Showing posts with label dynamic joint mobility. Show all posts
Showing posts with label dynamic joint mobility. Show all posts

Thursday, April 22, 2010

Eccentric Exercise - some cool ideas as to why it seems to heal certain tendinopathies (ps, ditch -itis and -osis)

ResearchBlogging.orgHave you been suffering with some kind of sore tendon/jointy pain? Rotator cuff area, achiles, elbow, forearm, rsi etc etc? Guess what? First we're not alone, but second, just about anything that's been tried to address it has no real evidence to support it working, especially over time. Indeed, as the authors of a 2009 review study put it, "Tendinopathy is common although pathology of this condition is poorly understood." In other words, we don't really know how this dis-ease works. The point of this article is to consider why, as these authors see it, Eccentric Exercise (EE) which has seemed to have some good, some neutral results in research, may actually be successfully addressing the effects of that pathology. So much so, that it gets rated as a good "conservative" therapy for these kinds of common, awful and sometimes career ending, painful problems.

By way of context, in 2008, the year before these authors proposed why EE might be useful, another group reviewed pretty much everything under the sun applied to tendinopathies, from NSAIDS to shock wave therapy (and anything else one's GP may recommend). THe paper has the remarkably useful title "Treatment of Tendinopathy: What Works, What Does Not, and What is on the Horizon"

They write of these therapies:
Tendinopathy is a broad term encompassing painful conditions occurring in and around tendons in response to overuse. Recent basic science research suggests little or no inflammation is present in these conditions. Thus, traditional treatment modalities aimed at controlling inflammation such as corticosteroid injections and nonsteroidal antiinflammatory medications (NSAIDS) may not be the most effective options. We performed a systematic review of the literature to determine the best treatment options for tendinopathy. We evaluated the effectiveness of NSAIDS, corticosteroid injections, exercise-based physical therapy, physical therapy modalities, shock wave therapy, sclerotherapy, nitric oxide patches, surgery, growth factors, and stem cell treatment. NSAIDS and corticosteroids appear to provide pain relief in the short term, but their effectiveness in the long term has not been demonstrated. We identified inconsistent results with shock wave therapy and physical therapy modalities such as ultrasound, iontophoresis and low-level laser therapy. Current data support the use of eccentric strengthening protocols, sclerotherapy, and nitric oxide patches, but larger, multicenter trials are needed to confirm the early results with these treatments. Preliminary work with growth factors and stem cells is promising, but further study is required in these fields. Surgery remains the last option due to the morbidity and inconsistent outcomes. The ideal treatment for tendinopathy remains unclear.

It's almost as bad as the common cold: ubiquitous and no idea how to cure it.
Aside: And if you have a type of rotator cuff tendinopathy, and your doctor is suggesting a steroid shot? I'm motivated here as this is me. You may want to point that caregiver to this 2007 review of the lack of proven efficacy of this approach.
This systematic review of the available literature indicates that there is little reproducible evidence to support the efficacy of subacromial corticosteroid injection in managing rotator cuff disease.
It's interesting that from that mix of "current data" strategies that look promising in the 2008 survey quoted above, the authors of the 2009 BJMS article are interested in eccentric exercises. In 2007, another group of researchers concluded a literature survey about Eccentric Exercise and chronic tendinopathy with the sad claim that
the dearth of high‐quality research in support of the clinical effectiveness of EE over other treatments in the management of tendinopathies.
In other words, good quality studies that would be taken as being say clinically significant are thin on the ground. They're not as rigerous as these scientists would like to see in the presciption of a protocol to treat something.

By 2009, however, the UK group of scientists seems ready to say that EE is a good "conservative" treatment for tendinopathy. What's quite remarkable is why they're making this claim, and that's at the heart of this article.

Tendinopathy?
But first things first, just to be sure we're all on the same page, what is tendinopathy? Tendinopathy is the umbrella term that includes, among other considerations, tendinosis and tendinitis. As for the differences between these two, on a functional level, Mike Nelson puts it nicely:
TendonITIS is normally from inflammation (itis). TendonOSIS is normally from messed up connective tissue.
To get into a bit more detail, the intro to the 2008 survey is very helpful
Traditionally, pain in and around tendons associated with activity has been termed tendonitis. This terminology implies the pain associated with these conditions results from an inflammatory process. Not surprisingly, treatment modalities have mainly been aimed at controlling this inflammation. The mainstays of treatment have included rest, nonsteroidal antiinflammatory medications (NSAIDs), and periodic local corticosteroid injections.

