February 2011 - Carlton Cullins

Fascia Research

Friday, February 18, 2011
The explosion of fascia research

This posting is a modified version of an article I have written for a British cranial osteopathic publication.

Because I am actively involved in the organizational aspects of next year’s Fascia Research Congress in Vancouver I have had only a limited amount of time to give to writing for the blog – hence this recycled – but I hope interesting – update on fascia.

When I was studying osteopathy in the late 1950s (BCNO – now BCOM) fascia entered into the lessons and lectures as a somewhat mysterious part of the economy of the body. It featured large in the historical aspects of osteopathy’s evolution, with early pioneers referring to its all-pervading nature – it was everywhere, and there were theories and assertions as to its relevance, but there was very little that was rooted in science. (Still 1902)

So, the question remained – what did fascia do?

Clues were to be found in American osteopathic writing. For example, decades ahead of his time Cathie (1974) described fascia’s potential for contractility as well as its rich neural supply – features that would not be validated by research until very recently. (Schleip 2006, Stecco 2008).

Osteopaths – and others – in the USA (Little 1969, Taylor 1958, Rolf 1962) made it clear that that fascia was not just a background material, with little function apart from its obvious supporting role, but rather a widespread, tenacious, connective tissue involved deeply in almost all of the fundamental processes of the body’s structure, function and metabolism.

In therapeutic terms it became clear there can be little logic in trying to consider muscles and joints as separate structures from fascia, because they are so intimately related. Remove connective tissue from the scene and any muscle left would be a jelly-like structure without form or functional ability, and joints would quite simply fall apart. (Cantu et al 1992)

We now know that there exists a state of structural and functional continuity between all of the body’s hard and soft tissues, with fascia being the ubiquitous elastic–plastic, gluey, component that invests, supports and separates, connects and divides, wraps and gives cohesion, to the rest of the body – the fascial, connective tissue network. (Ingber 2008, Myers 2009)

Any tendency to think of a local dysfunction, as existing in isolation needs to be discouraged as we try to visualize a complex, interrelated, symbiotically functioning assortment of tissues, comprising skin, muscles, ligaments, tendons and bone, as well as the neural structures, blood and lymph channels, and vessels that bisect and invest these tissues – all given shape, form and functional ability by the fascia. (Schleip 2006, Ingber 2008, Solomonow 2009)

Fascial function and dysfunction revealed

Fascia, when healthy, forms a gliding interface with underlying muscle [allowing] free excursion of the muscle under the relatively immobile skin. A plane of potential movement exists in the form of the areolar tissue layer, apparently lined with a lubricant, hyaluronic acid. (McCombe et al 2001)

This process of ‘sliding fascia’ can now be visualised, using real-time ultrasound and elastography – as was demonstrated recently by Langevin (2010b). Dramatic video images demonstrated the free movement of lumbodorsal fascia in pain free individuals, contrasted with that of individuals with low back pain.

Similar images were displayed of myofascial trigger points, during the same panel presentation, that I co-chaired (Shah 2010). Both elastography and ultrasound images show trigger points to be denser than surrounding, normal, tissue.

When fascia is excessively mechanically stressed, inflamed or immobile, collagen and matrix deposition becomes disorganized, resulting in fibrosis and adhesions, and fascial ‘thickening’ (Langevin et al 2009), also described as ‘densification’ (Stecco et al 2009). This process involves distortion of myofascial relationships, altering muscle balance and proprioception. Consequent binding among layers, that should stretch, glide and/or shift on each other, potentially impairs motor function (Fourie 2009), and leads to chronic tissue loading, which contributes to ‘global soft tissue holding patterns’ (Myers 2009).

Cramer et al (2010) in rat studies showed that “hypomobility results in time-dependent adhesion development within the zygapophyseal joints”. Such adhesion development may have relevance to spinal manipulation, which could theoretically break up Z joint intra-articular adhesions”

Some therapeutic implications

A review by Schleip (2003) has documented both myelinated and unmyelinated fibers in fascia, including sympathetic endings. Stecco et al. (2008) found that the outer layers of the deep fascia contained a rich vascular and nerve supply, with intrafascial nerve fibres seen throughout. Some of these were presumed to be stretch receptors.

