ABSTRACT There are numerous theories that attempt to explain how Rolfing Structural Integration (SI) works, but little evidence or research backing any of them. In this first of a series of columns reviewing these theories, Eric Jacobson discusses hypothesized mechanisms for Rolfing SI that are biomechanical. A future column will consider other possible mechanisms.

Investigations of the extent to which a particular  therapy  is   effective   against a specific disease or  disability,  known  as ‘clinical studies’, have long been distinguished from mechanistic studies of how those therapies produce their benefits by altering behavior, structure, physiology, biochemistry, and/or psychology. The mechanism of a therapy may be described at different levels, for instance as changes in posture or movement, changes in the function of organs or tissues including nerves, changes in cellular biology,  and/or changes at  the  molecular  level. In  contemporary  biomedical   science the latter is favored as the ultimate mechanistic explanation. In addition, it is possible for a therapy to have its effect through more than one mechanism at  any given level, and those can be active simultaneously or sequentially. A final important  point  is  that  confirmation that a therapy is clinically effective for a condition does not prove any particular theory as to the mechanism through which that benefit is produced. To assume that the first proves the latter is a very common mistake in reasoning. This is the first of a series of columns that will briefly review the most common theories about how Rolfing SI has its therapeutic effects, and what the evidence is, if any, for  them. We restrict our discussion of such evidence to reports published in peer- reviewed scientific journals, which is the prevailing standard. Part 1 summarizes hypothesized mechanisms that are essentially biomechanical at either gross, cellular, or interstitial levels.

Dr. Rolf’s (1977) original claim was that skillful manipulation of the soft tissues and movement education can alter the alignment and motility of the human structure toward specific ideals of whole- body biomechanical functioning,  and  that this confers long-term benefits in energy expenditure, stress, health, and personal psychology. On her account, the improvements in biomechanics were consequences of more local increases in motility and elasticity of the myofascia, which often spread spontaneously to anatomical regions that are broader than that which is directly manipulated. Rolf hypothesized that the greater elasticity that is clinically observed was due to an increase in the ratio of elastin to collagen content in the fibrous component of myofascia (Mithieux and Weiss 2005). However we currently have no evidence as to what  changes,  if  any,  occur  in the biological composition of fascia in response to SI manipulation.

Rolf also claimed that her techniques reduced adhesions between adjacent fascial planes, thus allowing freer gliding of such planes past each other during movement, and consequently of the muscles that they enveloped. In this respect it is noteworthy that a small n=10 pilot study found that a single session of Rolfing SI tended to increase the extent to which the myofascia enveloping the lumbar erector spinae were able to glide relative to the immediately overlaying connective tissue. However, the p value, a measure of the likelihood that an experimentally observed effect is due to random variation rather than to a systematic effect, was insufficient to regard this outcome as evidentiary (p=0.14) (Langevin et al. 2010). Recent work with mice has demonstrated that fascial adhesions  can  be  created  in the  intestines  of  laboratory  mice  and subsequently released by gentle manipulation of their abdomens, but a similar effect has not been investigated for myofascia (Bove et al. 2017). There is no current evidence as to how the changes in the fascial elasticity or motility that are clinically observed to result from Rolfing SI come about.

As a way of accounting for the effects of her manipulation, Rolf very tentatively invoked the ‘thixotropic’ property of the colloidal ground substance  that  makes  up  most  of the mass of fascial tissues. A colloid is   a substance that has properties of both solid and liquid. Common examples are butter and glass, both of which will begin to flow very slowly in response to an input of energy, including mechanical pressure. Rolf was doubtless thoroughly familiar with this phenomenon from her biochemical training. The problem, as Robert Schleip (2003) has pointed out, is that thixotropic flow of a colloid ceases as soon as the input of energy ceases, i.e. it is not a permanent change in the elasticity nor in the extensibility of the colloidal substance, so it cannot account for fascial changes that persist after the manual force is removed. It is entirely possible that thixotopic phenemona that occur during manipulation are part of a larger constellation of biological changes that do result in longer term changes in the properties of fascia, but this would be a different, far more complex hypothesis, and one that has not yet been articulated.

Another mechanisms that was hypothesized by Rolf at the level of local tissue change was an increase in interstitial fluid flow. In this connection she often noted that the majority of all the fluid movement in the body occurs as interstitial flow through soft connective tissues. The opposite sequence of effects is also often invoked by SI practitioners, that the applied pressure renders local regions of fascia more permeable to interstitial fluid, which upon the release of pressure, flows into that region and that thereby increases its elasticity. However, we have no evidence for either of these hypotheses.

Rolf taught practitioners to  approach joint pain and dysfunction by comparing the tone and motility of all the  soft-  tissue structures that  are  called  upon  to lengthen and contract as the joint flexes and extends. Pressure is then  then applied to structures  that  are  visibly less motile than others, resulting  in a subsequent increase in their ability  to flex and extend. Clients often report that an entire area – both the joint and surrounding tissues – subsequently feels less painful,  ‘‘better,’’  and  ‘‘stronger.’’ Rolf regarded this effect as due to a reduction in mechanical strain resulting from improved equality of tone  among the soft-tissue structures that span the joint that allows  mechanical  strain  to  be distributed more equitably among them, rather than the few that are more capable of stretch being  required  to bear excessive strain. However, neither this hypothesis, nor its association with improvements in joint pain and function, has been quantitatively studied.

