With Rolfing we attempt to change the shape and form of the body permanently. We have our ideas about balancing in gravity and improved function to guide questions about why to change structure. But then there are the questions about how. We have interventions that are our strategies and “moves,” formulas and techniques. Basic to all of these interventions is this intention for permanent change.
In recent years Robert Schleip has been promoting a theory that it is changes in muscle tonus via the nervous system that produce Rolfing’s permanent effects on structure. This is a radically different view than that of Dr. Rolf and in practice means using different interventions than she developed. It was Dr. Rolf’s view that we are changing the shape and form of structure by applying selective and educated pressure to the connective tissue matrix. As she, herself, wrote:
“Connective tissues, particularly the fasciae, are in a never-ending state of reorganization. The continuous metabolic interchange made possible through the intimate relation of fascia with water metabolism allows structural reorganization. While fascia is characteristically a tissue of collagen fibers, these must be visualized as embedded in ground substance. The universal distribution of connective tissue calls attention to the likelihood that this colloidal gel is the universal internal environment. Every living cell seems to be in contact with it, and its modification under changes of pressure would account for the wide spectrum of effects seen in Structural Integration. The observable speed of the changes that are induced supports this hypothesis in the light of what we know about the action of colloids and the physical laws governing them. The application of pressure is, in fact, the addition of energy to the tissue colloid. (It is well known in physics that the addition of energy can turn colloid gel into sol.) It is probably this more energized colloid that accounts for the different physical properties of the body undergoing Structural Integration.”1
From this point of view as Rolfers we have developed many modes of perception and techniques of interaction with tissue that we use every day in our practices to good result. In the second half of this article, Marilyn Beech describes the validity and interactions of the gel to sol operation. This intention toward softening, shifting, redirecting and sculpting the connective tissue matrix is fundamental to our work with fascia. Our notions of working with layers and sheaths of fascia and of connecting segments via a pervasive and integrated network of tissue are born fundamentally of our belief that we are working with the connective tissue network.
There are additional factors of connective tissue operation that could also be factors in Rolfing interventions. Dr. Oschman’s article in this issue of Rolf Lines discusses the electromagnetic conductive properties of the connective tissue. At the recent Annual Meeting, Michael Morrison, an earth systems scientist and recently certified Rolfer, presented information on connective tissue interactions at the cellular level that are determining the most primary life functions. It would seem that the information for many genetic operations is coming from the ground matrix around the cells, not from within the cells themselves. He presented research that demonstrates that the influence of the nervous system on the behavior of the body is secondary to the connective tissue both evolutionarily and qualitatively2.
The neurological theory as it is presented by Robert Schleip3 rejects any possibility of connective tissue involvement in structural shape or form and disbelieves the possibility of connective tissue change by a gel to sol operation or any other means. He has based this neurological theory of Rolfing change on certain foundational assumptions. He refers to calculations performed by Peter Levine that determined that it would take tons of pressure to produce a biochemical change in connective tissue. Yet, these calculations were done once while Peter was in graduate school and have not been reproduced since. We do not know what type of pressure on what parts of the connective tissue these calculations refer to. Dr. Levine has never presented these calculations for review, nor have they been tested in actual laboratory experiments. He has only told the story of the time when he and a professor worked them out.
Secondly, this neurological view is based on Robert’s experience of three persons under anesthesia. He found two out of the three had shoulders which would not fall backward before anesthesia that would fall backward during anesthesia. Yet, this does not prove that connective tissue is not producing. shape. To do this we would need to know what structural relationships existed in the structure prior to anesthesia and assess them during and afterward. And we would need to know to what degree muscle contraction and/or the connective tissue affected the restraint in the motion before, during and after anesthesia. It is true that surgeons and anesthesiologists have reported a lack of tone in anesthetized bodies. Certainly, muscle contraction can affect the range of motion in joints, but this does not indicate that muscle contraction is the exclusive determinate of structural shape and form. We also do not know what effects anesthesia might be having on the connective tissue. Our common sense assumption is that anesthesia shuts down the nervous system and anesthesiologists will give this explanation. But a search of the journals shows us two things: that there is no agreement on how anesthetics works, and that researchers for the most part are only looking at the nervous system.4 There is however research that shows that anesthetics disrupt functioning of microtubules and micro filiments at the cellular level. 16 Whether this is the primary affect that then determines neuronal action, or is concurrent or secondary has yet to be discovered. Any interpretation of why these anesthetized bodies changed under anesthetics will have to wait until more information is available.