Bialowski (2008) has hypothesised that mechanical force (soft tissue & manipulative) initiates neurophysiological responses – peripheral and central – possibly evoking and explaining the clinical outcomes of manual therapy. These hypotheses have been expanded on by Simmonds et al (2011) who suggest that HVLA manipulative therapies (i.e. rapid) stimulate fascial tissues (as in the Z-joint example described earlier), while myofascial therapies (such as myofascial release and muscle energy technique) deliberately stimulate fascial tissues

Langevin’s in vivo and in vitro studies have shown that loose connective tissue responds to light tissue stretch, which “may be key to the therapeutic mechanism of treatments using mechanical stimulation of connective tissue” (Langevin & Sherman 2006, Langevin 2010a)

Myers (2010) suggests that stretching can be applied not only to ‘length’ problems, but also to ‘stuck layer’ problems, using shear stress to allow the restoration of increased relative movement between the adjacent planes of fascia (Schwind 2004)

In Germany, Pohl (2010) has demonstrated, using real-time ultrasound imaging, changes in collagen density in various layers of skin before and after connective tissue massage (CTM) involving skin rolling

Mechanotransduction and strain transmission

What has now been established is the remarkable degree to which muscular effort depends on the multiple links that muscles have with connective tissue structures.

These connections mean that – for example – a hamstring stretch will produce 240% of the resulting strain in the Iliotibial tract – and 145% in the ipsilateral lumbar fascia – compared with the hamstrings.

The process of strain transmission that occurs during stretching, involves many other tissues beyond the muscle that is being targeted, largely due to fascial connections, making the use of the word ‘isolated’ – together with ‘stretching’ – difficult to justify. (Franklyn-Miller et al 2009)

A fascial hydraulic effect?

Klingler & Schleip (2004), at the University of Ulm, measured wet & dry “freshly harvested” human fascia and found that during an isometric stretch, water is extruded, refilling afterwards. As water extrudes temporary relaxation occurs in the longitudinal arrangement of the affected collagen fibres. If only moderate strain is involved there are no micro-injuries, and water soaks back into the tissue until it swells, becoming stiffer again. It therefore seems that some tissue responses to manual therapy may relate to this sponge-like squeezing and refilling in the semi-liquid ground-substance, with its water binding glycosaminoglycans and proteoglycans.

Fascia related therapeutic approaches

The range of methods and modalities that focus attention on fascial dysfunction are proliferating. A few of those where a degree of supporting validation exists are summarised below :

· Heat in the therapeutic range, relaxes many fascial contractures associated with myofascial dysfunction. External heat has been shown to be beneficial in low back pain (Klingler 2011)

· Graston Technique® (GT) is an instrument-assisted soft tissue assessment and mobilization method delivering load deformation via stainless steel instruments. Mechanical deformation influences the extracellular matrix (ECM,) modulating the synthesis of proteoglycans and collagen by fibroblasts, increasing collagen formation (Hammer 2007)

· Neurologically active scars can restrict back flexion, which the patient feels as low back pain. This can be relieved by treatment of scars on the abdomen and/or below the symphysis (Kobesová, 2007)

· Fryer & Fossum have suggested that apart from the influence of mechanoreceptors on pain (via both ascending and descending pathways), Muscle Energy Techniques induce in-vivo mechanical stretching of fibro-blasts that both alters interstitial osmotic pressure as well as increasing blood flow, so reducing concentrations of pro-inflammatory cytokines, reducing sensitization of peripheral nociceptors.

· Standley & Meltzer (2008) have demonstrated – on a cellular level – the beneficial effects, on fibroblasts, of both myofascial release and positional release (Strain/counterstrain) methods. “……strain direction, frequency and duration, impact important fibroblast physiological functions known to mediate pain, inflammation and ROM….”

