Anatomy Trains

Read here about Anatomy Trains, a model of the human musculoskeletal system that draws on tensegrity concepts. Anatomy Trains was originated by Tom Myers.

Essay: Relation of Fascial System to Tensegrity

This essay is based on chapter two of the Tom Myers' book, Anatomy Trains where he explains the model in terms of tensegrity.

Basic ideas: fascia form a whole and organs are double bagged

The human fibrous system is a body-wide responsive physiological network on a par in terms of importance and scope with the circulatory and nervous systems. The myofascial meridians are useful patterns discernible within the locomotor part of that system.

The body frequently deploys a "double bag" structure in the body’s fasciae, as all major organs, bones and joints are wrapped in this way, like a sphere turned in on itself. The myofascial meridians describe patterns of the ‘fabric’ within the outer myofascial bag connected down onto, and thus able to move, the inner bag.

Drawbacks of the classic musculoskeletal model of lever, angle and plane

Lastly, classic anatomical studies beginning with human dissection in the 17th century has been analytical, explaining the body as a series of isolated parts. These parts are found to work together kinematically in a strict Newtonian geometry of levers, angles, and inclined planes, based on an ‘isolated muscle’ theory.

The hundreds of distinct organs and body parts discovered in this way are considered as constructed in a continuous compression structure, like a brick wall, where the weight of the head rests on the 7th cervical, the head and thorax rest on the 5th lumbar, and so on down to the feet, which bear the weight of the body and transmit that weight to the earth. The concept is reinforced in the classic classroom skeleton, though the hundreds of bones in that model are reinforced with rigid hardware, or hung from an accompanying stand. According to the common concept, the muscles (read: myofascia) hang from this structurally stable skeleton and move it around, the way the cables move a crane. This mechanical model lends itself to the traditional picture of the actions of individual muscles on the bones: the muscle draws the two insertions closer to each other and thus affects the skeletal superstructure, depending on the physics.

This Newtonian force mechanical model still cannot produced convincing models of human movement, such as walking. It also engenders a mostly local therapeutic focus, since in this model forces are localized, just as they are in a brick structure. If a tree falls on one corner of your brick wall, that corner will collapse, perhaps without damaging the rest of the structure. Most modern manipulative therapy works out from this idea: if a part is injured, it is because localized forces have overcome local tissues, and local relief and repair are necessary.

To consider human body structure as a tensegrity, a macro- / micro- distinction is useful, being the macroscopic level of the body architecture as a whole, and the microscopic level of the connection between cell structure and the extracellular matrix. These two levels actually form part of a seamless whole.

Macrotensegrity: the global balance between tension and compression

The human myofasciae deploy a continuous network of restricting but adjustable tension around the individual bones and cartilage as well as the incompressible fluid balloons of organs and muscles. The latter organs push out against this restricting myofascic tensile membrane. Ultimately, the harder tissues and pressurized bags can be seen to ‘float’ within this tensile network, leading us to adjust the tensional members in order to reliably change any malalignment of the bones.

The tensegrity approach makes it obvious that forces are distributed, rather than localized. As Snelson discussed, compression members are islands, floating in a sea of continuous tension. Compression members push outwards against tension members that pull inwards. In the body, these tensile members often express themselves as fascial membranes, not just as tendinous or ligamentous strings. The two sets of forces are balanced, and the body is stable.

An overloaded tensegrity will break, but not necessarily anywhere near where the load was placed. Because the structure distributes strain throughout the structure along the lines of tension, the tensegrity structure may ‘give’ at some weak point at some remove from the area of applied strain, or it may simply break down or collapse. We know this to be true of human injuries. A bodily injury at any given site can be set in motion by such (often) long-term strains in other distant parts of the body. The injury happens where it does because of inherent weakness or previous injury, not purely and always because of local strain. Discovering these pathways and easing chronic strain at some remove from the painful portion then becomes a natural part of restoring systemic ease and order, as well as tending to prevent future injuries.

Tension and Compression: Bones and Myofascia

In this model bones are the primary compression members and the myofascia are the surrounding tension members. This is a simplification, of course. Bones can bear tension, and the double-bagged balloons in the body such as the abdomino-pelvic cavity and smaller cells can also carry compression forces.

