Originally published in Yearbook 2006 of
the International Association for Structural Integrators (www.theiasi.org
)
The European Fascia Research Project
Robert Schleip MA,
Adjo Zorn PhD, Mattheus Juan Els,
Werner Klingler MD
Introduction
A.T.Still, founder
of osteopathy, as well as I.P.Rolf, founder of Structural Integration,
suggested that skilled practitioners can feel a fascial release in response to
their manual touch. Standard biomechanical teaching however assumes that fascia
serves a passive mechanical role only, transmitting tension which is generated
by muscle activity or external forces. Recently, several indications have been
published which suggest that fascia may be able to actively contract in a
smooth muscle-like manner and consequently influence musculoskeletal dynamics.
If verified, the existence of such a smooth muscle-like fascial contractility
would have important implications for the understanding and further development
of fascial manipulation. Our basic research project specifically examines this
exiting possibility. While preliminary results of our project have already been presented
elsewhere[i][ii],
the following report includes some of our more recent findings.
Background
In what appears to be the most thorough
examination of the viscoleastic behavior of a normal (non pathological) fascial
sheet so far, Yahia et al. 1993[iii]
reported an unexpected discovery of
fascial behavior, which they termed ‘ligament contraction’. In
this in vitro study, pieces of human lumbar fascia were isometrically stretched
for 15 minutes, then allowed to rest for 30 or 60 minutes, and then stretched
again. Contrary to the authors’ expectation, the resistance force of the
tissues proved to be stronger at the repeated stretch compared with the
previous time, i.e. they had become stiffer. After carefully ruling out other
possible explanations for this response, the authors discussed the congruence
of this behavior with similar in vitro stretch responses of visceral
musculature, and they concluded that the most likely explanation would be the
presence of smooth-muscle like cells in this fascia. They therefore suggested a histological
study for these cells.
Three years later the German anatomist
Staubesand reported his
discovery of smooth muscle-like cells in the fascia of the lower leg. He documented this with electron microscopy[iv].
It was suggested by Staubesand[v] and others[vi] that these intrafascial cells might enable
the fascia to contract and relax via the control of the autonomic nervous
system independent of the muscular tonus. While this explanation opens some
exciting perspectives for myofascial bodyworkers, it has never been proven, and
reasonable questions have been raised as to whether the number of such
contractile cells in fascia is sufficient to have any significant effect[vii].
These two studies
motivated our group to start a special research project, to examine whether the
lumbar fascia can actively contract. We followed three major approaches: First - a literature review on what
is already known in this field. Secondly - a histological search for
contractile cells in human lumbar fascia. And finally, in vitro contraction
tests with fascia.
Fascial contractures
In the literature
review we found many examples of tissue contractions caused by connective
tissue cells called myofibroblasts. This happens naturally in wound healing,
but also in several chronic fascial contractures. In the hand, it presents as
palmar fibromatosis, a.k.a. Dupuytren disease, or as a pad like thickening of
the knuckles. In the foot the same process as Dupuytren disease is called
plantar fibromatosis. And in club foot, the myofibroblasts contraction is
focused on the medial side. In frozen shoulder, the contraction happens in the
shoulder capsule. Interestingly, the capsular contractures in frozen shoulder
often heal spontaneously, without any therapeutic intervention; whereas this is
almost never the case with the palmar fascia in Dupuytren contracture. Considering the wide spread existence of pathological fascial
contractures, it seems likely to us that there may be lesser degrees of fascial
contractions in normal people which may influence biomechanical behavior.
Fig. 1: Contracture of palmar fascia in Dupuytren disease.
The increased activity of a special contractile type of fibroblast causes a
permanent thickening and shortening of the palmar fascia, which then prevents
full extension of the hand and often includes visible nodules around flexor
tendons. Similar fascial contractures, which are due to the same cellular
activity, are reported to occur on other frequently loaded tissues, e.g. at the
foot or shoulder joint.
Contractile cells in
fascia
In our second approach, the histological
studies, we collected pieces of the deep fascia from human cadavers and treated
them with an antibody for smooth muscle actin stress fibers. Cells containing
these fibers are assumed to be either smooth muscle cells or contractile
myofibroblasts. Using monoclonal antibodies, more than 100 immunohistochemical
analyses of fascia have been carried out so far. While most of these were done
with tissue sections from human lumbar
fascia, we also included dozens of samples from plantar fascia and the Fascia
lata. Additionally we included lumbar fascia samples from quadruped mammals
(pigs, rats and mice). We found these
contractile cells in all our samples. But there was a significantly higher
density in the younger human age group than in the two older groups (Fig.2).
Fig. 2 . Comparison of density of intrafascial
contractile cells and amount of collagen crimp between 3 age groups. The youngest age group had a significantly higher
density of contractile cells than the two other age groups; and the density
generally correlated positively with the amplitude of collagen crimp
We also discovered
that there is a positive correlation between the density of contractile cells
and the amount of crimp formation (waves) in collagen fibers. I.e. in areas
with a more straight fiber arrangement, hardly any contractile cells are found;
whereas their density is much higher in areas with more wave-like collagen
fibers (Fig. 3). At this stage we do not know the causal relationship behind
this correlation. It could be that the cellular contraction creates the waves
(which is what some authors suggest for the contractile fibroblast in tendons[viii]); and it could be also that a fibroblast
suspension between waves increases tensional input to the fibroblasts in
everyday usage, so that these cells are stimulated to become more contractile. Another
interesting observation is that density of contractile cells tends to be higher
areas around blood vessels and/or fat cells.