There are two problems with this approach. First, several studies demonstrate little or no inflammation is actually present in tendons exposed to overuse [83, 96, 163]. Second, traditional treatment modalities aimed at modulating inflammation have had limited success in treating chronic, painful conditions arising from overuse of tendons. More recently, the term tendinopathy has been advocated to describe the variety of painful conditions that develop in and around tendons in response to overuse. Histopathologic changes associated with tendinopathy include degeneration and disorganization of collagen fibers, increased cellularity, and minimal inflammation [83, 163]. Macroscopic changes include tendon thickening, loss of mechanical properties, and pain [163]. Recent work demonstrates several changes occur in response to overuse including the production of matrix metalloproteinases (MMPs), tendon cell apoptosis, chondroid metaplasia of the tendon, and expression of protective factors such as insulin-like growth factor 1 (IGF-1) and nitric oxide synthetase (NOS) [10, 76, 93, 99, 154, 155, 174, 199]. Although many of these biochemical changes are pathologic and result in tendon degeneration, others appear beneficial or protective. Tendinopathy appears to result from an imbalance between the protective/regenerative changes and the pathologic responses that result from tendon overuse. The net result is tendon degeneration, weakness, tearing, and pain.
So for practitioners in the know, it seems the once-frequent diagnosis of "tendinitis" has gone down quite a bit - because inflammation may or may not be present, and when it is, may or may not be the main cause of pain. Also, there is an "imbalance" of protective/regenerative responses to overuse and pathological (diseease) responses. This is Mike's "messed up connective tissue."

Hence we circle back to the term tendinopathy to cover this not unusually mixed condition of perhaps some inflammation but in particular, "degeneration, weakness, tearing, and pain" Hence both osis (tears) and itis (inflammation) may neither be particularly pathologically accurate or diagnostically helpful. And so, tendinopathy is the new and more robust term for these conditions.

With that note in mind, let me also add that the following discussion is not meant to be a prescription of any course of action. Get yourself checked with your doctor before starting anything. In my own case i have been disappointed by the fact that the thing that has actually helped the most immediately has been taking NSAIDS - some inflammation, or -itis maybe?

After a month of other non-drug interventions, day one after finally breaking down and seeing the doc: bam - immediate reduction in the pain that was making putting on a jacket a painful experience. bugger. But ah ha, it ain't all better that's for sure. What to do next? My hope is that the following research may offer some insight into WHAT to do if not exactly how and when to do it.  


Eccentric Exercise and Tendinopathy
The authors of "Eccentric exercises; why do they work, what are the problems and how can we improve them?" J D Rees, R L Wolman, A Wilson write in the abstract:
Eccentric exercises (EE) have proved successful in the management of chronic tendinopathy, particularly of the Achilles and patellar tendons, where they have been shown to be effective in controlled trials. However, numerous questions regarding EE remain. The standard protocols are time-consuming and require very motivated patients. EE are effective in some tendinopathies but not others. Furthermore, the location of the lesion can have a profound effect on efficacy; for example, standard EE in insertional lesions of the Achilles are ineffective.

Until recently little was known of the effect of EE on tendinopathic tendons, although a greater understanding of this process is emerging. Additionally, recent in vivo evidence directly comparing eccentric and concentric exercises provides a possible explanation for the therapeutic benefit of EE. The challenge now is to make EE more effective. Suggestions on areas of future research are made.
So, the researchers are sitting with the 2007 surveyview that while there's some hints of promising evidence in the past about EE, it hasn't been super. They think that now, however, they have a better sense of what might be making it effective.

The body of the article focuses on Achilles tendinopathy (mid back of the leg - base of the calf muscles), Insertional Achilles tendinopathy (where the tendon inserts away from the calf muscles, down by the ankle where it attaches to the bone) , Patellar tendon (either side of the knee cap) in particular.

The authors' insight has been to look at where in the tendon the lesion is occuring. Is it where the tendon attaches to the bone or where it attaches to the muscle? The effects of EE in the small number of studies are all over the map, so it's hard to draw any conclusion except, it seems, that where the lesion is on the tendon seems to have a correlation between the degree to which EE will be successful. For insertional achilles, as opposed to "the main body" of the tendon, EE's not showing up as so great. With the paterllar tendons, while some studies have shown benefit, especially over CE or concentric, whether there's a difference around proximal or insertional hasn't been the focus of research in such a way as it's possible to make a distinction.


