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the latest in fascia as related to sports injuries

  Germany’s Ulm University is home to DR. ROBERT SCHLEIP’S Fasica Research Group, which recently got a group of 13 physicians and elite researchers from around the world together to determine the role of fascia rehab in regards to SPORTS INJURIES.  The results are found in one of the BMJ stable of publications; the British Journal of Sports Medicine (Fascial Tissue Research in Sports Medicine: From Molecules to Tissue Adaptation, Injury and Diagnostics: Consensus Statement).

The paper starts with these words, “Molecular crosstalk between extracellular matrix (ECM) molecules and cellular components is an important determinant of fascial tissue physiology and pathophysiology.”  The ECM (extracellular matrix) is the liquid portion of fascia.  What’s interesting is that sound / vibration travels much faster in water than it does in air (3,300 mph -vs- 767 mph) making the fascial web an ideal “SECOND NERVOUS SYSTEM” due to the fact that fascia connects every part of you to every other part of you.  Not to mention it’s a prime example of a phenomenon known as MECHANOTRANSDUCTION — the ability to convert mechanical stimulus to biochemical signals readily understood by the brain, nervous system, and receptors in various organs and tissues of the body.

“Strong alterations of the local ECM microenvironments are necessary to allow cellular adaptation and rebuilding of fascial tissues. All factors influencing cell or ECM behaviour can result in changes in the structure and homeostasis of tissues and organs.”

HOMEOSTASIS is the state your body should be in, the state where everything works and flows in harmony.  If you want to rebuild fascia, you will have to push your body’s ability to adapt to the limit.  Although there are many ways to push the body’s tissues (KETTLEBELL SWINGS would be an example), when it comes to dealing with hardcore FASCIAL ADHESIONS it’s critical to actually “BREAK” the adhesion.  Although different practitioners go about this in different ways, in my clinic I incite fibroblastic activity via something I call Tissue Remodeling (HERE & HERE).  “In fascial tissues such as tendons, acute and chronic loading stimulates collagen remodelling.”  What does it mean to “load” tissues?

In terms of physics, connective tissues are meant to resist shearing or pulling forces (these tissues must be elastic like fascia), or they must resist compressive forces (these must be more rigid like bone).  “The mechanical properties of fascial tissues can be modified by several factors, including a change in… crosslinks and molecular organization…  and the contractile activity of myofibroblast cells.”  In English this means that SCAR TISSUE can have issues with its organization.  If the tissue is structurally random and heavily crosslinked, it begins to take on characteristics that are more bone-like, losing elasticity in the process (look for my upcoming article about bone as fascia).  My goal is to find these areas and “UNTETHER” them (see ‘break’ link above).  Beyond the obvious — that fascial adhesions have the ability to cause pain — why does it make sense to actually address mechanical problems mechanically as opposed to chemically (drugs)?  

“Myofascial tissue that is stiffer or more compliant than normal has been shown to influence the magnitude of intermuscular force transmission and, arguably, may have a significant effect on muscle mechanics.”

The authors went on to reveal why, helping explain why things like MUSCLE RELAXERS or other BIG-FIVE DRUGS are not helpful in the long run because they cannot successfully address biomechanical issues such as fibrosis and densification (I’ll discuss it momentarily).  “Physiological ageing is a highly individual process characterized by a progressive degeneration of tissues and organ systems. Age-related alterations in fascial tissues include densification (alterations of loose connective tissue) and fibrosis (alterations of collagen fibrous bundles). Functionally, these pathological changes can modify the mechanical properties of fascial tissues and skeletal muscle, thereby contributing to pain-related and age-related reductions in muscle force or range of motion.

Although I addressed AGE-RELATED CHANGES IN FASCIA yesterday, what’s critical to remember is that this “aging” process (degenerative process) is not solely reliant on a person’s chronological age.  It has much to do — maybe even arguably more to do — with how well a person takes care of themselves, i.e. how much systemic inflammation they are generating or exposing themselves to.  “Although early inflammation after tissue damage due to physical exercise or injury is crucial for tissue remodelling and adaptation….  limiting the magnitude of inflammation might be beneficial for tissue regeneration and gains in muscle mass and strength, depending on the nature of the injury and in elderly people.”  Here is where things really start to get interesting.