· Borgini et al (2010) have demonstrated the influence of direct compressive force on dense fascial restrictions, using the Italian modality developed at the University of Padua, Fascial Manipulation®

· The benefits of Connective Tissue Massage have been demonstrated in a number of clinical trials – notably in relation to chronic pelvic pain (Fitzgerald 2009)

· The methods used in structural integration (Rolfing) are directed mainly at fascia and connective tissue, which are treated with fingers, open hands, clenched fists, and elbows, with pressure directed to release adhesions between what should be freely sliding structures. (Findley & Schleip 2007)

· Fernandez-de-las-Penas and Pilat (2010) have described the successful use of neuromuscular technique (NMT) in treatment of myofascial pain

Much more to learn

What has emerged from the first two Fascia research conferences – Boston 2007 and Amsterdam 2009 – suggests that there is far more yet to learn.

These conferences brought clinicians of all schools, together with scientific researchers, in the hope and expectation that this would lead to a cross-fertilization, in which the clinical needs, confusions and questions of practitioners and therapists would inform researchers, who in turn would help clinicians to better understand the real nature of fascial structure and function, in relation to their patient’s problems and their own therapeutic efforts. It was further hoped that researchers would be spurred to new directions of study fascia.

And this has happened, and continues, with studies emerging at a remarkable pace, that have further clarified the nature and multiple functions and roles of fascia in the body.

The theme of the 3rd Fascia Research Congress (Vancouver, Canada, March 28 – 30, 2012) will be: Fascia: What do we know? What do we feel? Continuing the Scientist/Clinician Dialogue.

As the organising committee have said : The 2012 Fascia Congress will centre on the latest and best research on human fasciae. Additionally—and recognizing the interests of clinicians in gaining insights that will bear on practical applications—the program will be designed to include more presentation time to relating the research findings to clinical issues, particularly the practical applications of fascial layers.”

The conference proper will be preceded (March 23-27) by a Fascial Dissection Workshop, with a range of additional pre and post-conference workshops, on March 27th and March 31st .

At this early stage the planning for the Vancouver conference is already advanced.

For example, among the confirmed keynote speakers are:

· Cesar Fernandez de las Penas DO PhD : Muscular and fascial aspects of myofascial Pain

· Al Banes PhD : Mechanical Loading and Fascial Changes – Tendon Focus

· Karen Sherman PhD : Existing trials on fascia in the context of manual therapies

· Carla Stecco MD : Fascial Anatomy Overview

· Dr. Rolf K. Reed : Fluid Dynamics and fascia (lymph, circulation etc)

· Mary Francis Barbe : Changes in Fascia Related to Repetitive Motion Disorders

A number of panel sessions are also in the planning stage that will highlight the needs and interests of all clinicians – including exploration of modern imaging methods

· The conference website is http://www.fasciacongress.org/2012/

· A call for Abstracts will soon be displayed on that website

Proceeding books and DVDs from the 2007 and 2009 congresses can be purchased via this link

British Osteopathic representation in fascia research?

There has to date been little evidence of interest from British osteopaths in current fascial research or the Research Congresses. In contrast, senior members of the American osteopathic profession (including Brian Degenhardt, Michael Kuchera, Frank Willard) are active in research as well as promotion of this trend via participation in the organisation of the 3rd Congress (Vancouver 2012). For example Dr Kuchera is co-chair of the Scientific Committee, of which I am a member, as are several US based chiropractic researchers.

The possibilities for active involvement in the next congress, via submission of abstracts, is something I would encourage British DOs to consider. In my studies of cranial concepts, the intercranial structures (Tentorium cerebelli, Falx cerebri and others) were always central considerations. Has there been any cranial research that could stand scrutiny in the form of an abstract – and/or possible oral presentation? Are there perhaps a series of cases that could be described, written up, presented?

And if not now – when?