With respect to other tendinopathies - like forearms (RSI kinda stuff) and elbows, the authors write:
A small number of studies have examined the use of eccentric exercises in the management of tendinopathy of the lateral extensors of the forearms.26–28 There is some evidence suggestive of an increase in function using EE compared with ultrasound in the treatment of lateral extensor tendons,29 and a recent study adopted an isokinetic eccentric protocol in the management of lateral elbow tendinosis and reported promising results.30 No randomised study on the effectiveness of EE on the rotator cuff has been published, although a small uncontrolled pilot study of nine patients did suggest a significant benefit of EE (patients with arthritis of the acromioclavicular joint or significant calcification were, however, excluded).31 Further trials on both tendinopathy of the rotator cuff and lateral extensor forearm tendons are required in order to evaluate EE more fully.
Just my luck: shoulders with EE haven't been evaluated. Time to become an experiment of one.


What are Eccentrics Doing?
Despite this rather promising but still arid, partial research landscape for EE and tendinopathy, the authors have some ideas about the mechanisms that may be at play in eccentric efforts
The pathophysiology of tendon injury and healing is incompletely understood. It does appear, however, that in established tendinosis the tendon often does not progress into an active (or at least successful) healing cycle. EE may work by providing a mechanical stimulus to the quiescent tendon cells
The authors propose several interesting ways in which this "mechanical stimulus" may work. The first is on that all important building block for tissue, collagen
Physical training in general has been shown to increase both the synthesis and degradation of collagen,39 and in the longer term this may lead to a net increase in collagen. Recently it has been recently elegantly demonstrated by Langberg and coworkers, by use of the microdialysis technique, that a chronically injured Achilles tendon responds to a 12 week EE programme by increasing the rate of collagen synthesis.40 In this study 12 patients (six with Achilles tendinosis and six normal controls) performed EE over a 12 week period. The EE group had increased collagen synthesis (peritendinous type I collagen) without a corresponding increase in collagen degradation. There was also a corresponding drop in pain levels (in line with other studies).
That collagen production - to repair tendon degredation - is a huge and good deal. Especially that the exercise is not causing breakdown, but actual rebuilding.

Another factor the authors consider is blood flow. When we see tendons illustrated in anatomy texts, they're usually white-ish. That's the lack of a whole lot of blood going through them. This limit is in no small part why tendons can take longer than just about anything else to heal. So improving blood flow to tendons - blood being a nutrient carrier - could seemingly be a big plus. The authors write
The effect of EE on Achilles tendon microcirculation has also been studied. Achilles tendon oxygenation was not impaired by an EE programme but was accompanied by a decrease in postcapillary venous filling pressures, the authors suggesting that this reflects improved blood flow. Again this study looked only at eccentric exercise so it is not possible to determine whether this is a specific effect of EE.
In other words, concentric exercise may have the same benefit on blood flow as eccentric exercise - we don't know - but what we do seem to know is that exercise (in the studied case, eccentric) keeps the blood moving, circulating rather than sitting somewhere. The anti pump? in a good way?


Where using the Force Mayn't Matter. All this is cool, but it doesn't explain WHY these effects are occuring from EE. In particular, something the scientists can conclude rather strongly from the work that's been carried out is that the magnitude of the force has nothing to do with it. So lifting a big weight, or lifting a lighter weight faster (F=M*A) isn't what's getting the job done.

The key question the authors ask is:
If the efficacy of EE cannot be explained by the magnitude of force, then what is responsible?
Great Question. They have one very intersting finding about eccentric exercise - the shape of control of the muscle when it's lengthening and contracting at the same time:
Intriguingly, we observed a pattern of sinusoidal loading and unloading in EE which was not demonstrated in CE. The fluctuations in force probably reflect the difficulty in controlling a dynamic movement with a lengthening muscle; similar to the experience that it is easier to lift a heavy weight under precise control than to lower the same weight. We propose that these fluctuations in force may provide an important stimulus for the remodelling of tendon. Certainly in the remodelling of bone it is known that bone responds to high-frequency loading and appropriate mechanical signals can lead to a dramatic increase in bone density.

Frequency rather than Force. This is so cool - it sounds great too: that the sort of cycling on and off of the muscle (the sinusoidal loading and unloading) during the eccentric may be the biggie in stimulating that good collagen rebuilding in particular associated with EE and maybe the blood flow too. The other interesting part is that there is a possible parallel to bone remodelling here (and Woolf's law).