There is little actual evidence to support the idea that Rolfing changes are the result of neural action. Dr. Levine’s calculations are also unsubstantiated in the light of subsequent biochemical analysis of connective tissue function. Robert’s evidence from anesthetized bodies needs to be gathered in a well designed study that considers all of the variables. Robert also cites reports of nerves being found penetrating the connective tissue sheath, but these nerves can be, and often are, passing through to other structures. Noting the presence of nerves should not lead to the assumption of some sort of motoric effect. There has never been any evidence or demonstration of a direct neurological contraction of any connective tissues. And though smooth muscle fibers have occasionally been found in connective tissue, their presence is too rare to be considered a factor in determining connective tissue behavior.
In my (Liz’s) experience of Rolfing, I do find contracted muscles. It is often necessary to get these contracted muscles to release in order to accomplish Rolfing goals. Using my understanding of the golgi tendon reflex from early massage training, I will put pressure on the attachments of the muscles to get them to release. Then I will proceed to apply pressure to the connective tissue matrix to get further alteration to the shape of the structure in this local area or globally I will also interact with the tonus of muscles in doing functional education before, during and after a session.
This brings up the distinction between what might be called postural changes and what might be called structural changes. We could consider the changes in shape and alignment that can be produced by relaxing or contracting muscles as postural changes. These would be under some level of voluntary control. The changes in shape and alignment that are structural are associated with tissues that require outside intervention or significant and/or repetitive stress to transform. In Rolfing, we work with both postural and structural changes. These neurological interfaces affect postural change, the work we do with the connective tissue matrix affects structural change.
PROPERTIES OF CONNECTIVE TISSUE
What we are faced with here is a dilemma concerning whether the nervous system or the connective tissue system is primary in the control of structure. This dichotomy itself may be misleading. Often we humans set up dichotomies or develop principles that are not found in nature. The history of science is full of these well-intentioned mistakes. The fact is that the nervous system does exert great control over the functioning of our bodies, but so do other biochemical elements which are not always under direct control of the nervous system. In order to avoid artificial dichotomies we need to stay close to what is actually known about these two systems, what the research tells us, and try our best not to theorize in the absence of facts. To this end I will outline a brief overview of what is known about the physical properties of gels in order to clarify how connective tissue does what it does. This information comes mainly from the research of Toyoich: Tanaka7. See the article by Jim Oschman in this issue for further information on the repair, information and tensegrity functions of connective tissue, as well as the interview with Gil Hedley as he describes the fascinating “centipede arms” that wrap the tubes in the body. This suggests to me that structures function much more holistically and with less separate distinction than we are accustomed I looking for.
Human connective tissue has two distinct parts: a liquid matrix and a fibrous network. The liquid matrix i., composed of macromolecules called proteoglycans, which have a protein core covalently bonded to glycosami noglycan (polysaccharides) side chains. Six types of glycosaminoglycans have been found. One of them, hyaluronate, differs from the rest in that it is not bonded to the protein core, has an expanded structure which gives it great viscosity, and is evolutionarily the oldest glycosaminoglycan and the first to appear in the embryo. Proteoglycans function as barriers that regulate the flow of macromolecules through connective tissue, act as shock absorbers for weight bearing tissues, and bind to other molecules that regulate cell function8.9.
The fibrous network is embedded in the proteoglycan liquid, and is composed of rigid molecules of polypeptides arranged in a triplechain helix. Five types of collagen have been identified and seem to be specific to tissue and function. They differ in their protein composition and in their extensibility. Tendon and bone are 95% Type I collagen, which is the least elastic type, while basement membranes are 95% Type IV(the thin layer that attaches cells to connective tissue), an open collagen network that provides support but also allows a lot of molecular flow through the tissue. Most tissues contain more than one type of collagen so that they complement each others’ functions.10
PHYSICAL PROPERTIES OF GELS
Connective tissue is an organic gel, and like all gels has two basic elements: a liquid through which particles circulate, and a fibrous network that gives structure to the liquid. Equilibrium needs to be maintained between these two components. If conditions in the liquid medium create enough instability in the fibrous medium the gel will experience a phase transition from an expanded, swollen state to a collapsed one, or vice versa. The fibrous network can tolerate a wide range of changes, but when the critical point is reached a very minor degree of change will cause a complete phase transition.