The skeleton is only apparently a continuous compression structure: eliminate the soft tissues and watch the bones clatter to the floor, as they are not locked together but perched on slippery cartilage surfaces. It is evident that soft-tissue balance is the essential element that holds our skeleton upright--especially those of us who walk precariously on two small bases of support while lifting the center of gravity high above them.

In this model, bones are seen as ‘spacers’ pushing out into the soft tissue, and the tone of the tensile myofascia becomes the determinant of balanced structure. To change the relationships among the bones, change the tensional balance through the soft tissue, and the bones will rearrange themselves. This metaphor speaks to the strength of sequentially-applied soft-tissue manipulation, and implies an inherent weakness of short-term repetitive high-velocity thrust manipulations aimed at bones. A tensegrity model of the body--unavailable at the time of their pioneering work--is closer to the original vision of both Dr Andrew Taylor Still and Dr Ida Rolf.

The Anatomy Trains model identifies a set of myofascial meridians as the major (though by no means exclusive) continual tension bands along which this tensile strain runs through the outer myofasciae from bone to bone. Muscle attachments (‘stations’ in Anatomy Trains) are where the continuous tensile net attaches to the relatively isolated, outwardly-pushing compressive struts. These continuous meridians are not theoretical constructs--they can be seen in human dissection by turning the scalpel on its side to separate these stations from the bone underneath, while retaining the connection through the fabric from one ‘muscle’ to another. Body work and movement therapy based on this model seeks balanced tone along these tensile lines and sheets so that the bones and muscles will float within the fascia in resilient equipoise, such as is seen in any healthy athlete or dancer.

The tensegrity can also be fractally extended down into organs and cells, but this is outside the scope of Anatomy Trains.

Lacunae of this model

This model is more qualitative than quantitative. Tensegrity mathematics, itself in its infancy, has not yet described human dynamics. Further research is required to quantify the constituent tensional and compressional forces around a joint or around the system as a whole, to see if it can be analyzed in a manner consistent with tensegrity engineering. No method has been found yet to measure the actual tensions in vivo.

The long tension lines described by the model are relatively isolated from one another. More work is needed to describe their interaction, to close the truly global nature of tension as deployed about the body.

Lastly, the human body is a dynamic tensegrity with varying stress. Variation in stress is only just beginning to be explored in dynamic tensegrites. More on this below.

The tension-dependent spectrum

Allowances must be made in this vision of tensegrity for the reality of the body in motion. The body runs the gamut, in different individuals, in different parts of the body, and in different movements in various situations, from the security of a continuous compression structure to the sensitive poise of pure, self-contained tensegrity. We term this point-of-view ‘tension-dependent spectrum’--the body operating through different mechanical systems in different situations and in different parts of the body.

A herniated disc is surely the result of trying to use the spine too completely as a continuous compression structure, contrary to its design. On the other hand, a long jumper landing at the far end of his leap relies momentarily but definitively on the compressive resistance of all the leg bones and cartilages taken together. (Though even in this case, where the bones of the leg could be thought of as a ‘stack of bricks’, the compressive force is distributed through the collagen network of the bones, and out into the soft tissues of the entire body in ‘tensegrity’ fashion.) In daily activities, the body employs a spectrum of structural models from tensegrity to more compression-based modeling.

Analogies with Tensile Structures (rather than complete tensegrities)

Tensile structures and tension-reinforced structures help explicate the tension-dependent spectrum.

A sailboat provides a good ‘middle ground’ structure. It is not a tensegrity in toto, but is extensively structured by tensile elements. At anchor, the mast will stand on its own, but when you sails full of wind, the fully loaded mast must be further supported by the tensional shrouds and stays or it will snap. By means of the tensile wires, forces are distributed around the boat, and the mast can be thinner and lighter than it otherwise would be. Our spine is similarly constructed to depend on the balance of tension member ‘stays’ (the erector spinae, longissimus specifically) around it to reduce the necessity for extra size and weight in the spinal structure, especially in the lumbars.

Frei Otto deployed a tension mast at the Munich Olympiazentrum. Its flexible core is held aloft by a balance of the cords attached to its ‘processes’. With the cords in place, pulling on them can put the mast anywhere within the hemisphere defined by its radius. Cut the cords, and the flexible core would fall to the ground, unable to support anything. This arrangement parallels the iliocostalis muscles.

