ASICs required for immediate exercise-induced muscle pain

pattismith

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ASICs are required for immediate exercise-induced muscle pain and are downregulated in sensory neurons by exercise training

Tahsin Khataei
,
Anne Marie S. Harding
,
Mahyar Janahmadi
,
Maram El-Geneidy

23 JUN 2020

Abstract
Exercise training is an effective therapy for many pain-related conditions, and trained athletes have lower pain perception compared with unconditioned people.

Some painful conditions, including strenuous exercise, are associated with elevated levels of protons, metabolites, and inflammatory factors, which may activate receptors and/or ion channels, including acid-sensing ion channels (ASICs), on nociceptive sensory neurons.

We hypothesized that ASICs are required for immediate exercise-induced muscle pain (IEIP) and that exercise training diminishes IEIP by modulating ASICs within muscle afferents.

We found high-intensity interval training (HIIT) reduced IEIP in C57BL/6 mice and diminished ASIC mRNA levels in lumber dorsal root ganglia, and this downregulation of ASICs correlated with improved exercise capacity.

Additionally, we found that ASIC3 −/− mice did not develop IEIP; however, the exercise capacity of ASIC3 −/− was similar to wild-type mice.

These results suggest that ASICs are required for IEIP and that diminishment of IEIP after exercise training correlates with downregulation of ASICs in sensory neurons.

NEW & NOTEWORTHY Exercise performance can be limited by the sensations of muscle fatigue and pain transmitted by muscle afferents. It has been proposed that exercise training abrogates these negative feedback signals. We found that acid-sensing ion channels (ASICs) are required for immediate exercise-induced muscle pain (IEIP). Moreover, exercise training prevented IEIP and was correlated with downregulation of ASICs in sensory neurons.
 

Wishful

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This might apply to some PWME, but I'm guessing that the level of exercise training required for a noticeable effect will be beyond what most PWME can tolerate. It's possible that it's a non-linear function, and those with the lowest fitness could see the most improvements from small increases in exercise. Anyone for experimentation? :)

A safer way to test this is from existing observations. Has anyone here noticed a significant reduction in muscle pain from increases in exercise?
 

pattismith

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This might apply to some PWME, but I'm guessing that the level of exercise training required for a noticeable effect will be beyond what most PWME can tolerate. It's possible that it's a non-linear function, and those with the lowest fitness could see the most improvements from small increases in exercise. Anyone for experimentation? :)

A safer way to test this is from existing observations. Has anyone here noticed a significant reduction in muscle pain from increases in exercise?
yes I think that some of us have hyperexcitable ASIC 3 in muscles' small nerve fibers (C and Adelta), which would explain the pain during exercise and also the pain after the exercise lasting for days.
This last one is called Delayed onset muscle soreness (DOMS) and the link with ASIC 3 and small fibers was shown in this study ;

https://forums.phoenixrising.me/thr...ensitivity-after-exercise.80584/#post-2283295
 

wabi-sabi

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Has anyone here noticed a significant reduction in muscle pain from increases in exercise?
No- the more I exercise the more I hurt. Pain goes away with enough rest and time on the heating pad. In fact, my pain pretty much only comes on in response to exercise- if you can call getting myself to the mailbox exercise.
 

pattismith

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No- the more I exercise the more I hurt. Pain goes away with enough rest and time on the heating pad. In fact, my pain pretty much only comes on in response to exercise- if you can call getting myself to the mailbox exercise.
the pain reduction with training is suppose to work for healthy people, not for CFS/ME.

It doesn't work for me either.

The muscle pain with exercise comes from hyper reactivity of the small berve fibers (C and A delta) and ASIC 3 receptors excitation.

This mean that our muscle pain is a small nerve fiber dysfunction, with probable hyper reactivity of ASIC 3.
 

Pyrrhus

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From Wikipedia:

Wikipedia said:
Acute muscle soreness (AMS) is the pain felt in muscles during and immediately, up to 24 hours, after strenuous physical exercise. The pain appears within a minute of contracting the muscle and it will disappear within two or three minutes or up to several hours after relaxing it.

The following causes have been proposed for acute muscle soreness:
  • Accumulation of chemical end products of exercise in muscle cells such as lactic acid and H+
  • Muscle fatigue (the muscle tires and cannot contract any more)
Source: https://en.wikipedia.org/wiki/Acute_muscle_soreness


From other papers I've read, the mechanism behind acute muscle soreness may actually be a mix of:
  1. H+ leaking from the stressed muscle mitochondria activate the acid sensors (ASICs) on neighboring cells.
  2. ATP leaking from the stressed muscle cells activate the purine sensors (P2X) on neighboring cells.
Despite a prior misconception, the contribution from lactic acid appears to only be temporary, as lactic acid is quickly removed from muscle tissue and carried in the blood to the liver, where it is converted to glucose and released back into the blood in a matter of minutes.
 
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