That is, as force is applied to a bone it will get bigger (the outer shell gets pushed out it seems, as the inner lace work architecture increases) and so stronger to respond to that demand. Davis's law on tissue seems a wee bit similar: "If soft tissue is placed under unremitting tension, the tissue will elongate by adding more material. "

Bottom line: the particular type of muscular demands to maintain control of a load in extension (force fluctuations not force magnitude) may play a particular role in remodeling tendons in these various opathies.


Whither, Voyager for Futuer EE / Tendinopathy Research?
The authors are now happy to say EE seems to have sufficient basis to be considered viable. Time to figure out how to optimize it. THey write in the Future Work section:
Little is known of the optimal protocol for EE. Indeed, fundamental questions remain unanswered, such as how fast the exercises should be performed and progressed. This is certainly an area worthy of future research. The specific location of the pathology within a tendon has increasingly been shown to have an effect on the efficacy of EE, and further study in this area is also suggested. Other potential areas of research include studying the effect of periodisation of training, a technique currently perhaps more familiar to athletes and their coaches than to sports medicine physicians.
Goodness, that's interesting. Periodization combined with frequency may be the sweet spot for rehab. Why not? It's excellent for anti-fatigue strength building; why not repair?

As an example of eccentric exercises that have been tried out among at least a small population of elbow-opathies,  Mike T Nelson's developed some nice eccentrics work with a kettlebell. Well worth a look and a go.

What i've been working lately for my shoulder/painful arc thing:

 put a wee kettelbell or light db in the hand of the sore side. bring hand up to chest (with weight in it), then lift elbow so it's parallel or close to shoulder height WITH NO PAIN - only go as high as you can with no pain
- slowly abduct the hand away from the chest, and potentially rotate wrist down (like pouring a jug) - if the load feels too heavy - brings on pain - bring hand in a bit; reduce turn in wrist; then lower the whole arm (not just the elbow but this L shape you're holding) so you're working the shoulder.

that lets one do the concentric pretty much unloaded and focus on a safe eccentric.
if you give that a go for a while let me know how that feels - just don't move into pain.

Concludium 
Perhaps the main take away from this summary of recent research reviews and primary work is that tendinitis vs osis is largely a non-starter; tendinopathy is where it's at. And saying that, the pathology or dis-ease of tendinopathy is not well understood, which may also explain why treatements - in particular long term ones - don't have much evidence to support their efficacy. There are some prospective treatements on the horizon, however, with eccentric exercise amongthem. This latest study on EE and tendinopathy seems to propose the best hypothesis so far as to why eccentric exercises is showing up as particularly effective for at least main body tendinopathy.


Citations:
Rees, J., Wolman, R., & Wilson, A. (2009). Eccentric exercises; why do they work, what are the problems and how can we improve them? British Journal of Sports Medicine, 43 (4), 242-246 DOI: 10.1136/bjsm.2008.052910

Andres, B., & Murrell, G. (2008). Treatment of Tendinopathy: What Works, What Does Not, and What is on the Horizon Clinical Orthopaedics and Related Research, 466 (7), 1539-1554 DOI: 10.1007/s11999-008-0260-1

Woodley, B., Newsham-West, R., Baxter, G., Kjaer, M., & Koehle, M. (2007). Chronic tendinopathy: effectiveness of eccentric exercise * COMMENTARY 1 * COMMENTARY 2 British Journal of Sports Medicine, 41 (4), 188-198 DOI: 10.1136/bjsm.2006.029769

Koester MC, Dunn WR, Kuhn JE, & Spindler KP (2007). The efficacy of subacromial corticosteroid injection in the treatment of rotator cuff disease: A systematic review. The Journal of the American Academy of Orthopaedic Surgeons, 15 (1), 3-11 PMID: 17213378

Related Resources

Wednesday, October 28, 2009

Move or Die? Movement as Optimal Path to Strength and Well Being, Part 1

This post is an intro to why *good* movement is a big frikin' panacea to most of what ails us. No kidding. Move well; be well. In this series, we're going to look at different attributes of movement - joints, muscles, skin, lymph everything - but first, let's start with an overview of what movement seems to mean to our governing system - the "always on" part of our bodies that monitors and messages about every process in our bodies, our nervous system - and then consisder a pretty direct route to cuing up those happy messages to it via dynamic joint mobility.

Movement = well being. We are designed to move. And apparently to move at speed: our bodies are apparently designed to support running more so than even walking. Perhaps not surprisingly, Use it or Lose it for humans could be redefined potentially as Move It or Lose It.