Stress variation and active contraction of fascial cells

The clsasic tensegrity model needs even more adjustment when we consider human motion and human load bearing. Loose tensegrity structures are ‘viscous’--they exhibit easy deformation and fluid shape change. Tighten the tensile membranes or strings--especially if this is done evenly across the board--and the structure becomes increasingly resilient, approaching rigid, columnar-like resistance until they reach their breaking point.

Tensegrity structures show resiliency, getting more stiff and rigid (hypertonic) the more they are loaded. Though load impacts one location on the tensegrity, all the interconnected structural elements of a tensegrity model rearrange themselves in response. And as the applied stress increases, more of the members come to lie in the direction of the tensional part of the applied stress, resulting in a linear stiffening of the material (distributed in a non-linear manner). This is reminiscent of the reaction of the fibrous system to mechanical stress, just as when you take a wad of loose cotton wool and gently pull on the ends--the multidirectional fibers line up with the direction of the pull until the stretching comes to a sudden stop as the fibers line up and bind. Our fibrous body reacts similarly when confronted with extra strain, like a tensegrity structure or a Chinese finger puzzle.

If a tensegrity structure is loaded beforehand, especially by tightening the tension members in ‘pre-stress’, the structure is able to bear more of a load without deforming. Being adjustable in terms of ‘pre-stress’ allows the biological tensegrity-based structure to quickly and easily stiffen in order to take greater loads of stress or impact without deforming, and just as quickly unload the stress to that the structure as a whole is far more mobile and responsive to smaller loads.

The myofascial system remodels in two ways in response to stress or the anticipation of stress. In the obvious way, muscle tissue can contract very quickly at the nervous system’s whim within the fascial webbing to pre-stress an area or line of fascia, and 2) long-term stresses can be accommodated by the remodeling of the ECM around piezo-electric charge patterns, adding matrix where more is demanded. Recently a third way to pre-stress the fascial sheets has emerged (the research was begun some time ago, but the story has only recently made it to bodywork and osteopathic circles), so we include a brief report on this new class of fascial response--the active contraction of a certain class of fibroblasts on the ECM itself.

The reader may well ask, if fascial cells display active contractility within the matrix, why it has taken us this long into the chapter to say so? All our previous discussion has centered on the passive response of the cells and the matrix itself to outside forces coming through the matrix. Might not an element this important have come up earlier in the discussion of the fascial net?

The reason for placement of this new research is that the unique role of the myofibroblasts provides a perfect transition between the tissue-and-bone world of macrotensegrity to the cytoskeletal world of microtensegrity which will occupy us for the rest of the chapter. Aside from that, the exact therapeutic implications of this discovery are as yet unclear.

Suffice it to say that fascia has long been thought to be plastic or visco-elastic, but otherwise inelastic and non-contractile. Both these shibboleths are being revised in light of new research. According to Schleip, “It is generally assumed that fascia is solely a passive contributor to biomechanical behavior, by transmitting tension which is created by muscles or other forces … (but) there are recent hints which indicate that fascia may be able to contract autonomously and thereby play a more active role.”


In fact, fascia can now be said to be contractile. But the circumstances under which such a contraction is exerted are limited and therefore quite interesting. We now know that there is a class of cells in fascia that are capable of exerting clinically significant contractile force in particular circumstances--enough, for instance, to influence low-back stability. This class of cell has been termed myofibroblasts. MFBs represent a middle ground between a smooth muscle cell (commonly found in viscera at the end of an autonomic motor nerve) and the traditional fibroblast (the cell that primarily builds and maintains the collagenous matrix). Since both smooth muscle cells and fibroblasts develop from the same mesodermal primordium, it comes as little surprise (in retrospect, as usual) that the body might find some use for the transitional cell between the two, but some surprising characteristics of these cells kept them from being recognized earlier. Apparently, evolution found variable uses for such a cell, as MFBs have several major phenotypes from slightly modified fibroblasts to nearly typical smooth muscle cells.