References

Bialosky J et al 2009 The mechanisms of manual therapy in the treatment of musculoskeletal pain Manual Therapy 14:531–538

Borgini E et al 2010 How much time is needed to modify fascial fibrosis? Jnl Bodywork & Movement Therapies 14(4):318-325

Cantu R Grodin A 1992 Myofascial Manipulation Gaithersburg Maryland; Aspen Publications

Cathie A 1974 Selected writings. Academy of Applied Osteopathy Yearbook 1974, Colorado Springs

Cramer G et al 2010 Zygapophyseal joint adhesions after induced hypomobility. Journal of Manipulative and Physiological Therapeutics 33:508-518

Fernandez-de-las-Penas C Pilat A 2010 IN: Chaitow L Lovegrove R (Eds.) Practical Physical Medicine Approaches to Chronic Pelvic Pain (CPP) & Dysfunction Elsevier IN PRESS

Findley T Schleip R 2007 Fascia Research. Basic Science and Implication for Conventional and Complementary Health Care vols. 2–3, Elsevier, Germany

FitzGerald, M.P. et al 2009 Randomized Multicenter Feasibility Trial of Myofascial Physical Therapy for the Treatment of Urological Chronic Pelvic Pain Syndromes. Journal of Urology 182(2):570-580

Fourie W 2009 IN: Fascial Research II: Basic Science and Implications for Conventional and Complementary Health Care Munich: Elsevier GmbH

Fryer G Fossum C 2009 Therapeutic Mechanisms Underlying Muscle Energy Approaches. In: Physical Therapy for tension type and cervicogenic headache: physical examination, muscle and joint management Fernández de las Peñas C Arendt-Nielsen L Gerwin R (eds): Jones & Bartlett, Boston

Hammer W 2007 Functional Soft-Tissue Examination & Treatment by Manual Methods 3rd ed. Sudbury, MA, Jones & Bartlett pp 33-161

Ingber D 2008Tensegrity and mechanotransduction, Jnl Bodywork and Movement Therapies 12(3):198–200, 2008.

Klingler W Schleip R Zorn A 2004 European Fascia Research Project Report. 5th World Congress Low Back and Pelvic Pain, Melbourne, November 2004

Klingler W 2011 IN: Chaitow L Lovegrove R (Eds.) Practical Physical Medicine Approaches to Chronic Pelvic Pain (CPP) & Dysfunction Elsevier IN PRESS

Kobesova A et al M 2007 Twenty-year-old pathogenic “active” postsurgical scar: a case study of a patient with persistent right lower quadrant pain. Journal of Manipulative and Physiological Therapeutics 30(3):234-238

Langevin H, Sherman K 2006 Pathophysiological model for chronic low back pain integrating connective tissue and nervous system mechanisms. Medical Hypotheses 68(1):74–80

Langevin H 2009 Fibroblast Cytoskeletal Remodeling Contributes to Viscoelastic Response of Areolar Connective Tissue Under Uniaxial Tension, as reported in Fascial Research II, Elsevier GmbH Munich

Langevin H et al 2010a Tissue stretch induces nuclear remodelling in connective tissue fibroblasts. Histochem. Cell Biol. 133(4):405-15

Langevin H 2010b Presentation: Ultrasound Imaging of Connective Tissue Pathology Associated with Chronic Low Back Pain. 7th Interdisciplinary Congress on Low Back & Pelvic Pain (Los Angeles, November 11 2010)

Little L 1969 Towards more effective manipulative management of chronic myofascial strain and stress syndromes. Jnl American Osteopathic Association 68:675-685

McCombe D et al 2001Jnl. Histochemical structureof the deep fascia and its structural response to surgery. Hand Surgery 26B:2: 89-97

Meltzer K et al 2009 In vitro modelling of repetitive motion injury and Myofascial Release. Jnl Bodywork & Movement Therapies 14:162-171

Myers T 2009 Anatomy Trains, 2nd edition Edinburgh: Churchill Livingstone

Myers T Fascial Stretching. IN: Schleip, Findley, Huijing & Chaitow. Fascia in Manual Therapy. Elsevier, Edinburgh IN PRESS

Pohl H 2010 Changes in structure of collagen distribution in the skin caused by a manual technique J. Bodywork Movement Th. 14(1):27-34