Our physiology works on a move it or lose it principle: by Woolf's Law and Davis' Law, we get to keep only what we use, and use is determined by - yes - movement. Don't move our muscles, function degrades; don't use our bones, bones degrade, don't move the joints, joints degrade. Movement means strength, fitness, digestion, respiration, skin tone, joint health, heart health, everything health. Could it be that simple?

Everything about our beings responds best to movement: movement therefore seems to mean a big neurological thumbs up. If we are able to move, we're good to go, to flee, to hunt or to gather.

On the other hand, if our nervous system either perceives or receives a threat of any kind, movement is what pays: sore shoulder means reduced range of motion; shoes too tight so joints are compressed and less able to function as designed means less muscle power for a deadlift. Loosen up those shoes (or get rid of them), do some foot mobilization work (ankle circles; toe waves) and power is restored to the system. We react *that* quickly, as reflected in the SAID principle.

SAID stands for "specific adaptation to imposed demand." Eric Cobb, DC, c0-founder of Z-Health adds "exactly and immediately" to the SAID mix. In other words, our bodies respond exactly and immediately to what we're doing.

We see evidence of this immediacy all the time. Go to pick something up, our muscles don't wait to turn on to support that position; they do so right away, courtesy of the nervous system. We are about to go on stage to give a talk, and our heart rate accelerates right at that moment pumping more blood to our peripheral limbs; likewise hormones are released to prepare for flight to deal with the perceived threat of our anxiety. That response happens as soon as we perceive the moment of threat - which may be long before, right before or during the event.

A huge part of that immediate adaptation is the speed at which information travels through the nervous system. Most fibers are sending info at 300miles per hour. That's fast. One might almost say immediate.

Not moving = We have a Problem, Houston. Movement is so basic, so fundamental an indicator of well being, that *not* moving is, on a gross scale, a sign of illness or duress. Our movement is reduced seemingly in proportion to the degree of perceived or actual threat to the system. Our movement is reduced if we have: a broken limb, a gut ache, a head ache, if we feel depressed. Likewise, we think of aging as a process of movement deterioration: the aged are often slower, less mobile, suffer from movement debilitations - or are entirely bed ridden, just like the acutely ill.

Irony. We are, despite our awesome craniums, embodied beings. Our modern lives, however, have moved us to a place where, to our nervous system we generally operate, if ya think about it, from postures of illness: we don't move; we sit at desks; we sit in cars, trains and planes. We are more sedentary than ambulatory.

Likewise those postures often closely resemble what's know as threat response or startle positions: hunched shoulders, head lowered, legs raised towards chest (from sitting) - if our legs and hands were pushed up a bit more we'd be in total fetal posture. And the rolling up into a ball is the big threat protection posture: cover the internal organs, protect the head, eyes and ears. That's a little, er, sick, isn't it?

Response to Modern Life:
Dynamic Joint Mobility as a first step, or movement.

If we tell our bodies that we are non mobile, our bodies also respond immediately to this - as we have seen - with Wolff's Law and Davis's Law: we are rebuilding tissue ALL the time. If we continually sit slumped, the body will work to maintain that position - go to get out of it, we feel stiff. Over a long enough time, the bones remodel to better maintain that position.

A painless and effective way to counteract less mobility is to move: move every joint in the body through its range of motion - that is - through the degree of motion we can voluntarily control. Another name for moving each joint in the body in a focused way is dynamic joint mobility work.

(Eric Cobb demo'ing cross body figure 8's in the z-health Neural Warm Up 1)

There are lots of joint mobility systems out there; the one i prefer, practice and teach is z-health. I've written lots about why (article index) and here's Z-Health's FAQ, but the main reason is that the movements in the R, I and S continuum are designed to move each joint
  • really: each joint, from head to foot, precisely
  • through as many positions as possible
  • as many speeds as possible
  • with varying loads
The outcome is building up lots and lots of practice for being mobile in all these positions, means reduced likelihood of getting jammed up such that the nervous system shuts down mobility. For more info on this, you may wish to take a peek at this article on mobility and injury prevention with I-Phase.

Range of motion is a great way to see how our nervous system may be doing with our body. We may feel fine but if we go to raise our arm in front of us to beside our ear and it usually gets to beside our ear but today it's only going to beside our cheek something's up. We might not perceive what it is clearly, but our nervous system does.

Doing a few joint mobility drills will often improve that range of motion. Some joints, like the wee bones in the feet and hands don't have a great deal of motion - but they do move. They're joints for a reason - if there wasn't a need for a joint, there'd be a bone, as Cobb puts it.