“Excessive or prolonged loading or direct trauma to fascial tissues initiates micro and macro changes necessary for tissue repair. These effects may also contribute to pathological changes that modify tissue function and mechanics, leading to compromised function of the healthy tissue. Effects may become systemic, and thus not limited to the injured/loaded tissues.”

In other words, it essentially takes controlled trauma of varying degrees to both break down the old injury and create the local inflammation needed for the repair process.  The train, however, starts going off the rails once the inflammatory process moves from local to systemic (more on that process can be found on my COLLAGEN SUPER PAGE).  The authors go on to talk about the fact that this systemic inflammation has the ability to generate the scar tissue that the medical community refers to as “FIBROSIS“.  If you follow my site you are already aware that the endgame of inflammatory processes are fibrotic changes to tissues and organs.

“An acute inflammatory response is typically short-lived and reversible and involves the release of a range of molecules, including proinflammatory cytokines from injured cells and macrophages, along with other substances that sensitize nociceptive afferents and promote immune cell infiltration. If loading is prolonged or repetitive, persistent inflammation may develop leading to the prolonged presence of macrophages and cytotoxic levels of cytokines in and around tissues, ultimately resulting in ongoing tissue damage. Some tissue cytokines are fibrogenic and can promote fibrosis via excessive fibroblast proliferation and collagen matrix deposition.”

Inflammation will cause sensory nerves (afferents) to become much more pain sensitive.  How much more? When scar tissue itself becomes sensitized due to exposure to inflammatory mediators, the result is incredible pain sensitivity, which DR. CHAN GUNN describes as potentially being over 1,000 times more pain-sensitive than normal tissue.  This is part of the scenario that sets up the unholy brain-based ‘loop’ of chronic pain known in the medical community as CENTRAL SENSITIZATION, where damaged tissue itself is no longer generating pain, but instead, the brain has become the pain generation.  But it gets worse. Once tissues and organs start to experience the process of inflammation infiltration, they start to undergo fatty infiltration as well — the process by which muscles and other connective tissues turn to fat (HERE).  And if this weren’t bad enough, the ECM-based fibrosis and “DENSIFICATION” that occurs right along with, is actually the world’s #1 leading cause of death (HERE).  Bottom line, if you have not been taking INFLAMMATION seriously, you must change your thought process if you hope to have any chance of reversing these physiological aberrations.

What did these authors say was good for reversing the processes above — particularly in cases where it was not yet severe?  How about some STRETCHING and RESISTANCE TRAINING; things I’ve dealt with on my site at length.  I have always said that if you are unsure whether or not your pain is centralized, try a Tissue Remodeling treatment and see if it helps (HERE).  Moving forward, the paper discussed what it takes to IMAGE FASCIA.  While MRI can be used for certain tissues like the PF, the authors spoke at length about DIAGNOSTIC ULTRASOUND.  From there they went on to the topic we are all waiting eagerly for — treatment.  In other words, are there other forms of treatment that may successfully help a person address adhesed fascia?

The authors stated that in all but rare cases, surgery for fascia is out, as are the medical community’s number one treatment theme; NSAIDS and CORTICOSTEROIDS.  Why?  Because they “may impair regeneration and diminish tissue adaptation.”  There were warnings issued against FLUOROQUINOLONE ANTIBIOTICS as well, along with a limited endorsement of PRP INJECTIONSFOAM ROLLING was mentioned as were several types of body work, including MYOFASCIAL TRIGGER POINT THERAPY.  And while CHIROPRACTIC CARE was not mentioned, OSTEOPATHY was (not surprising considering the study was done in Europe).  They also warned about the effects of certain drugs on fascia, speaking specifically about ESTROGEN / HRT.  “While estrogen replacement in elderly, postmenopausal women impairs collagen synthesis in response to exercise…. Oral contraceptives have an overall depressing effect on collagen synthesis.

People are thinking and talking about fascia more than ever.  While that’s certainly cool, the fact that more people than ever are beginning to grasp the importance of lessening and controlling their inflammatory load is, at least in my mind, an even bigger deal.  What I have done is put together a post (no charge to you) to help you in this endeavor.  While I am not claiming to be a “cure all,” I would suggest that for the vast majority of you it will provide a starting point or launching pad as far as addressing systemic inflammation; a first step in the process of taking your life back (HERE).  If you appreciate this sort of work, be sure to like, share or follow on FACEBOOK as it’s a great way to reach the people you love and care about most.


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