Rolf I 1962 Structural Dynamics. British Academy of Applied Osteopathy Yearbook 1962. BAAO London

Schleip R, Naylor I, Ursu D, et al 2006 Passive muscle stiffness may be influenced by active contractility of intramuscular connective tissue, Med Hypotheses 66(1):71

Schleip R 2003 Journal of Bodywork & Movement Therapies 7:104-116

Schwind P 2006 Fascia and Membrane Technique, Edinburgh: Churchill Livingstone

Shah J 2010 Ultrasound techniques reveal objective abnormalities of myofascial trigger points and surrounding connective tissue. 7th Interdisciplinary Congress on Low Back & Pelvic Pain (Los Angeles, November 11 2010)

Simmonds N et al 2011 A theoretical framework for the role of fascia in manual therapy. Jnl. Bodywork & Movement Therapies IN PRESS

Solomonow M 2009 Ligaments: A source of musculoskeletal disorders, Journal Bodywork and Movement Therapies 13(2):136-154

Standley PR, Meltzer KR 2008 In vitro modeling of repetitive motion strain and manual medicine treatments: potential roles for pro- and anti-inflammatory cytokines. Journal of Bodywork & Movement Therapies 12:201-203.

Stecco A et al 2009 Anatomical study of myofascial continuity, anterior upper limb. J Bodyw Mov Ther. 13: 53-62

Stecco C et al 2008 The expansions of the pectoral girdle muscles onto the brachial fascia: morphological aspects and spatial disposition. Cells Tissues Organs. 188: 320-9.

Still AT. 1902 Philosophy and mechanical principles of osteopathy. Kansas City, MO: Hudson-Kimberly Pub. Co.

Taylor R 1958 Bioenergetics of man. Academy of Applied Osteopathy Yearbook 1958. Carmel California

February 24, 2011/0 Comments/by Carlton Cullins

To Stretch or Not to Stretch?

Articles by Smart People, Flexibility & Mobility Training, Flexibility Training, Foam Rolling/Soft Tissue Work, Myths

Static Stretching (Balanced Body Series)

by Gray Cook

Mike Boyle is talking about killing kittens and other terrible things…………….

Recently I had an opportunity to hear my good friend, Mike Boyle give a talk at a Perform Better Summit. In his opening statements he made mention to the effective use of static stretching in some of his programs. Some attendees in the room would have had a more positive response if Mike had said, “hey guys let’s go kill some kittens”. It was almost like Mike had to defend static stretching, even though there is some research showing its effectiveness. Research also shows some more efficient ways to get muscle length to change. I’m not going to waste your time with those references at this point; A Goggle or Medline search can help you with that. Dr. Stuart McGill has stated that “static stretching deadens the muscle from a neural perspective – diminishing the stretch reflex and reducing peak strength and power” and I agree with this statement. Over a long period of time I feel that indiscriminately holding static stretches will create more problems than it will correct. So why am I saying Mike and Stuart both have a point. Let me explain:

I would like to lend my support and admiration to Mike for sticking to his guns about static stretching. Mike is an excellent teacher and coach. He teaches by example with a quick eye for practical application. I think he talks about static forms of stretching because of the results he observes when trying to change and improve movement patterns as well as educate his athletes and clients. Many people would be surprised that I’m an advocate of static stretching but, I definitely think it has its place. Scientifically, there may be better, quicker and faster ways to develop muscle length or change and maintain muscle length; however, they require a higher level of expertise, are more technique intensive, and usually have a more significant learning curve for the user than static stretching. Let me go over some of the benefits of static stretching for the user.

