Injuries to a variety of fascial tissues cause a significant loss of performance in sports and have a potential role in the development and perpetuation of musculoskeletal disorders, including lower back pain. A major goal of clinicians is to return athletes and patients to activity, training and competition after injury.
Earlier this month and just ahead of the 2018 INTERNATIONAL FASCIA CONGRESS, the British Journal of Sports Medicine issued a ‘Consensus Statement’ titled Fascial Tissue Research in Sports Medicine: From Molecules to Tissue Adaptation, Injury and Diagnostics, which was put together by 13 of the world’s premier fascia researchers, including Drs. Schleip and Findley.
After giving a definition of FASCIA and then letting readers know that it is an extremely important tissue for sports medicine practitioners (not to mention recreational and elite athletes), the authors stated, “Advancing this field will require a coordinated effort of researchers and clinicians combining mechanobiology, exercise physiology and improved assessment technologies.” So, while we can’t all be professional athletes, we should all endeavor to higher levels of physical fitness, athletic prowess, and knowledge about how the body functions and repairs itself (HERE).
One of the first things discussed was the difference between structure (anatomy) and function (physiology). “The proposed terminology distinguishing the terms ‘fascia’ and ‘fascial system’ allows for the precise identification of individual structures as well as grouping them for functional purposes.” Part of the problem with the anatomical study of fascia is that historically it’s been considered an afterthought — a tissue that always seems to be in the way of visualizing the more ‘important’ tissues such as muscles, joints, and organs.
There are, however, several groups doing anatomy dissections for the express purpose of visualizing fascia (Gil Headley, Julian Baker, and the ANATOMY TRAINS group immediately come to mind, as well as the recent Human Fascial Net Dissection & Plastination Project). It’s a start but the whole thing is still problematic.
While it’s true that we are making incredible strides with our knowledge of fascia (HERE are my blog posts on the subject), the fact remains that it is at best, difficult to study in vivo (in living conditions). While imaging is slowly improving (HERE), neither imaging nor dissections on cadavers will ever tell the whole story as far as function in living humans is concerned.
The authors continued by attempting to connect the information on fascial healing and repair on a cellular level to it’s mechanical function as a unified tissue ultimately connecting all parts of the body together, making it in many ways, similar to a SECOND NERVOUS SYSTEM. Take a look at these cherry-pickings having to do with fascia “HOMEOSTASIS“.
“Molecular adaptation of fascial tissues: effects of physical exercise, ageing, sex hormones and inflammation: Molecular crosstalk between extracellular matrix (ECM) molecules and cellular components is an important determinant of fascial tissue physiology and pathophysiology. Small functional and structural alterations in the ECM result in complex cellular adaptation processes and, vice versa, changes in cell function and structure leading to ECM adaptation. All factors influencing cell or ECM behaviour can result in changes in the structure and homeostasis of tissues and organs.”
Frankly, this is one of the reasons that DR. DAVID SEAMANS, chiropractor, educator, functional neurologist, and expert on the effects of inflammation, recently wrote a piece for the American Chiropractor titled Is Mechanical Back Pain an Unscientific Myth that Should be Abandoned? Although I am going to respond to his article, I’ll give you a preview by saying that while I don’t think the concept should be totally abandoned, it certainly needs to be altered. Why? Chiefly because “mechanical back pain” underestimates the crazy effects of inflammation.
INFLAMMATION is the collective name for a cluster of chemicals made by your body in response to damaged tissue. While we usually think of tissue damage in mechanical terms (sprains, strains, bruises, broken bones, etc, etc, etc), the harsh reality is that it’s easy to create massive amounts of tissue damage through totally controllable factors such as what we eat. And while diet is not the only reason for non-mechanical inflammation (HERE), it’s not only by far the most common, it’s also the easiest for you to take charge of, control, and manipulate.
