Myofascial Adhesions (Muscle Knots)

Myofscial Adhesions (also known as myofascial pain syndrome) arises from the muscle and are caused by myofascial trigger points. The symptoms are a collection of the sensory, motor, and autonomic systems that include local and referred pain, decreased range of motion, and weakness. Patients suffer from decreased functional status associated with musculo-skeletal pain and loss of function, but also suffer from impaired mood as well as decreased quality of life.

The trigger points are associated with areas in muscle that have stiff, tender nodules under palpation. It is believed that this stiffness might arise from hypercontracture of the sarcomere in the affected area

There are several massage treatments that relax myofascial trigger points such as passive rhythmic release, active rhythmic release, and trigger point pressure release. What seems to be common is that they alleviate muscle stiffness and pain and may be combined with therapies that stretch and improve metabolism at the hypercontracted trigger point region.

It is widely believed that massage increases blood flow. For example, it has been shown that massage of the lower left extremity in young females increased blood flow in the tibial artery as measured by Doppler ultrasound. If this occurred on the local level in muscle, this would in principle break the cycle in the above theories. However, this finding does not necessarily affect the microcirculation which is thought to be constricted in a myofascial trigger point. Furthermore, massage activated the mechano-transduction signaling pathways FAK and ERK (focal adhesion kinase and extracellular signal-regulated kinase, resp.), decreased inflammatory cytokines, and increased mitochondrial biogenesis. which improve energy metabolism in the muscle. Therefore, one way massage may reduce muscle stiffness is by the reduction of focal adhesions through activation of the FAK pathway.

Stretching involves a series of stretching exercises of the muscle where pain is experienced. Muscle stretching training may increase circulation as shown in ballet trained individuals. This might explain the observed long-term benefit. Recent experiments have shown that stretching skeletal myocytes activates NADPH oxidase. This occurs through the microtubules serving as mechano-transducers, resulting in the production of reactive oxygen species. In muscular dystrophic cells this response is greater due to the increase in microtubule density in these myocytes. In addition, this presents the possibility that stretching of muscle, similar to massage, activates the FAK and ERK pathways.