(demo'ing target locations for z-health R-Phase toe pulls: alternatives to hip flexor stretches)


So smaller joint motions mean smaller range of motion, but still movements - and precise movements at that for optimal efficiency (more on efficient movement here). How to hit the target and what those targets are are important to maximize benefit of this joint librating work.

Repetition Only One Way: Bad; All ways, good. Other joints, like the wrist, pretty big obvious range of motion as we bend the hands back and forth at the wrists. But also therefore important to move those joints through those ranges of motion. Carpal Tunnel or RSI is not usually the result of too many reps, but too many reps in only ONE direction of a possible set of motions. Like typing on a keyboard - flexion flexion flexion, no extension; same with musicians. And here's one: elbows have fabulous movement possibilities but do you know some ways to move them through their complete ranges of motion in multiple directions/speeds? How often do lifters in the gym complain of tennis elbow? More than 9 times out of ten, this is the similar problem as the typing desk jockey: too many reps in one direction, exacerbated by potentially poor form with load, or just overuse.

If i could talk to the Animals - or the Nervous System...
Simple concept of why joint mobility work, like doing ZHealth R-Phase and I-Phase is so important: mechanorecption and nociception.

Mechanoreceptors populate the muscles and the tendons around joints. The give our brain information, through the nervous system of where we are in space and how fast we're moving. The other big proprioceptor around the joints are nocicpetors - nerves that react to noxious stimulus, like a cut or a kick or an impingement. If limbs are not moving well, the number of mechanoreceptors fired are way less than if they do move. Significantly. Nociceptors, which are far fewer in ratio to most mechanorecpetors are free to fire. And 1 is always louder than zero.

Signal Processing. Pain is something the brain says about a signal through the nervous system. A nociceptor may fire, but if the signal from the mechanorecptors is louder because more of these are firing, the brain mayn't interpret the action as something that needs to fire up as pain. If however the nociceptor is the only thing talking because the other mechanorecpetors in the area are inhibited from lack of mobility, then that pain signal may just get amplified.

Oh, Canada! Here's a way you might model this signal processing concept. At a recent mobility seminar, i started to sing O Canada - large room but everyone heard me. No one else was speaking. I then asked participants in the room to sing - at a normal volume not shouting or anything - God save the queen - while i sang O Canada while someone at the door listened in. What song do you think the person listening heard?

Movement Sings. So movement, on one simple level - movement through the fullest possible range of motion - helps to send positive "all clear" signals to the nervous system.

Practicing movement helps the joints learn to move through their full range of motion. Here's an example. When i started doing R-Phase in Z-Health, i looked with amazement on the thoracic circles - moving *just* the upper spine in a circle - of a fellow RKC. Me doing thoracic glides just front at back: ok i'm doing them! And there was no movement. Practicing them even though it felt like nothing was happening eventually caused rather a lot to happen, to the point the other day where a master trainer said "well you have such excellent thoracic mobility this isn't a problem for you; most people need...."

One gets joint mobility the same way one gets to carnegie hall it seems: practice practice practice.

Healing off the Table: Doing it For Ourselves:




Self movement more so than manual work (being worked on by others or having limbs moved passively) engages motor learning. That self-initiated action to control a motion fires up way more of the nervous system, building new patterns of movement with each rep. This is fabulous for self-care. Practically, the number of athletes i work with and whom colleagues work with who come in complaining of shoulder pain, elbow pain or back pain, generally speaking
  • a) get their pain significantly lessened if not eliminated in a single session by getting at a movement pattern that is not firing correctly so good mobility is inhibited
  • b) are able to take care of themselves afterwards because they know and have the tools on how to reduce the problem by the mobility work, so they can get on with their strength or health or life practices
  • c) as their mobility improves, they have fewer flare ups

It's that simple. And while we've focused on the benefit of moving joints for the nervous system due to mechanorecptors around the joints, in future we can look at movement of the skin, fascia, lymph and gut that also comes into play - how mobilty assists these other movements to feel better and perform better.

In the meantime, i hope this for me unusually brief overview helps get a handle on why mobilty work may be a good practice to consider if it's not already part of your daily practice. And here's an example of controlled movement:

Full Motion: Herman Cornejo executes a seeming impossible
double tours en l’air as part of David Michalek's slow dancing project.



Next Time: threat, pain and threat modulation.

Related Posts

ShareThis

Related Posts with Thumbnails