As a personal trainer, performance specialist, or rehabilitation professional, you may screen or assess someone who has less than optimal range of motion. You may identify that muscle length is a problem and therefore want to improve muscle length. The first order of business is achieving agreement with the client, athlete, or patient. You must make sure that the individual has an appreciation of that which you have discovered. You can take the movement pattern (squatting, lunging, backward bending, etc.) that presents them with difficulty and find safe static stretching positions within that pattern that actually make them completely aware of their specific limitation. It only takes a few other individuals doing the same stretch with no difficulty to let them know they have a deficiency. You then have an opportunity to say to them, “This is your priority”. They are immediately aware, both externally by watching others move, and internally by feeling their own restrictions that a barrier does exist. All the exercise in the world will not change their movement without attention to this limitation. It may be obvious to you, but you must drive this point for them. Further more, if a left-right asymmetry is present, there is yet another dimension of appreciation afforded to the user. This opens a discussion of injury prevention and movement efficiency. Most of the research data that we are currently collecting points towards left-right asymmetry as a huge problem and underlying reason for compensation. Using a static stretch position to allow your client, athlete, or patient to have an appreciation of a left-right asymmetry is invaluable. You have given them both a perspective of a problem or limitation that they currently have and a baseline measure that they can re-check every day before and after every training session. They can gauge the effectiveness of the other mobility techniques you employ on their simple and primitive baseline static stretch. The static stretch offers them a safe, proprioceptive awareness of where the restriction is, and making that awareness raise to the conscious level will help them appreciate the holistic approach that you are taking with them.

Now that you have shown them a barrier, you can educate them as to how this barrier can be overcome. You can break out some cool foam roll stuff, or fancy Stick work or even some great PNF technique to accelerate the resetting of normal muscle tone.

Then ask them to try the static stretch again. Sit back and enjoy the “Wow” moment.

Here are the steps:

1. Identify the most significant faulty pattern (screen). If muscle length / tone (identified by assessment) is the problem then –
2. Reset tone in the area of limited muscular length
3. Introduce normal ROM and length to the muscle group
4. Reset pattern with a corrective maneuver that utilizes the basic mobility and stability needed in the primary pattern.
5. Don’t be surprised if you can reduce time and activity in step 2 and then step 3 as things improve. Invest the extra time in step 4. Eventually if you have successfully addressed the primary problem, you can effectively use step 4 as movement preparation.

Note that I’m now using the word tone instead of length because muscle length is usually a physical representation of muscle tone. Tone is simply a characteristic of a skeletal muscle brought about by the constant flow of nerve stimuli. This tone creates the resistance to stretching. Abnormal muscle tone can be defined as:

* hypertonus – increased muscle tone, as in spasticity in extreme cases when the neurological system is functioning abnormally, and tight muscles when the neurological system is considered normal. The tight muscles are usually the result of poor habits in posture and movement and usually respond to corrective exercise.
* hypotonus – reduced muscle tone, as in flaccid paralysis in extreme cases when the neurological system is functioning abnormally, and long, sloppy, and weak muscles when the neurological system is considered normal. The long, sloppy, and weak muscles are usually the result of poor habits in posture and movement and usually respond to corrective exercise.

You can also introduce yoga postures. Yoga can be very helpful because the focus is on breathing. Many don’t understand the natural, protective reflex response, to tighten up, when we come upon a barrier like a tight muscle. We breathe shallow, grimace with our facial muscles, and push, thinking that if we just push a little harder, the barrier will yield. We somehow think the tight muscle will give in. But, very often, the individual with a flexibility problem will actually tighten and contract the muscle that they are trying to stretch. The reason the muscle is tight in the first place, is probably because it is being used improperly. This muscle may be activated twice as frequently as it should because of a lack of muscle strength or coordination in another area of the body. This muscle is actually tight because it’s protecting itself; it’s been overused and it’s generally fatigued. Part of its protection involves shortening its length to reduce its workload (contractile length) and guard against unforeseen stretching. Pushing the stretch can actually, in some cases, make the muscle you’re stretching contract even harder. This is a great opportunity to educate your athlete, client or patient and talk to them about breathing. Deep slow breaths with a relaxed expression can make a huge difference. Take a big, deep inhale breath, and enter the stretch on the super slow exhale breath. Repeat this same slow cycle the entire time you are in the stretch position.

