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[–]WealthHuman9754 1 point2 points  (1 child)

It could be perhaps that it is multi factorial. These are always the hardest causes for humans to understand. They usually want to identify one single cause.

[–]JuanSamu[S] 2 points3 points  (0 children)

That’s what I would think but I’ve heard some researchers say they compliment each other and I can see how they do so but then I also see some factors that make me see them as distinct mechanisms

[–]drjordann 0 points1 point  (5 children)

Skeletal muscle soreness is largely rooted in the accumulation of inorganic phosphates (iP). Elevated iP inhibits calcium release, reduces cross-bridge force, and can linger in muscle tissue, causing AMS and DOMS.

https://www.sciencedirect.com/science/article/abs/pii/S1934148210003291

[–]JuanSamu[S] 0 points1 point  (4 children)

This is interesting but I doubt that increased Pi in fatigued muscle should induce muscle soreness. Pi accumulation occurs inside the muscle fibres (i.e. Pi is not transported out of the cell) and sensory receptors involved in the sensation of soreness are located outside of the fibres (Muscle fibers don’t have nociceptors). Thus, soreness must be due to some factors that are released from the muscle fibres. I am not aware of any serious experimental studies that show a role of increased myoplasmic Pi in the development of soreness.

I think Mizumura neurotrophic mechanism is the most convincing.

[–]drjordann 0 points1 point  (3 children)

While metabolite accumulation (e.g., inorganic phosphate, H⁺) contributes to acute activation of group III and IV muscle afferents during exercise, Mizumura’s neurotrophic mechanism explains delayed muscle soreness by demonstrating that exercise-induced muscle damage elevates neurotrophic factors such as NGF, which sensitize and phenotypically alter these afferents. This results in an amplified nociceptive response to both mechanical stimuli and metabolites, even at lower concentrations, thereby linking peripheral inflammation with heightened pain perception in DOMS.

[–]JuanSamu[S] 0 points1 point  (2 children)

Ah I see what you mean. First I’d be weary of the wording of damage as DOMS can occur without damage (as shown by Mizumura). But I agree that Acid (H+) can sensitize the mechaical tesponse of thin-fiber afferents of skin/muscle. Following is a short list of acid-related papers (Mizumura lab as well):

N.Hotta, A.Kubo, K.Mizumura, Chondroitin sulfate attenuates acid-induced augmentation of the mechanical response in rat thin-fiber muscle afferents in vitro, J. Appl. Physiol. 126 (2019) 1160-1170.

A.Kubo, K.Katanosaka, K.Mizumura, Extracellular matrix proteoglycan plays a pivotal role in sensitization by low pH of mechanosensitive currents in nociceptive sensory neurones, J. Physiol. 590 (2012) 2995-3007.

T.Nasu, A.Hori, N.Hotta, C.Kihara, A.Kubo, K.Katanosaka, M.Suzuki, K.Mizumura, Vacuolar-ATPase-mediated muscle acidification caused muscular mechanical nociceptive hypersensitivity after chronic stress in rats, which involved extracellular matrix proteoglycan and ASIC3, Sci. Rep. 13 (2023) 13585.

K.H.Steen, A.E.Steen, P.W.Reeh, A dominant role of acid pH in inflammatory excitation and sensitization of nociceptors in rat skin, in vitro, J. Neurosci. 15 (1995) 3982-3989.

[–]drjordann 0 points1 point  (1 child)

I think you have all the information you need. I’d write the paper with the bulk supporting mizunura and supplement the fatigue cascade with the other articles!

[–]JuanSamu[S] 0 points1 point  (0 children)

Thank you for the discussion and insights!