Deep fascia

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Deep fascia
Latin fascia profunda
Gray's p.378

Deep fascia (or investing fascia) is a fascia, a layer of fibrous connective tissue which can surround individual muscles, and also divide groups of muscles into compartments.

This dense fibrous connective tissue interpenetrates and surrounds the muscles, bones, nerves and blood vessels of the body. It provides connection and communication in the form of aponeuroses, ligaments, tendons, retinacula, joint capsules, and septa. The deep fasciae envelop all bone (periosteum and endosteum); cartilage (perichondrium), and blood vessels (tunica externa) and become specialized in muscles (epimysium, perimysium, and endomysium) and nerves (epineurium, perineurium, and endoneurium). The high density of collagen fibers is what gives the deep fascia its strength and integrity. The amount of elastin fiber determines how much extensibility and resilience it will have.[1]

Examples[edit]

Examples include:

Fascial dynamics[edit]

Deep fascia is less extensible than superficial fascia. It is essentially avascular,[2] but is richly innervated with sensory receptors that report the presence of pain (nociceptors); change in movement (proprioceptors); change in pressure and vibration (mechanoreceptors); change in the chemical milieu (chemoreceptors); and fluctuation in temperature (thermoreceptors).,[3][4] Deep fascia is able to respond to sensory input by contracting; by relaxing; or by adding, reducing, or changing its composition through the process of fascial remodeling.[5]

Deep fascia can contract. What happens during the fight-or-flight response is an example of rapid fascial contraction. In response to a real or imagined threat to the organism, the body responds with a temporary increase in the stiffness of the fascia. Bolstered with tensioned fascia, people are able to perform extraordinary feats of strength and speed under emergency conditions.[6] How fascia contracts is still not well understood, but appears to involve the activity of myofibroblasts. Myofibroblasts are fascial cells that are created as a response to mechanical stress. In a two step process, fibroblasts differentiate into proto-myofibroblasts that with continued mechanical stress, become differentiated myofibroblasts.[7] Fibroblasts cannot contract, but myofibroblasts are able to contract in a smooth muscle-like manner.[8]

The deep fascia can also relax. By monitoring changes in muscular tension, joint position, rate of movement, pressure, and vibration, mechanoreceptors in the deep fascia are capable of initiating relaxation. Deep fascia can relax rapidly in response to sudden muscular overload or rapid movements. Golgi tendon organs operate as a feedback mechanism by causing myofascial relaxation before muscle force becomes so great that tendons might be torn. Pacinian corpuscles sense changes in pressure and vibration to monitor the rate of acceleration of movement. They will initiate a sudden relaxatory response if movement happens too fast.[9] Deep fascia can also relax slowly as some mechanoreceptors respond to changes over longer timescales. Unlike the Golgi tendon organs, Golgi receptors report joint position independent of muscle contraction. This helps the body to know where the bones are at any given moment. Ruffini endings respond to regular stretching and to slow sustained pressure. In addition to initiating fascial relaxation, they contribute to full-body relaxation by inhibiting sympathetic activity which slows down heart rate and respiration.[10][11]

When contraction persists, fascia will respond with the addition of new material. Fibroblasts secrete collagen and other proteins into the extracellular matrix where they bind to existing proteins, making the composition thicker and less extensible. Although this potentiates the tensile strength of the fascia, it can unfortunately restrict the very structures it aims to protect. The pathologies resulting from fascial restrictions range from a mild decrease in joint range of motion to severe fascial binding of muscles, nerves and blood vessels, as in compartment syndrome of the leg. However, if fascial contraction can be interrupted long enough, a reverse form of fascial remodeling occurs. The fascia will normalize its composition and tone and the extra material that was generated by prolonged contraction will be ingested by macrophages within the extracellular matrix.[12]

Like mechanoreceptors, chemoreceptors in deep fascia also have the ability to promote fascial relaxation. We tend to think of relaxation as a good thing, however fascia needs to maintain some degree of tension. This is especially true of ligaments. To maintain joint integrity, they need to provide adequate tension between bony surfaces. If a ligament is too lax, injury becomes more likely. Certain chemicals, including hormones, can influence the composition of the ligaments. An example of this is seen in the menstrual cycle, where hormones are secreted to create changes in the uterine and pelvic floor fascia. The hormones are not site-specific, however, and chemoreceptors in other ligaments of the body can be receptive to them as well. The ligaments of the knee may be one of the areas where this happens, as a significant association between the ovulatory phase of the menstrual cycle and an increased likelihood for an anterior cruciate ligament injury has been demonstrated.[13][14]