Conditions that can cause instability in the liquid medium are pH, salt content, temperature, electrical fields and hydration. Changing conditions in the liquid medium puts pressure on the fibrous network to maintain equilibrium. It does this with a three part balancing mechanism called osmotic pressure. It is the osmotic pressure that determines whether a gel absorbs or releases fluids. Osmotic pressure is described as having two positive forces, rubber elasticity and hydrogen-ion pressure; and one negative one, fiber affinity.
Phase transitions in gels are not gradual. Rather, changes in the liquid need to reach a certain critical point and then the expansion or collapse of the gel is abrupt and drastic, resulting in the expulsion of fluids or expansion with maximum uptake of fluids.
This describes the attraction between the liquid and fiber mediums. If the chemical composition of the liquid is such that it repels the fibers then the fibers will be attracted to each other, clumping up. This attraction is a negative force and causes collapse of the gel. The ability of this force to affect the gel depends on the gel’s volume. The fibers must be in contact before the attraction is enough to collapse the gel. As the volume increases, the fibers separate more and the attraction decreases.
This is a positive force and is affected mainly by temperature. Collagen fibers are in constant motion because of the thermal energy created by the temperature of the gel. This motion is a rapid rotation around the axis of the fiber that spirals up and down. The fibers are made up of sectioned chains. When these are held in a completely extended position with the ends immobile, the rotational motion tends to pull the ends together. When the fibers are collapsed, the motion of the segments tends to push the ends apart. When the fiber is in a state of equilibrium, this force is zero and the fiber neither extends or collapses, merely rotates. Changing the temperature of a gel will accentuate the extension or collapse of the fibers.
Hydrolysis, the splitting of water molecules, occurs in a gel when it has been saturated with water. Hydrolysis releases H+ ions into the liquid medium, the negative ions lining up on the fiber chain. H+ concentration depends on how much hydrolysis has occurred, and that is a consequence of how much water is in the liquid and how long it has been there. The presence of hydrogen ions creates pressure within the gel. This pressure tends to create expansion until volume has increased enough to lower the pressure.
Ionization is a positive pressure that combines with rubber elasticity to oppose fiber affinity attraction. Without it fiber affinity can overpower rubber elasticity and collapse of the gel cannot be stopped. This extra pressure can keep fluid in the gel at greater temperature ranges so that phase transitions do not happen gradually as temperature or solution components change. Instead, pressure is maintained for a high degree of change until a critical point is reached and the change in gel volume is drastic. It helps maintain the “all or nothing” approach to stability. I imagine that many of us have experienced this effect in our work when, after working diligently for minutes or sessions on a piece of gristle, it suddenly changes with almost no input.
There is one more property of gels that is important for us as Rolfers to be aware of, and this is amplification. When a phase transition occurs in a localized region, that area begins to expand, creating a positive osmotic pressure compared to the surrounding areas. This puts pressure on the surrounding areas and as this pressure reaches a critical point, phase transitions occur in these outlying areas. The same happens with contraction. In this way a tendency toward movement in one direction in a local area can be amplified to surrounding areas. This is why we don’t have to touch all the connective tissue in a person and can work at a bit of a distance and still cause phase transitions.
Connective tissue is a non-genetic organic gel that evolved first out of a need to move freely through an aqueous environment and provide information to the organism concerning internal and external conditions. Later, as life rolled out onto the beaches, it was pressed into service to provide structural support against the full force of gravity and to give life forms a way to take their water with them.” Some forms of connective tissue, those that contain elastin and hyaluronate, are evolutionarily ancient12. We still have this same substance providing the same support services: information carrier, structural support, fluid control. It managed this without the direction of a nervous system for many millennia. Gels have physical properties that cause them to act in certain ways under certain conditions and these conditions do not include input from neurons.
