Trigger points are in reality part of what I call a tendinous myofascial unit, i.e. an entire myofascial unit in which the muscles are contracted and myofascia is extended (relaxed) with muscles hypertonia.

I think that the molecule responsible for this is nitric oxide and that the NOS inhibition throught local injection of NOS inhibitor can make myofascia to contract, promoting the contraction of myofibroblasts which was before inhibited by NO, and the muscle to lose hypertone restablishing the physiological lenght of the muscle.

is there anyone who can test this hypothesis throught experiments? Let me know