Soreness probably not caused by inflammation, but by something it prevents

PainSci » bibliography » Deyhle et al 2015
updated Aug 1, 2017

Tags: inflammation, biology, DOMS, pain problems, exercise, self-treatment, treatment, muscle

One article on PainSci cites Deyhle 2015: A Deep Dive into Delayed-Onset Muscle Soreness

PainSci commentary on Deyhle 2015: ?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.

Soreness after workouts goes down as you get used to it (“repeated bout effect”). If the soreness is caused by inflammation, then there must be less inflammation after repeated workouts than initial workouts. These researchers tried to confirm that inflammation reduction, and found, “overwhelmingly,” exactly the opposite. Inflammation after subsequent workouts either fails to go down or actually goes up! Huh? Maybe that even calls for a “WTF”!

So, exercise soreness is probably not caused by inflammation … but by something else that inflammation itself actually prevents. •mind blown• Here’s a jargon-free version of the authors’ explanation of what might be going on, from the full text of the article:

Overwhelmingly, our data undermines the idea of a muted inflammatory response after a second bout of exercise. On the contrary, the data suggest an neutral or increased inflammatory response! … We saw that inflammatory indicators only increased after a second workout. This suggests that the initial workout may have sensitized the muscle toward a stronger, longer inflammatory response after the second workout. In other words, the muscle seems to “remember” the stress of the first workout, and responds with a stronger recruitment of immune cells when the stress is repeated — much like the way our immune system responds to an invader by preparing for an even stronger response the next time. Furthermore, muscle soreness goes down when the inflammation goes up, indicating that’s unlikely the soreness is caused by inflammation.

Fascinating!

~ Paul Ingraham

original abstract †Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Skeletal muscle responds to exercise-induced damage by orchestrating an adaptive process that protects the muscle from damage by subsequent bouts of exercise, a phenomenon called the repeated bout effect (RBE). The mechanisms underlying the RBE are not understood. We hypothesized that an attenuated inflammation response following a repeated bout of lengthening contractions (LC) would be coincidental with a RBE, suggesting a potential relationship. Fourteen men (n = 7) and women (n = 7) completed two bouts of lengthening contractions (LC) separated by 28 days. Muscle biopsies were taken before the first bout (B1) from the non-exercised leg, and from the exercised leg 2- and 27-d post-B1 and 2-d following the second bout (B2). A 29-plex cytokine array identified alterations in inflammatory cytokines. Immunohistochemistry quantified inflammatory cell infiltration and major histocompatibility complex class 1 (MHC-1). Muscle soreness was attenuated in the days following B2 relative to B1, indicating a RBE. Intramuscular monocyte chemoattractant protein (MCP1) and interferon gamma-induced protein 10 (IP10) increased following B2 relative to the pre-exercise sample (7-52 and 11-36 pg/ml, respectively p < 0.05). Interleukin 4 (IL4) decreased (26-13 pg/ml, p < 0.05) following B2 relative to the pre-exercise sample. Infiltration of CD68(+) macrophages and CD8(+) T-cells were evident following B2, but not B1. Moreover, CD8(+) T-cells were observed infiltrating apparently necrotic muscle fibers. No changes in MHC-1 were found. We conclude that inflammation is not attenuated following a repeated bout of LC and that CD8(+) T-cells may play a role in muscle adaptation following LC. Moreover, it appears that the muscle or the immune system becomes sensitized to an initial bout of damaging exercise such that inflammatory cell infiltration into the muscle is enhanced upon a repeated bout of damaging exercise.

original abstract †Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

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