Chronic contraction of MFBs plays a role is chronic contractures like Dupuytren’s contracture of the palmar fascia or adhesive capsulitis in the shoulder. MFBs are clearly very active during wound healing and scar formation, helping to draw together the gap in the metamembrane and build new tissue. To be brief, we will let the reader follow the references for these possible intriguing roles in body pathology so that we can hew closely our stated goal of describing how fascia works normally.

It is now clear that MFBs occur in healthy fascia, and in fascial sheets in particular--such as the lumbar fascia, fascia lata, crural fascia, and plantar fascia. They have also been found in ligaments, the menisci, tendons, and organ capsules. The density of these cells may vary positively with physical activity and exercise, but in any case, the density is highly variable among people.

One very surprising aspect of these cells is that their contraction--unlike every other muscle cell in the body, smooth or striated--is that they are not stimulated to contract via the usual neural synapse. Therefore they are beyond the reach of conscious control, or even unconscious control as we would normally understand it. The factors that induce the long-duration, low-energy contraction of these cells are 1) mechanical tension going through the tissues in question, and 2) specific cytokines and other pharmacological agents such as nitric oxide (which relaxes MFBs) and histamine, mepyramine, and oxytocin (which stimulate contraction). Unexpectedly, neither norepinephrine or acetylcholine (neurotransmitters commonly used to contract muscle), nor angiotensin or caffeine (calcium channel blockers) has any effect on these MFBs. Many MFBs are located near capillary vessels, the better to be in contact with these chemical agents.

The contraction, when it occurs, comes on very slowly compared to any muscle contraction, building over 20--30 minutes and sustaining for more than an hour before slowly subsiding. Based on the in vitro studies to date, this is not a quick-reaction system, but rather one built for more sustained loads, acting as slowly as it does under fluid chemical stimulation rather than neural. One aspect of the fluid environment is of course its pH, and a lower, acidic pH in the matrix tends to increase the contractility of these MFBs. Therefore, activities that produce pH changes in the internal milieu, such as breathing pattern disorder, emotional distress, or acid-producing foods could induce a general stiffening in the fascial body. Here endeth this brief foray into chemistry, which is so well-covered elsewhere.

MFBs also induce contraction through the matrix in response to mechanical loading, as would be expected. With the slow response of these cells, it takes 15-30 minutes or more before the fascia in question gets more tense and stiff. This stiffness is a result of the MFBs pulling on the collagen matrix and ‘crimping’ it (Fig. 1.70).

The manner in which the MFB contacts and tenses the fiber matrix of the ECM is instructive, and will lead us into the wonderful world of tensegrity on a cellular level.

Regular fibroblast cells contain actin, as do most cells, but they are incapable of mounting the degree of tension or forming the kinds of intracellular and extracellular bonds necessary to pull significantly on the ECM (Fig 1.71A). Under mechanical stress, however, the fibroblast will differentiate into a proto-MFB, which builds more actin fibers and connects them to the focal adhesion molecules near the cell surface (Fig. 1.71B). Further mechanical and chemical stimulation can result in full differentiation of the MFB, characterized by a complete set of connections between the fibers and glycoproteins of the ECM through the MFB membrane into the actin fibers connected with the cytoskeleton (Fig 1.71C).

The contraction produced by these cells--which often arrange themselves in linear syncitia as muscle cells also do, like boxcars on a train - can generate stiffening or shortening of large areas in the sheets of fascia where they often reside (Fig. 1.72).

This discovery, though still in its early stages in terms of research, promises myriad implications about the body’s ability to adjust the fascial webbing. This form of ‘pre-stress’--a middle ground between the immediate contraction of pure muscle and the fiber-creation remodeling shown by the pure fibroblast - can prepare the body for greater loads or facilitate transfer of loads from one fascia to another. In terms of the responsiveness of fascia, we see a spectrum of contractile ability from the instant and linear pull of the skeletal muscle through the more generalized spiral contraction of the smooth muscle cell on into the varying degrees of MFB expression to the more passive but still responsive fibroblast at the other end of the connective tissue spectrum.

Given how these MFBs can be stimulated by mechanical (fibrous) loading or by fluid chemical agents, we can also discern in this system the dance among the neural, vascular, and fibrous web that goes into making what we have here termed ‘Spatial Medicine’, how the body senses and adapts to changes of shape caused by internal or external forces.

