Om triggerpunkter og hvordan muskelspenninger gir oksygenmangel som så fører til melkesyreopphopning. Nevner også at capillærer trekker seg sammen. En annen studie som det refereres til viser bilder og grafer av hvordan dette skjer; økt blodoppsamling pga trange kapillære vener der blodet strømmer ut fra triggerpunktet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3440564/#__ffn_sectitle

«Since the capillary blood pressure ranges from approximately 35 mm Hg at the beginning (arterial side) to 15 mm Hg at the end of the capillary beds (venous side), the capillary blood flow is temporarily obstructed during muscle contractions. The blood flow recovers immediately with relaxation, which is consistent with its normal physiological mechanism. In dynamic rhythmic contractions, intramuscular blood flow is enhanced by this contraction-relaxation rhythm, also known as the muscular pump. During sustained muscle contractions, however, muscle metabolism is highly dependent upon oxygen and glucose, which are in short supply.»

«Since oxygen and glucose are required for the synthesis of adenosine triphosphate (ATP), which provides the energy needed for muscle contractions, sustained contractions may cause a local energy crisis due to the lack of oxygen. To guarantee an adequate supply of ATP, the muscle can switch within a few seconds to anaerobic glycolysis. »

«Under anaerobic circumstances, however, most of the pyruvic acid produced during glycolysis is converted into lactic acid, thereby increasing the intramuscular acidity (pH). Most of the lactic acid diffuses out of the muscle into the bloodstream; post-exercise lactic acid is washed out within 30 minutes after exercise. Unfortunately, when the capillary circulation is restricted, as in sustained low-level contractions, this process comes to a standstill.»

«Small increases of the H+ concentration, as seen with inflammation, heavy muscle work, and ischemia, are sufficient to excite muscle group IV endings, contributing to mechanical hyperalgesia and central sensitization (15).»

«They identified 2 contributing factors, namely an increase in the volume of the vascular compartment, and an increased outflow resistance. Increased outflow resistance could be due to muscle contractures at the TrP that compress the capillary or venous bed. Sustained low-level contractions are common in the workplace where many occupations rely on prolonged postures, as seen in musicians, supermarket cashiers, computer operators, hairdressers, and dentists, among others.» Bilder ref til denne studies: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493167/

«Hägg suggested that the continuous activity of these motor units in sustained contractions causes overuse muscle fiber damage, especially to the Type I fibers during low-level activities, which he summarized in his Cinderella hypothesis21. It is conceivable that in sustained low-level contractions and in dynamic repetitive contractions, ischemia, hypoxia and insufficient ATP synthesis in type I motor unit fibers are responsible for increasing acidity, Ca2+ accumulation, and subsequently sarcomere contracture. Furthermore, starting with the sarcomere (super-) contraction, the intramuscular perfusion slows down and ischemia and hypoxia will occur. This may lead to the release of several sensitizing substances causing peripheral sensitization15,22.»

«A key factor is the local ischemia, which leads to a lowered pH and a subsequent release of several inflammatory mediators in muscle tissue. Hocking proposed an interesting counterargument, which deserves further exploration. Whether overuse mechanisms are the crucial initiating factor or persistent nociceptive input remains a point of debate and further study.»

Forklaring på hva Hocking mener:
«Rather than looking at overuse mechanisms, Hocking maintains that persistent nociceptive input causes the formation of TrPs through central sensitization of the C-fiber nociceptive withdrawal reflex and plateau depolarization of withdrawal agonist alpha-motor neurons and compensatory reticulospinal motor facilitation of antigravity muscles and plateau depolarization of withdrawal antagonist alpha-motor neurons (33). «