Another thing we learn from yoga is that many of the stretches actually require you to support or brace your body in such a way, that you are not just lengthening one muscle, you are statically stabilizing with another. It is this static stability that allows you to elongate the muscle on stretch. Many of the yoga postures require you to hold yourself up in proper postural alignment while elongating one segment. This proper alignment is not simply done for aesthetic purposes; statically stabilizing your body while elongating another part of your body is more functional. It looks like static stretching, but there is a lot of stabilization going on. You do not sink and sag into a stretch, you hold your body erect, breathe into your diaphragm, and allow the segment that you are stretching to elongate. If you force it, it will contract. As you reach your barrier, breathe, tighten or hold the supporting parts of your body with more conscious control and watch the length come back to the area of your stretching focus.

I truly feel that there’s a lesson in life here. When you reach a barrier, do you push and grimace and force, or do you breathe, assess your surroundings, check your alignment and ease with patients and caution into unfamiliar territory?

One last thing you need to consider is how you actually think about muscle tightness. To help work this out, ask yourself this question on a daily basis for at least two weeks; what drives the tightness? Obviously, we are talking about static stretching because we’ve all uncovered tightness. We all know the need to reduce or resolve that tightness, but tightness in and of itself is not the problem. There is something causing the tightness. What is behind it? What is driving the tightness? Usually you will find muscle tightness is a by-product of inefficient movement patterns where muscles unnecessarily have to compensate or work overtime to help you achieve your fitness and athletic goals. Many people think, ‘well, if I just push harder or exercise longer or lift more, the problem will work itself out’. Not necessarily so. If anything, activity will reinforce a compensation, unless it is identified and addressed at its most primitive and fundamental level. My point is, if you don’t have the basic mobility and stability for a ground based activity, like a posture from yoga, a deep squat or side plank position, then performing a hang clean, plyometrics or an advanced Pilates moves is really not what you need to be doing. You need to go back and get that fundamental primitive mobility and stability when you are connected to the ground. When you become proficient you can build on that.

Learning for yourself to answer the question, ‘where does the tightness come from’, will help you educate clients and athletes about their own flexibility. When they say to you, ‘why do you think my hamstrings are so tight’, say, ‘I think they’re tight because you are using them that way’. I think that improving your movement patterns such as squatting and lunging and balancing on one leg may activate your glutes, and by activating those glutes, we reduce the dependence on extra hamstring work. Those hamstrings will actually become more flexible and functional, when they are not overworked. One of the catch-phrases I always like to state in my workshops is very simple, but very complex in its application:

“Don’t go for length in one place, if you don’t plan on adding strength in another place.”

And, for every small bit of length that you gain in one place, make sure you add a piece of strength in the other. That length you are taking away is the body trying to create stability in a muscle that wasn’t made as a stabilizer. These muscles are often found to be tight.

Below is a list of muscles prone to tightness and prone to weakness. You can see that the muscles prone to tightness are actually movers, and if they are used as postural stabilizers, will often get tight. You will also notice that the muscles prone to weakness are actually postural stabilizers, and if they are not used efficiently, or if poor alignment does not allow them to activate automatically with movement, they will actually become weak with disuse.

Janda’s functional division of muscle groups:

Muscles Prone to Weakness:

* Peronei
* Tibialis anterior
* Vastus medialis and lateralis
* Gluteus maximus, medius, and minimus
* Rectus abdominis
* Serratus anterior
* Rhomboids
* Lower portion of the trapezius
* Short cervical flexors
* Extensors of the upper limb

Muscles Prone to Tightness:

* Gastroc/Soleus
* Tibialis posterior
* Short hip adductors
* Hamstrings
* Rectus femoris
* Iliopsoas
* Tensor fasciae latae
* Piriformis
* Erector spinae
* Quadratus lumborum
* Pectoralis major
* Upper trapezius
* Levator scapulae
* Scalenes
* Flexors of the upper limb

*This list is not intended to create controversy. I realize that this list was constructed some years ago and some may consider one or two muscles are misplaced. I prefer to look at the concept that Janda has introduced. He is showing us a concept of patterns. The weakness causes the tightness and the tightness causes the weakness. You cannot just fix only one because they are mutually dysfunctional. Also note that the list of ‘muscles prone to weakness’ usually function as stabilizers and the ‘muscles prone to tightness’ usually function as movers. Why not consider one of the underlying causes of muscle tightness to be a dysfunctional stabilizer system that causes movers to shorten in an attempt to create support. Simply stretching muscles that appear tight will only address part of the problem and will rarely get to the cause.

