reason cited is to reduce inflammation around the injured area. The RICE (Rest, Ice, Compression, and Elevation) technique is the current ‘best practice’ for accomplishing this. Mounting evidence suggests, however, that this may in fact worsen the long-term recovery of injured areas, specifically for the reason that it reduces inflammation. Inflammation is a critical process necessary for injured areas to fully recover, so why try and reduce it? More concerning is the widespread evidence that doctors, physical therapists and chiropractors still prescribe the RICE treatment while years of contrarious evidence suggest they should do otherwise.
Case in point, in my last semester at UMD I also took a class called “The Principles of Exercise and Rehabilitation”. One of the primary 'take home' points of that class was to ice any and all injuries. The instructor drilled it into our heads, but with virtually no scientific research presented, I was a little dubious, and according to my thesis icing actually made injuries worse. Tens of thousands of doctors, physical therapists and chiropractor’s recommend these icing and NSAID's as treatment for musculoskeletal injuries, so are they wrong? Science seems to say so. Icing and NSAID's have been shown time and again to reduce pain and elevate subjective feelings of betterment. If you make the patient feel better, they’ll think the treatment is working, come back for more and tell their friends too. Certainly this isn't always the case, and a good cadre of sports and physical rehab doctors dutifully keep up with current research. Even then, it's somewhat surprising to see how this subject remains hotly debated when the science says its all but a moot point. Witness the opposing viewpoints of the physical therapist and the track coach in this Washington Post article for an illustration. The physical therapist is grounded in science, while the track coach is anything but objective.
Here are a few relevant sections from my thesis that specifically concern the effects of icing and NSAID’s on muscle regeneration post-injury:
These findings raise the question of whether commonly used modalities in sports medicine for treating musculoskeletal injuries such as icing and prescription of non-steroidal anti-inflammatory drugs (NSAID’s) actually promote muscle regeneration or are simply used for pain reduction (Orchard et al., 2008). A study by Takagi et al. (2011) demonstrated that the application of ice for 20 minutes five minutes after a crush injury of the EDL muscle in rats actually delayed the degeneration and necrosis of muscle cells by approximately 1 day, potentially via the slowing of calpain enzyme activity, a calcium-dependent neutral protease that plays a central role in the degeneration and necrosis of injured muscle fibres. This delay in degeneration with icing also resulted in the delay of the inflammatory response, evidenced by a reduction in Mp’s in the degenerating area at 6 and 12 h post injury as compared with the nonicing group, suggesting that icing impaired Mp migration to the injured area, likely through the impairment of muscle degeneration post injury and the associated lack of secretion of chemo-attractant substances such as CCL2. Furthermore, at 14 d post injury, centrally nucleated (immature) muscle fibers were more prevalent in the icing group than in the nonicing group, and the CSA of regenerating fibres in the icing group were significantly smaller than those in the nonicing group at 28d post injury, indicating that icing could have impaired differentiation and maturation of regenerating muscle fibres. As a result, in the icing group, the production of TGF-β1 and IGF-1 from Mp’s was delayed. TGF-β1 stimulates proliferation and differentiation of satellite cells, while IGF-1 stimulates the differentiation and growth of regenerating muscle fibres via increases in protein synthesis (Takagi et al., 2011; Strle et al., 2006).Lastly, fibrosis of the EDL muscle was significantly upregulated in the icing group at 14 and 28 days post injury, with a total proportion of 8.5% collagen fibres in the non-icing group and 18.7% collagen fibres in the icing group at 28d post injury. This may be explained by the delay in induction of TGF-β1, expression of which was evident at 5d post injury in the icing group, but only up to 3d post injury in the nonicing group. TGF-β1 has been shown to stimulate fibroblast differentiation and collagen synthesis, leading to the development of fibrosis. Thus, the timing of expression of TGF-β1 may be critical to the development of fibrosis (Takagi et al., 2011). This suggests that delaying the degenerative and inflammatory phases of muscle regeneration could prolong TGF-β1 secretion and contribute to the aberrant development of fibrosis. TGF-β1 has been found to auto-induce its own expression in myoblasts and to act in a time-and dose-dependent manner in stimulating myoblasts to express myofibroblastic protein while decreasing their expression of myogenic proteins (Li et al. 2004).In a similar vein, a study assessing the effects of the NSAID flurbiprofen on functional recovery from eccentric exercise-induced injury demonstrated a short-term increase in muscle torque between 3 and 7d post injury with NSAID treatment, but a decreased torque at 28d post injury compared with the untreated group. Interestingly, there appeared to be a protective effect of treatment on structural proteins such as desmin with NSAID treatment, which were significantly reduced in the untreated as compared to treated group, a biologically plausible phenomenon considering the reduction in infiltrating neutrophils and resultant impairment of degeneration and necrosis of injured muscle tissue with NSAID’s. This impairment is also evidenced by the significantly greater expression of embryonic myosin 3d post injury in the untreated group than in the treated group, which was reversed at 7d post injury with greater amounts of embryonic myosin in the treated group than in the untreated group, although this was not significant (Mishra et al., 1999). This suggests that NSAID treatment post injury can have beneficial short-term effects on preservation of ultrastructural proteins and hence relative maintenance of muscle torque, but the accompanying impairment in muscle regeneration resulted in a diminished torque in the long-term as compared with the untreated group.
I personally experienced what these researcher’s describe when I unfortunately succumbed to conventional medical ‘wisdom’ and popped NSAID’s left and right in an attempt to speed the recovery of a hamstring injury. Unsurprisingly, full recovery of the muscle took far longer under these circumstances, and the residual fibrosis that I was left with was only subdued by months of constant stretching and ROM exercises.