Returning to our discussion of tensegrity, we introduced the myofibroblasts at this point because they show how the body can alter the ‘pre-stress’ of the body’s tensegrity to stiffen it for greater loading. Because of the time involved, there has to be an anticipation of further stress and loading to put the contraction in place. Thus one is tempted to question whether emotional stress can induce similar loading and MFB response, creating a generally ‘stiffer’ (literally), less sensitive (interstitial sensory nerve endings would be rendered inert), and less adaptable person biochemically.

Moving to the other end of the scale, this discussion also leads us to how microtensegrity works to connect the entire inner cell workings to the ECM of the fascial net. It is not only MFBs that are capable of hooking up to the ECM. On this microscopic level, the tensegrity applications are more unambiguous, and have every promise of revolutionizing our approach to medicine by bringing to the fore the spatial and mechanical aspect as a complement to the predominant biochemical view.

Microtensegrity: how the cells balance tension and compression

Up to this point, we have been discussing tensegrity on the macroscopic level, as it relates to our Anatomy Trains model. In discussing the MFBs, we saw how the internal cell structure could hook to the macrostructure of the ECM. This end of the tensegrity geometry argument has recently been boosted with extensive research, now reaching more common knowledge under the name mechanobiology, with relevance to myofascial work and manual intervention of all types. Before we leave tensegrity for the main body of the book, we repair once again to the microscope. Here we find a new set of connections with an unexpected glimpse into the possible effect of manual work on cellular function, even including genetic expression.

On the basis of this book, one could be forgiven, saving the last few paragraphs about MFBs, for thinking that the cells ‘float’ independently within the extracellular matrix (ECM) we have been describing, and indeed that is how I myself taught it for years. ‘Medicine has done great things,’ I would pontificate, ‘by concentrating on the biochemistry within the cells, while manual and movement therapists concentrate on what goes on between the cells.’ The cell has been viewed as ‘a balloon filled with Jello’, in which the organelles float, in the same way the cell floats in the medium of the ECM.

This new research--and here we rely heavily on the work of Dr. Donald Ingber and his faculty at Children’s Hospital in Boston - has knocked any such separation into a cocked hat. It has been definitively shown that there is a very structured and active ‘musculo-skeletal system’ within the cell, called the cytoskeleton, to which each organelle is attached, and along which they move. The cytoskeleton is slightly misnamed in that it also contains actomyosin molecules that can contract to exert force within the cell, on the cell membrane, or--as we saw with the MFBs--through the membrane to the matrix beyond, so it is really the cell’s musculoskeletal or myofascial system. These mechanically active connections--compressional microtubules, tensile microfilaments, and interfibrillar elements - run between the inner workings of nearly every cell and the ECM, a mutually active relationship that forever puts to rest the idea that independent cells float within a sea of ‘dead’ connective tissue products (Fig. 1.73).

It has been known for some time that the ‘double bag’ of the phospholipid cell membrane is studded with globular proteins that offer receptor sites both within and without the cell, to which many but highly particular chemicals could bind, changing the activity of the cell in various ways (see Fig. 1.34). Candace Pert’s research summarized in the ‘Molecules of Emotion’, making endorphins a household word, is one example of the kinds of links in which the chemistry beyond the cell, binding to these cross-membrane receptors, affects the physiological workings within the cell.


The newer discovery, and one even more relevant to our work, is that in addition to these chemoreceptors, some of the membrane-spanning globular proteins--a family of chemicals known as integrins--are mechanoreceptors which communicate tension and compression from the cell’s surroundings--specifically from the fiber matrix--into the cell’s interior, even down into the nucleus (Fig. 1.74). So, in addition to chemoregulation, we may now add the idea of mechanoregulation.

By the early 1980s, it was understood in scientific circles that the ground substance and adhesive matrix proteins were linked into the system of the intracellular cytoskeleton. It is that linkage--from the nucleus to the cytoskeleton to the focal adhesion molecules inside the membrane, through the membrane with the integrins, and then via the proteoglycans like fibronectin to the collagen network itself (Fig. 1.75). This set of connections is extraordinarily strong in the MFBs, working generally from the cell out onto the matrix, but the same kind of mechanoregulatory process extends to every cell, often working from the outside in: movements in the mechanical environment of the ECM can affect, for better or worse, how the cell functions.