In other words, it’s the lowest of the low-hanging fruit as far as solving inflammatory problems is concerned. And if you’d rather spend your days eating SUGAR and GRAINS? Inflammation is the cause of fibrosis (scar tissue), which just happens to be the cause of death for nearly half of all Americans (HERE). This is one of the reasons so many of today’s elite fascial researchers are saying that problems with the fascia are related not simply to chronic pain, but to one’s overall state of health (HERE or HERE).
Another topic of discussion in this paper was the importance of “mechanical stress” on fascia for an almost unlimited number of reasons. Firstly, when we talk about mechanical stress, this stress can be normal or abnormal. And just like Wolf’s Law that deals with the remodeling of bones, mechanical stress will likewise “remodel” soft tissues along similar lines. This is known as DAVIS’ LAW and can be better understood in my post on world record powerlifter, Donnie Thompson (see link).
The authors go on to talk about the effects of aging on fascia, referring to it as “inflammaging“. “The ECM is the main site of inflammatory responses taking place in tissues, it is not surprising that the ECM can interact with immune cells to change their function, which is important for growth and regeneration of tissues.” Are you starting to see why it’s difficult for any doctor to truly “fix” patients who are not serious about reducing their levels of SYSTEMIC INFLAMMATION? Oh; take a look at what was said about sex differences in fascial healing, regeneration, and repair.
“As the exercise-induced increase in collagen synthesis is lower in women than in men, and as injury frequency and the expression of oestrogen receptors in human fascial tissue are sex-dependent, oestrogens may play an important regulatory role in ECM remodelling. The effects of oestrogens on collagen synthesis appear to differ between rest and response to exercise. While oestrogen replacement in elderly, postmenopausal women impairs collagen synthesis in response to exercise, oestrogen has a stimulating effect on collagen synthesis at rest. Oral contraceptives, on the other hand, have an overall depressing effect on collagen synthesis.”
Two things here ladies. The first is that before you start any sort of HORMONE REPLACEMENT THERAPY, you need to study this issue yourself since the average family physician or OB is going to give you a less-than-accurate picture of what it’s really doing to you. Secondly, while oral contraception is certainly the easiest and most convenient form of contraception, there are hundreds of studies showing how bad it is on so many levels.
For more information on this topic, head over to DR. CHANDLER MARRS site, Hormones Matter. And not to leave the men out of this equation; if you are struggling with low T for any reason (HERE, HERE, or HERE), you are going to adversely affect your fascial system’s ability to heal as well.
The authors went on to discuss via a very cool little diagram, at least a dozen factors that influence fascia stiffness. Why are these so critical to know whether you are an athlete or not? For instance, we know that fascial adhesions are associated with tissue thickening (HERE), and that furthermore, following the earlier theme of fascia being related not just to pain but to health, we know that numerous disease processes, including cancer, live, thrive, and grow in stiff, dense, environments (HERE).
Basically, the circle diagram was made of of fascia-affecting entities that I’ve mentioned numerous times on my site. SURGERY, CORTICOSTEROIDS, TRAUMATIC & REPETITIVE INJURIES, TISSUE HYDRATION, and cross-linking (I refer to this as “TETHERING” with patients) are some of the things they discussed. Listen to how it was put together to give you a glimpse into the bigger picture.
“Fibrosis (eg, collagen deposition) around the tendon, nerve and myofascial tissues influences dynamic biomechanical properties secondary to tissue adherence and can tether structures to each other or induce chronic compression. Increased collagenous tissues surrounding the nerves can tether the nerves and also enhance pain behaviours. Furthermore, inflammatory cytokines can ‘spill over’ into the bloodstream, leading to widespread secondary tissue damage and central nociceptor wind-up. Circulating TNF is elevated in chronic lower back pain, and recent data highlight a relationship between elevated TNF and greater risk for progression to chronic pain in some individuals.”
