The integrated hypothesis: why a taut band forms and stays

The model starts at the motor endplate: excessive acetylcholine release keeps a small cluster of sarcomeres contracted. Sustained contraction compresses local capillaries, so oxygen delivery falls exactly where energy demand is highest.

The resulting energy crisis lowers pH and releases sensitising substances, which in turn increase acetylcholine release. The loop closes on itself, which is why a point can persist for months without any new injury.

For the terminology and interpretation used here, compare What are trigger points?; Primary vs secondary trigger points; How to read referred pain maps. These guides distinguish the definition of a trigger point, its classification and the limits of a referred-pain map.

Local chemistry alone does not explain pain felt in a distant area. The expanded model adds central sensitisation: persistent nociceptive input from the muscle lowers the threshold of dorsal horn neurons, which then respond to input from convergent territories, and the brain localises the pain there.

That is why referred zones are reasonably consistent between people, follow neurological convergence rather than dermatomes, and often shrink as the source point calms down.

If the loop is the problem, then anything that interrupts it should help: mechanical disruption of the contracted band, restored circulation, reduced sustained load, and less nociceptive drive overall. That is precisely the treatment set with the strongest clinical support today.

It also predicts relapse when perpetuating factors are ignored — the same postural, ergonomic and sleep factors listed on every muscle page here.