Summery of static stretching points with comments:

* A static stretch creates awareness of tightness and sets a baseline for future comparison. It can function as a quick self appraisal of limitation, changes in limitation, or lack of limitation. It can also create awareness of appreciable asymmetries between functional units of the right and left side of the body. Dr. McGill supports static stretching in the presence of asymmetry.
* A static stretch creates safety because a stretch should be felt in the belly or midsection of a muscle, not the tendon, and not over a joint. If this is felt, something more than a tight muscle is going on here. You probably have a joint problem or tendonitis. “No pain no gain” does not apply here. If a static stretch produces pain, over a joint or tendon, you have a problem that stretching alone will not fix. Do not proceed to exercise or training without getting this assessed.
* A static stretch creates perspective with respect to movement. If the muscles that cross your ankles, knees, and hips are tight they will probably limit your squatting movement pattern. If the muscles that cross your ankles, knees, and hips are not tight and are considered normal and you cannot perform a squatting movement pattern you may have a stabilization problem. If your stabilizers do not support your skeletal system as you lower into the squat you must use your movers as a secondary support system. This will distort joint alignment and create poor postural control within the movement pattern. Consider this next time you pick exercises that do not utilize postural control (leg press, bench press etc…).
* A static stretch creates education if you take the time to discuss the potential causes of muscle tightness during the stretching session. Ask ‘where does tightness come from’ and see what responses you get. Here are some hints. One or all may fit any situation.
o Movement habits drive tightness – focus on better exercise and athletic techniques.
o Postural habits drive tightness – look at the positions of the body during sitting, sleeping, driving, and standing. Some habitual positions can create muscle shortness so consider the four positions above.
o Emotional stress can drive tightness – This is often overlooked and avoided in discussions about muscle tightness, but it is a big part of excess muscle tension (See Yoga and Breathing).
o Trigger points – are extra electrical activity in a small part of a muscle that can create muscle tightness and pain. They can result from an old muscle injury to chronic muscle tension (see all of the above). They respond best to manual pressure and stick work followed by stretching and correct exercise habits.

In closing, I would like you to understand that I do support static stretching, for the simple fact that it helps make the individual aware of their most basic limitation. It makes them think! It causes an open exchange of ideas of where the limitation has come from and what can potentially result if the limitation is not addressed. It’s easy, simple and uncomplicated. They can reproduce it, and hopefully, you will start adding more functional movements on top to keep the flexibility issues from returning. Assure them that the static stretching is necessary but only temporary. If you do your job you can turn the improved muscle length into functional movement. If movements remain functional then muscle length has no reason to return to its previous limited state. Mike is right on the money with his static stretching comments. People need time to understand and get reconnected with their body. Once this understanding is present then introduce them to more advanced techniques. I can’t think of a better way to make this point, than with some simple static stretches to show people, ‘here’s your problem’, ‘here is what I’ve found’, ‘here is where you will need to focus’. This sets you up to say ‘now, I’m going to show you some advanced and fancy stuff’, but you will always have a baseline and a perspective of where that original limitation was. If you don’t show them that, they’re not going to know how good you are.

Oh yeah…. I don’t really think Mike has problems with kittens.

Our poster series reviews in great detail how we use the Functional Movement Screen to identify faulty patterns. We use the stick and various stretches to reset tone and movement training to create harmony between stabilizers and movers. These are foundation of the corrective strategy for the movement patterns in the Functional Movement Screen. Two companion CD-roms walk you through my powerpoint presentation for each poster and guide you through the exercises that correct each pattern in the Functional Movement Screen. See a full line of our Functional Movement Screen products.

February 21, 2011/0 Comments/by Carlton Cullins