While it is obvious that some kind of cell adhesion is necessary to hold the body together, the extent and importance of this mechanical signaling, now called mechanotransduction, is being seen to have a role in a wide variety of diseases, including asthma, osteoporosis, heart failure, atherosclerosis, and stroke, as well as the more obvious mechanical problems such as low back and joint pain. ‘Less obviously, it helps to direct both embryonic development and an array of processes in the fully formed organism, including blood clotting, wound healing, and the eradication of infection.’

For instance:

A dramatic example of the importance of adhesion to proper cell function comes from studies of the interaction between matrix components and mammary epithelial cells. Epithelial cells in general form the skin and lining of most body cavities; they are usually arranged in a single layer on a specialized matrix called the basal lamina. The particular epithelial cells that line the mammary glands produce milk in response to hormonal stimulation. If mammary epithelial cells are removed from mice and cultured in laboratory dishes, they quickly lose their regular, cuboidal shape and the ability to make milk proteins. If, however, they are grown in the presence of laminin (the basic adhesive protein in the basal lamina) they regain their usual form, organize a basal lamina, and assemble into gland-like structures capable once again of producing milk components.

In other words, the mechanical receptors and the proteins of the ECM are linked into the cell in a communicating system via the integrins on the cell’s surface. These connections act to alter the shape of the cells, and with that, their physiological properties. How do cells respond to changes in the mechanics of their surroundings?

The response of the cells depends on the type of cells involved, their state at the moment, and the specific makeup of the matrix. Sometimes the cells respond by changing shape. Other times they migrate, proliferate, differentiate, or revise their activities more subtly. Often, the various changes issue from the alterations in the activity of genes.

Information conveyed on these spring-like ‘mechanical molecules’ travel from the matrix into the cell to alter genetic or metabolic expression, and, if appropriate, out from the cell back to the matrix:

We found that when we increased the stress applied to the integrins (molecules that go through the cell’s membrane and link the extracellular matrix to the internal cytoskeleton), the cells responded by becoming stiffer and stiffer, just as whole tissues do. Furthermore, living cells could be made stiff or flexible by varying the prestress in the cytoskeleton by changing, for example, the tension in contractile microfilaments.

The actual mechanics of the connections between the extracellular matrix and the intracellular matrix is generally achieved by numerous weak bonds--a kind of Velcro® effect--rather than a few strong points of attachment. The MFBs, with their very strong connections, would be an exception. These focal adhesion and outside integrin bonds respond to changing conditions, connecting and unconnecting rapidly at the receptor sites when the cell is migrating, for instance. Mechanically stressing the chemoreceptors on the cell’s surface--the ones involved in metabolism, as in Pert’s work--did not effectively convey force inside the cell. This job of communicating the picture of local tension and compression is left solely to the integrins, which appear ‘on virtually every cell type in the animal kingdom.’

This brings us to a very different picture of the relationship between biomechanics, perception, and health. The cells do not float as independent ‘islands’ within a ‘dead’ sea of intercellular matrix. The cells are connected to and active within a responsive and actively changing matrix, a matrix that is communicating meaningfully to the cell, via many weak connections (see Fig. 1.74B and 1.75). The connections are linked through a tensegrity geometry of the entire body, and are constantly changing in response to the cell’s activity, the body’s activity (as communicated mechanically along the trails of the fiber matrix), and the condition of the matrix itself.

Microtensegrity and optimal biomechanical health

It appears that cells assemble and stabilize themselves via tensional signalling, that they communicate with and move through the local surroundings via tension, and that the musculo-fascial-skeletal system as a whole functions as a tensegrity. According to Ingber: ‘Only tensegrity, for example, can explain how every time that you move your arm, your skin stretches, your extracellular matrix extends, your cells distort, and the interconnected molecules that constitute the internal framework of the cell feel the pull--all without any breakage or discontinuity.’ This is a very up-to-date statement of the sentiment from The Endless Web with which we started this chapter.