Three of the objections that have been made to the gel-sol theory are that the length of time required to induce a phase change is too long to explain the affects of Rolfing; it is not clear why connective tissue doesn’t harden again immediately; and that it is hard to understand why everyday movements don’t cause constant phase changes. To the first objection I will quote Tanaka: “The time required is proportional to the square of the linear dimensions of the gel…. A cylindrical gel one micrometer in diameter, the size of a muscle fiber, would swell or shrink in a few thousandths of a second. “(p.138) To the second objection, a gel will not harden immediately because once it is in equilibrium it requires quite a bi of force to change it again. As to the third, everyday movements do cause constant phase changes and, in fact, may be how muscles operate. (Again, see Tanaka.) As to why repetitive postures or movements cause the tissue to collapse permanently, I can only guess. I imagine it is a combination of voluntary use of muscles in a particular manner (postural change), with a subsequent drastic phase change in the connective tissue (structural change) after many repetitions, perhaps years, of doing the same thing. The point is that there are many fascinating and sketchily understood interactions at the atomic and molecular level that if understood may very well explain our dilemmas. It is at these levels that the primary forces of matter-gravity, electromagnetism, hydrostatic pressure, temperature-affect tissue and can cause DNA and enzymes to turn on or off operations, and gels to collapse or expand. This is where some good research would come in handy, but I don’t think these objections are unanswerable to the point that we have to dispense with the idea that connective tissue has a primary role to play in structure.
There are certainly fascinating factors in understanding the interactions between the nervous system and structure that result in posture. There is great potential in understanding state shifts in the autonomies that result from the permanent alteration of shape, form and position. There is much to be understood about the nervous system’s role in movement and expression. However, these avenues of inquiry are not closed off by an assumption that there is a permanent modification of the connective tissue network that is affected by Rolfing. The potentials for transformation in the connective tissue matrix are well-founded and promising. It is troubling that this neurological approach is being presented not as an additional explanation for change but as a replacement of Dr. Rolf’s understanding, closing off the connective tissue matrix as an avenue of inquiry.
1. Rolf, Ida. Rolfing: The Integration of Human Structures, Dennis-Landman, Santa Monica, 1997. pp. 41, 42.
2. Michael Morrison presented this information in a panel discussion chaired by Patrick Ellinwood with Jim Oschman and John Cottingham. Tapes of this discussion are available from Goodkind of Sound, 800-476-4785.
3. Robert Schleip’s presentation of his neurological theory are collected in “Talking to Fascia – Changing the Brain” available from the Rolf Institute. These were previously published as “Talking to Fascia-Talking to the Brain,” Rolf Lines, April/May 1991; “Rolfing and the NeuroMyofascial Net,” Ro/f Lines, March 1993; “Primary Reflexes and Structural Typology,” Rolf Lines, October 1993; “Adventures in the Jungle of the NeuroMyofascial Net,” Rolf Lines, November 1998.
4. Franks, N.P. and W.R. Lieb. Molecular and Cellular Mechanisms of General Anaesthesia, Nature, Vol 367, February 1994. pp. 607-613.
5. Poste G., D. Papahadjopoulos and F.L. Nicolson, Local Anesthetics Affect Transmembrane Cytoskeletal Control of Mobility and Distribution of Cell Surface Receptors, Proc. Nat. Acad. Sci. USA, Vol. 72:11, pp. 4430-4434.
6. Freedman, David H., Quantum Consciousness, Discover, June 1994. pp.89- 98.
7. Tanaka, Toyoichi. Gels, Scientific American, 244:1, 1998, pp. 124-138.
8. Heinegard, D. and M. Paulsson. Structure and Metabolism of Proteoglycans. In: K.A. Piez and A.H. Reddi, eds., Extracellu/ar Matrix Biochemistry, Elsevier: New York, 1984.
9. Comper, Wayne D. and T.C. Laurent. Physiological Function of Connective Tissue Polysaccharides, Physiological Reviews, 58:1, 1978. pp. 255-307.
10. Miller, Edward J. Chemistry of the Collagens and Their Distribution. In: K.A. Piez and A.H. Reddi, eds., Extracellular Matrix Biochemistry, Elsevier: New York, 1984.
11. Margulis, Lynn and D. Sagan. Mystery Dance: on the Evolution of Human Sexuality, Summit Books: New York, 1991.
12. Garrone, Robert. The Evolution of Connective Tissue, Phylogenetic Distribution and Modifications During Development, In: Z. Deyl and M. Adam, eds., Connective Tissue Research, Alan R. Liss, Inc.: New York, 1980. pp. 141- 147.How Rolfing Produces Change