It has been suggested that manipulation of the fascia by acupuncture needles is responsible for the physical sensation of qi flowing along meridians in the body,[15] even though there is no physically verifiable anatomical or histological basis for the existence of acupuncture points or meridians.[16][17]

References[edit]

  1. ^ Hedley, Gil (2005). The Integral Anatomy Series Vol. 2: Deep Fascia and Muscle (DVD). Integral Anatomy Productions. Retrieved 2006-07-17. 
  2. ^ Rolf, Ida P. (1989). Rolfing. Rochester, VT: Healing Arts Press. p. 38. ISBN 0-89281-335-0. 
  3. ^ Chaitow, Leon (1988). Soft Tissue Manipulation. Rochester, VT: Healing Arts Press. pp. 26–28. ISBN 0-89281-276-1. 
  4. ^ Schleip, R. (2003). "Fascial plasticity – a new neurobiological explanation: Part 1". Journal of Bodywork and Movement Therapies (Elsevier) 7 (1): 15–19. 
  5. ^ Myers, Thomas W. (2002). Anatomy Trains. London, UK: Churchill Livingstone. p. 15. ISBN 0-443-06351-6. 
  6. ^ Schleip, R.; Klingler W.; Lehmann-Horn, F. (2005). "Active fascial contractility: Fascia may be able to contract in a smooth muscle-like manner and thereby influence musculoskeletal dynamics". Medical Hypotheses (Elsevier) 65 (2): 274. doi:10.1016/j.mehy.2005.03.005. PMID 15922099. 
  7. ^ Tomasek, J.; Gabbiani, G.; Hinz, B.; Chaponnier, C.; Brown, R. (2002). "Myofibroblasts and Mechanoregulation of Connective Tissue Remodelling". Molecular Cell Biology (Nature Publishing Group) 3: 350–352. 
  8. ^ Schleip, R.; Klingler, W.; Lehmann-Horn, F. (2005). "Active fascial contractility: Fascia may be able to contract in a smooth muscle-like manner and thereby influence musculoskeletal dynamics". Medical Hypotheses (Elsevier) 65 (2): 273–277. doi:10.1016/j.mehy.2005.03.005. PMID 15922099. 
  9. ^ Chaitow, Leon (1988). Soft Tissue Manipulation. Rochester, VT: Healing Arts Press. pp. 26–27. ISBN 0-89281-276-1. 
  10. ^ Schleip, R. (2003). "Fascial plasticity – a new neurobiological explanation: Part 1". Journal of Bodywork and Movement Therapies (Elsevier) 7 (1): 11–19. doi:10.1016/S1360-8592(02)00067-0. 
  11. ^ Schleip, R. (2003). "Fascial plasticity – a new neurobiological explanation: Part 2". Journal of Bodywork and Movement Therapies (Elsevier) 7 (2): 104–116. doi:10.1016/S1360-8592(02)00076-1. 
  12. ^ Paoletti, Serge (2006). The Fasciae: Anatomy, Dysfunction & Treatment. Seattle, WA: Eastland Press. pp. 138, 147–149. ISBN 0-939616-53-X. 
  13. ^ Wojtys, E.; Huston, L.; Lindenfeld, T.; Hewett, T.; Greenfield M.L. (1998). "Association Between the Menstrual Cycle and Anterior Cruciate Ligament Injuries in Female Athletes". American Journal of Sports Medicine (American Orthopaedic Society for Sports Medicine) 26 (5): 614–619. PMID 9784805. 
  14. ^ Heitz, N.; Eisenman, P.; Beck, C.; Walker, J. (1999). "Hormonal Changes Throughout the Menstrual Cycle and Increased Anterior Cruciate Ligament Laxity in Females". Journal of Athletic Training (National Athletic Trainers' Association) 32 (2): 144–149. PMC 1322903. PMID 16558557. 
  15. ^ Kimura M, Tohya K, Kuroiwa K, Oda H, Gorawski EC, Hua ZX, Toda S, Ohnishi M, Noguchi E. “Electron microscopical and immunohistochemical studies on the induction of "Qi" employing needling manipulation.” Am J Chin Med. 1992;20(1):25-35.
  16. ^ Felix Mann. Chinese Medicine Times, vol 1 issue 4, Aug. 2006, "The Final Days of Traditional Beliefs? - Part One"
  17. ^ NIH Consensus Development Program (November 3–5, 1997). "Acupuncture --Consensus Development Conference Statement". National Institutes of Health. Retrieved 2007-07-17. 

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