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Neurological growing pains: the nature of exercise soreness

 •  • by Paul Ingraham
Weekly nuggets of pain science news and insight, usually 100-300 words, with the occasional longer post. The blog is the “director’s commentary” on the core content of a library of major articles and books about common painful problems and popular treatments. See the blog archives or updates for the whole site.
Woman playing tennis, getting ready to serve.

Racquet sports are always hard on my forearm muscles — sore for days, every time.

One of the more enduring little puzzles in medicine is the nature of the soreness that crops up after exercise (post-exercise or delayed-onset muscle soreness). Vague ideas like “microtrauma” are probably true in some sense, but it’s not nearly that simple, and ongoing research has been slow.

But I’m now cautiously optimistic that the mystery of exercise soreness has more or less finally been solved. A series of Japanese studies since 2010 have showed that the pain is probably related to neurotrophic factors [Wikipedia]: substances secreted by muscles cells that goose nerve growth (see Mizumura 2016).

Nerve growing pains, in other words.

Exercise pushes our nerves to develop, and apparently that’s uncomfortable.

This accounts for the vivid “repeated bout effect”: the great reduction in discomfort when you repeat the same workout a few days later.

It would also explain the curious findings of Ayles et al, who showed that exercise soreness can spread to adjacent muscles groups that were not exercised at all.

All of this was demonstrated in rats, not humans, and all by the same group of researchers, so it’s not time to uncork the champagne and declare victory quite yet. But it’s extremely interesting and promising, and it gets better: based on this theory, the Japanese researchers did demonstrate that the development of DOMS was “completely suppressed” by a drug that stifles neurotrophic factors. Yahtzee?

And what was that drug?

Mizumura et al prevented exercise soreness using COX-2 inhibitors, which specifically inhibit neurotrophic growth factors. This is not their primary purpose: COX-2 inhibitors are anti-inflammatory meds by nature, a much-maligned type of NSAID with major safety issues, and the only remaining drug of this type for sale in the US is Celebrex (celecoxib).

If Celebrex can be clearly shown to prevent DOMS in humans, that’s a huge deal, not because it’s a viable treatment — preventing DOMS almost certainly isn’t valuable enough to be worth the side effects of COX-2 inhibitors — but because it would prove the mechanism of DOMS. And that's a cool and substantive knowledge upgrade.

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