The sum total of the matrix, the receptors, and the inner structure of the cell constitute our ‘spatial’ body. Though this research definitively demonstrates its biological responsiveness, a question remains concerning whether this system is ‘conscious’ in any real sense, or whether we perceive its workings only via the neural stretch receptors and muscle spindles arrayed throughout the muscle and fascia of the fibrous body.

Structural intervention--of whatever sort--works through this system as a whole, changing the mechanical relations among a countless number of individual tensegrity-linked parts, and linking our perception of our kinesthetic self to the dynamic interaction between cells and matrix.

Research into integrins has just begun to show us the beginnings of ‘spatial medicine’--and the importance of spatial health:

To investigate the possibility further [researchers in my group] developed a method to engineer cell shapes and function. They forced living cells to take on different shapes--spherical or flattened, round or square--by placing them on tiny adhesive ‘islands’ composed of extra-cellular matrix. Each adhesive island was surrounded by a Teflon-like surface to which cells could not adhere.

By simply modifying the shape of the cell, they could switch cells between different genetic programs. Cells that were stretched and spread flat became more likely to divide, whereas rounded cells that were prevented from spreading activated a death program known as apoptosis. When cells are neither too expanded nor too hemmed in, they spend their energy neither in dividing nor in dying. Instead they differentiated themselves in a tissue-specific manner; capillary cells formed hollow capillary tubes, liver cells secreted proteins that the liver normally supplies to the blood, and so on.

Thus, mechanical information apparently combines with chemical signals to tell the cell and cytoskeleton what to do. Very flat cells, with their cytoskeletons stretched, sense that more cells are needed to cover the surrounding substrate--as in wound repair--and that cell division is needed. Rounding and pressure indicates that too many cells are competing for space on the matrix and that cells are proliferating too much; some must die to prevent tumor formation. In between those two extremes, normal tissue function is established and maintained. Understanding how this switching occurs could lead to new approaches in cancer therapy and tissue repair and perhaps even to the creation of artificial-tissue replacements.

The New Proportion

This research points the way toward a holistic role for the mechanical distribution of stress and strain in the body that goes far beyond merely dealing with localized tissue pain. If every cell has an ideal mechanical environment, then there is an ideal ‘posture’--likely slightly different for each individual, based on genetic, epigenetic, and personal use factors--in which each cell of the body is in its appropriate mechanical balance for optimal function. This could lead to a new and scientifically based formulation of the old search for the ‘ideal’ human proportion--an ideal not built on the geometry of proportion or on musical harmonics, but on each cell’s ideal mechanical ‘home’.

Thus, creating an even tone across the myofascial meridians, and further across the entire fascial net, could have profound implications for health, both cellular and general. ‘Very simply, transmission of tension through a tensegrity array provides a means to distribute forces to all interconnected elements, and, at the same time to couple or ‘tune’ the whole system mechanically as one.’

For manual and movement therapists, this role of tuning the entire fascial system could have long-term effects in immunological health, prevention of future breakdown, as well as in the sense of self and personal integrity. It is this greater purpose, along with coordinating movement, augmenting range, and relieving pain, that is undertaken when we seek to even out the tension to produce an equal tonus--like the lyre’s string or the sailboat’s rigging--across the Anatomy Trains myofascial meridians (Fig 1.76).

In fact, however, every cell is involved in what we could term a ‘tensile field’ (see also the Appendix 3 on Acupuncture meridians for more in this vein). When the cell’s need for space is disturbed, there are a number of compensatory moves, but if the proper spatial arrangement is not restored by the compensations, the cell function is compromised--that is what this research makes clear. The experiences therapist’s hand or eye can track disturbances and excesses in the tensile field, although an objective way to measure these fields would be welcome. Once discovered, a variety of treatment methods can be weighed and tried to relieve the mechanical stress.

The microvacuole theory

The body has to relieve and distribute such stress continually, sometimes without benefit of manual therapy. The mechanism for doing so--a fascinating fractal adapting system in the connective tissues--has recently been uncovered and documented. So, finally, we cannot leave the world of fascia without sharing some of the insights and beautiful images that have come from the work of the French plastic and hand surgeon Dr. Jean-Claude Guimberteau.120 These images show the interface between microtensegrity and macrotensegrity (an artificial distinction in the first place) in action in the living body (Fig. 1.77).