Because this paragraph describes the crux of the injury process, allow me to break it down a bit. Bathe normal tissues in inflammation (cytokines and tumor necrosis factor), and you end up with fibrosis. Bathe fibrotic tissues in chronic inflammation, and you are far more likely to end up with TYPE III PAIN. Inflammation creates microscopic tissue adhesions that cause various tissues (and even organs) to “tether” themselves to each other, leading to RESTRICTION, ABNORMAL BIOMECHANICS, and CHRONIC PAIN.
What’s interesting about this situation is that in most cases, I tell my patients they will know in a single treatment whether or not I can help them (HERE is an example of this claim in action). The problem is that it can be difficult to tell whether a person is truly dealing with Type III pain or rather a severe and ongoing case of Type II.
Depending on the circumstances, I frequently suggest one treatment to see if there is improvement (HERE), because while worst case scenario, treatment may fire the situation up temporarily, it will not make you worse. For most people in chronic pain, the risk of a temporary flare-up is worth the potential reward of long term pain solutions.
These authors also discussed something I’ve discussed on my site when talking about LOW BACK PAIN and the THORACOLUMBAR FASCIA — the fact that abnormally moving tissues will turn to fat (ADIPOSE TISSUE) via a process known as “fatty infiltration” that will actually self-generate more inflammation. That’s right folks; without some sort of intervention, body fat begats more of the same via inflammatory pathways.
“Adipose tissue is a potential source of proinflammatory cytokines and has been implicated in a range of musculoskeletal conditions, including osteoarthritis. Regardless of the underlying mechanism, fibrotic changes in the muscle have a substantial potential impact on tissue dynamics and force generation capacity.”
Are you starting to get the picture that whether you call it SCAR TISSUE, FIBROSIS, or FASCIAL ADHESIONS, this stuff is bad and will have effects that reach far beyond the original area of pain or dysfunction?
As far as solutions are concerned, not only did the authors mention various “MODALITIES,” EXERCISES, and STRETCHING for inducing tissue repair and healing, they mentioned NSAIDS as well. I would largely disagree with this, as this class of drug is not only heavily prone to overuse and abuse (KENNY EASLEY for example), but carries a wide range of nasty and UNDER-REPORTED side effects as well (HERE), including the fact that soft tissues tend to heal weaker and with less elasticity when under the effects of NSAIDS.
“Anti-inflammatory drugs are used for sports-related overuse pathologies; however, they may impair regeneration and diminish tissue adaptation.”
In other words, they make you feel better while weakening the tissue. This is why I would argue that in most cases NSAIDS are palliative and not therapeutic.
The paper summed things up by talking about IMAGING FASCIA, which as I stated at the beginning of the paper, is difficult in the best of circumstances. As far as treatment, beside what’s already been mentioned, they touched on PRP, Extracorporeal Shockwave Therapy, FOAM ROLLING, massage, MANIPULATION, and various sorts of bodywork.
Interestingly, the authors admitted that the evidence for any of these as far as fascia is concerned is scant, but promising (“evidence suggests increases in arterial perfusion, enhanced fascial layer sliding and modified corticospinal excitability following treatment“). I would suggest that this is probably due to limitations in the research, but then again I’m a “homer” who has proven over and over that Tissue Remodeling as a form of treatment is not only beneficial, but potentially life changing (HERE).
Because few of us know a professional athlete, let alone plan on being one, my takeaway for the average recreational athlete is that you need to address more than fascia in order to best-address your fascia. How do I suggest you do this? Easy — start by diminishing your inflammatory load. Although some of you reading this have SYSTEMIC ISSUES that will require the services of a functional doctor of some sort, how cool is it that a huge amount of the recovery process can be done on your own?
In fact, along with my FASCIA SUPER POST that gives you all 180+ articles I’ve written on the subject, nicely categorized in one spot, I’ve also provided you a generic protocol completely free of charge (HERE), so that you can start the process of change that will hopefully lead you to start taking charge of your life and your health. And if you appreciate what you find on our site, be sure and like, share, or follow on FACEBOOK, as it’s a great way to reach those you love and care about most.