In a review of clinical records that found significant benefits from SI for a variety of chronic musculoskeletal pain syndromes, Deutsch and associates discussed three ways that it might reduce nociception (pain signaling) from local nerves (Deutsch et al. 2000). They first extend Rolf’s thesis that balancing the pliability of connective tissues around problematic joints can realign force vectors along more physiologic lines by  noting  that  this might also reduce pain producing nerve  irritation  at  the  joint.  Second, that SI is often reported to increase the flexibility of scar tissue, the rigidity of which is theorized to be another source  of nociceptive irritation. Finally, that the increased rate of interstitial fluid  flow  that Rolf believed SI produced might relieve local hypoxia, acidosis, and the accumulation of bradykinins, potassium ions, and prostaglandins, all of  which  are known nociceptive amplifiers  (Shah et al. 2005). However, none of these hypothesized mechanisms have been quantitatively investigated.

Schleip and colleagues (2006, 2019) hypothesized and then demonstrated that fascial stiffness can be altered by increases or decreases in the contractile activation of myofibroblasts to various stimuli including stretching, and that such alterations in stiffness could influence biomechanical performance at least minimally. This finding has also been reported by other research groups, including Langevin’s (2013). Schleip has built on this by  theorizing  that changes in autonomic activation might account for longer term changes in fascial biomechanics. That theory will be discussed in Part 2 of this column.

Whatever the mechanism producing them, the immediate increase in elasticity, motility, and glide that Rolfing practitioner sobserve clinically has been regarded since Rolf as in the service of larger improvements in whole-body biomechanics. As hallmarks of that ideal she emphasized increased vertical alignment of the major body masses, increased bilateral symmetry, and ‘grace’ of movement,  and  taught  her students to strategize their manual interventions toward the achievement of those goals. Given the importance what Rolf and subsequent generations have given to those hallmarks, which most practitioners observe, it is surprising that we have almost no quantitative evidence that they are predictable  consequences of Rolfing SI.

In Part 2 of this column we will review some other hypothesized therapeutic mechanisms that are psychological and neurophysiological in nature, and what, if any, evidence there is in their favor. At this point, however, it is already clear that we have a large number of theories that are plausible in view of what is known about the relevant properties of connective tissues and their components, but very little evidence to confirm any of them. This presents a wealth of  opportunities for fundamental research.

Eric Jacobson, PhD, MPH was trained by Ida Rolf in 1974 and completed advanced Rolfing training with the Rolf Institute® in 2005. He has a private practice of Rolfing Structural Integration in Boston. He also teaches medical anthropology and investigates alternative medicines at Harvard Medical School. In 2009 he completed an NIH-funded, randomized clinical trial of structural integration  for chronic low back pain; the study  is available at https://www.ncbi.nlm. nih.gov/pmc/articles/PMC4405211/ pdf/ECAM2015-813418. Eric can be contacted by email at eric_jacobson@ hms.harvard.edu.

References

Bove G.M., S.L. Chapelle, K.E. Hanlon, M.P. Diamond, and D.J. Mokler 2017. “Attenuation of Postoperative Adhesions Using a Modeled Manual Therapy.” PLOS One June 2, 2017:1–18.

Deutsch, J., L.L. Derr, P. Judd, B. Reuven 2000. “Treatment of Chronic Pain Through the Use of Structural Integration (Rolfing)”. Orthopedic Physical Therapy Clinics of North America 2000(9):411–427.

Langevin, H.M., M. Nedergaard, and A.K. Howe 2013. “Cellular Control of Connective Tissue Matrix Tension.” Journal of Cellular Biochemistry 114(8):1714–1719.

Langevin, H.M., H.R. Fox, E. Jacobson 2010. “Structural Integration (A Manual Therapy) May Increase Myofascial Lateral Shear Strain in Human Chronic Low Back Pain.” 13th World Conference on Pain. Montreal: International Association for the Study of Pain.

Mithieux, S.M. and A.S. Weiss 2005. “Elastin.” Advances in Protein Chemistry 70:437–461.

Rolf, I.P. 1977. Rolfing: The Integration of Human Structures. Santa Monica, California: Dennis Landman Publishers, 1977.

Schleip, R., G. Gabbiani, J. Wilke, I. Naylor, B. Hinz, A. Zorn, H. Jager, R. Breul, S. Schreiner, and W. Klingler 2019. “Fascia Is Able to Actively Contract and May Thereby Influence   Musculoskeletal   Dynamics:  A Histochemical and Mechanographic Investigation.” Frontiers in Physiology 2019; April 2(10):336.

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2006. Zorn, H.J. Wilke, F. Lehmann-Horn, and W. Klingler 2006. “Passive Muscle Stiffness May Be  Influenced  by   Active Contractility of Intramuscular Connective Tissue.” Medical Hypotheses 66(1):66–71.

Schleip, R. 2003. “Fascial Plasticity – A New Neurobiological Explanation:  Part 1”. Journal of Bodywork and Movement Therapies 7(1):11–19.

Shah, J.P.,  T.M. Phillips,  J.V.  Danoff, and L.H. Gerber 2005. “An In Vivo Microanalytical Technique for Measuring the Local Biochemical Milieu of Human Skeletal Muscle.” Journal of Applied Physiology 99(5):1877–1884.