So many of the images, both verbal and visual, that we present here are taken from in vitro experiment or from cadaverous tissue. The microvacuolar photos in this section were photographed in vivo during hand surgery, with permission. How well they demonstrate the healthy functioning of normal fascia, revealing a surprising new discovery of how fascial layers slide on each other.

Fascial layers in the hand, specifically in the carpal tunnel, must slide on each other more than any other apposite surfaces, so it is understandable that a hand surgeon would seek more precision on this question. Every fascial plane, however, has to slide on every other if movement is not to be unnecessarily restricted. Yet, when doing dissection in either fresh-frozen or preserved cadavers, one does not see fascial planes sliding freely on each other; one sees instead either a delicate fascial ‘fuzz’ or stronger cross-linkages that connect more superficial planes to deeper ones, as well as laterally between the epimysia. This fits with the ‘all-one’fascia’ image of continuity that is the motif for this book, but it calls into question what constitutes ‘free’ movement within the fascial webbing (Fig. 1.78).

Such movement within the carpal tunnel and with the lower leg tendons around the malleoli is usually depicted in the anatomies as having tenosynovial sheaths, or specialized bursae for the tendons to run in--often rendered in blue in the anatomy atlases like Netter and Gray’s.121, 122 Dr Guimberteau has poked his camera inside these supposed bursae of the ‘sliding system’ and come up with a startling revelation that applies not only to his specialized area of the hand, but to many of the loose interstitial areas of the body: there is no discontinuity between the tendon and its surroundings. The necessary war between the need for movement and the need for maintaining connection is solved by a constantly changing fractally divided set of polyhedral bubbles which he terms the Multimicrovacuolar Collagenic Absorbing System.

Pictured here (Fig 1.79), the skin of these bubbles is formed from elastin and collagen Types I, II, IV and VI. The bubbles are filled with 80% water, 5% fat, and 15% hydrophilic proteoglycoaminoglycans. The fern-like molecules of the sugar-protein mix spreads out through the space, turning the contents of the microvacuole into a slightly viscous jelly. When movement occurs between the two more organized layers on either side--the tendon, say, and the flexor retinaculum, these bubbles roll and slide around each other, joining and dividing as soap bubbles do, in apparently incoherent chaos. ‘Chaos’, understood mathematically, actually conceals an implicate order. This underlying order allows all the tissues within this complex network to be vascularized (and therefore nourished and repaired), no matter which direction it is stretched, and without the logistical difficulties that present themselves whenever we picture the sliding systems the way we have traditionally done (Fig. 180).

This kind of tissue arrangement occurs all over the body, not just in the hand. Whenever fascial surfaces are required to slide over each other in the absence of an actual serous membrane, the collagen--ground substance bubbles ease the small but necessary movements between the skin and the underlying tissue, between muscles, between vessels and nerves and muscles--this arrangement is literally almost everywhere in our bodies--tensegrity at work on a second-by-second basis.

There is little to add to these images; they speak for themselves. To see this system in motion, we offer the references for Dr Guimberteau’s video. The photographs here show the complexity, but not the diversity in how the microvacuoles and microtrabeculae rearrange themselves to accommodate the forces exerted by internal or external movement. The trabecular ‘struts’ (actually parts of the borders between vacuoles) shown in Fig. 1.81, which combine collagen fibers with the gluey mucopolysacchraides, spontaneously change nodal points, break and reform, or elasticize back into the original form. Also not visible in the still pictures is how each of these sticky guy-wires is hollow, with fluid moving through the middle of these bamboo-like struts.

Guimberteau’s work brings together the tensegrity concepts on both a macroscopic and microscopic level. It shows how the entire organismic system is built around the pressure balloons common to both cranial osteopathy and visceral manipulation. It suggests a mechanism whereby even light touch on the skin could reach deeply into the body’s structure. It demonstrates how economical use of materials can result in a dynamically adjusting system.

Links and References

Portal to Structural Anatomy
A series on the body's musculoskeletal structure
Anatomy:Animals, Bone, Lungs, Spine, Elbow
Concepts: Anatomy Trains, Biotensegrity, Birth, Mechanobiology, Movement Therapy
Tools: Clothing, Prosthetics
People: Earnhardt, Flemons, Guimberteau, Levin, Myers, Scarr