Fig. 3: Left side: Typical tissue section of
lumbar fascia from a 19 year old man
with dense population of cells staining positively for alpha smooth
muscle actin (here in black) and a
high degree of collagen crimp. Contrasting that on the right side is a
section from a 76 year old man with hardly any collagen crimping and no
positively stained cells in this area. (F
The surprising matrix
In our in vitro
tests, we take pieces of porcine or rat lumbar fascia, and suspend thin strips
in an organ bath. This allows us to add specific drugs to the bath and measure
the tensional response with a force transducer (Fig. 4). Recently we were also
able to repeat these test with fresh human fascia from surgeries. Based on
Staubesand’s suggestion, that the contractile cells in fascia might behave
similar to smooth muscle cells, we started with adrenaline and acetylcholine, at
different dosages. There was no response. Then we used the vasodilator
substance nifedipine, again without any clear response. That was when we began
to question whether there may be other factors aside from cellular contraction,
which may explain the reported tissue hardening in repeated stretches.
Fig.4 : A portion of
our Fascia Research Lab at the University of Ulm, Germany. The test vessel
with the organ bath is hooked up to the computerized force displacement
transducer which records any changes in tissue resistance force. Solutions can
be exchanged and titrated in a controlled fashion. Tissues can be stimulated
electrically as well as pharmaceutically while tensional changes are
registered.
Based on the work
of Alfred Pischinger[ix], James
Oschman[x]
and Mae-Wan Ho[xi] we looked
at the water binding qualities of the matrix, specifically the ground
substance. We took strips of porcine lumbar fascia and measured the water
content at various stages. Our results are shown in Fig. 5. Before the stretch,
the average water content was 68%. Immediately after a 15-minute stretch, the
water content was significantly lower. Within approximately 30 minutes, the
water content had returned to the original level. Then we had a real surprise. We discovered that if the strain
was strong enough and the rest period long enough, the water content would
continue to rise to an even higher value than before the stretch.
Fig. 5: Water content (in % of total
tissue weight) of lumbar fascia before and after a 15 minute stretch.
In order to
understand the visoelastic effect of this, we increased the tissue hydration by
putting distilled water into the bath. Here we measured the elastic stiffness
in Mpa (mega-Pascale), compared with the effects of a sucrose solution, which
dehydrates the tissue. The results were quite clear: an increase in water
content increased the elastic stiffness of the tissues (see Fig. 6).
|
|
Water content
|
Stiffness (Mpa)
|
|
Hypotone solution n=6
|
↑
|
+42%
|
|
Hypertone
solution n=6
|
↓
|
-27%
|
Fig. 6: Water content effects stiffness. An
increase in water content, induced by immersion of the fascial tissue in a
hypotone solution, resulted in an increased tensional stiffness. Conversely, a
decrease in water content, induced by a hypertone solution, resulted in a
decreased tensional stiffness
This led us to the
following conclusion. When
the fascia is stretched, there are longitudinal relaxation changes in the
collagen fibers and the water is squeezed out, much like what happens when you
squeeze water out of a sponge. Within a few minutes the collagen fibers recover
their original state. Meanwhile, water continues flooding into the tissue to an
even higher percentage than before, substantially increasing the elastic
stiffness.
One possible and profound conclusions is that:
Fascia seems to adapt with very complex and dynamic water changes to mechanical
stimuli, to the degree that the matrix
reacts in smooth-muscle-like contraction and relaxation responses of the whole
tissue. It seems likely that much of what we do with our hands in Structural
Integration and the tissue response we experience may not be related to
cellular or collagen arrangement changes, but to sponge like squeezing and
refilling effects in the semi-liquid ground substance with its intricate
scrub-like arrangement of water binding glycosaminoglycans and proteoglycans.
Since age related tissue changes are associated with a decreased water content,
this brings up the question: Could slow but strong tissue draining moves that
are a part of our work prove to
increase hydration? Future studies with in-vivo measurements of
the tissue water content taken hours and days after such treatments might offer
interesting ‘anti aging’ perspectives for our field.
Test tube fascial contractions
While this may not
be regarded as an active contraction process, we finally had some success with
our in vitro contraction experiments (Fig.7). When we applied
glyceroltrinitrate – a powerful nitrous oxide donator, which works a little
like viagra - and applied that to the lumbar fascia of mice, we got a clear and
significant relaxation response.
Fig. 7: In vitro contraction test: a piece of fresh
porcine lumbar fascia is vertically suspended inside an organ bath. The tissue
is isometrically stretched for 1 hour; then a pharmaceutical agonist is added
into the bath and any tension changes in the tissue are registered.
Fig. 8: Example of an IVCT
experiment. The addition of a NO-donator
substance at minute 5 and minute 10 is followed each time by a tension
decrease.
We also found, that
Dr. Ian Naylor and his research group at the University of Bradford (U.K.) had
recently reported positive results with a number of additional substances. This group, which we are now collaborating
with, is specialized in research on the pharmaceutical regulation of wound
healing and Dupuytren disease. For this purpose they have also started to
conduct tests with normal uninjured fascia. Using the lumbar fascia from rats,
they reported a clear contraction response with the substance mepyramine which
is generally considered to be the most reliable agonist in myofibroblast
research [xii].
On our invitation Dr. Naylor visited our
lab, and in return, we worked with Dr. Naylor in his laboratory at Bradford
university during two one-week visits so far. We were able to repeat his
positive contraction results with rat lumbar fascia in response to mepyramine.
Additionally with rat testicular capsule (a fascial organ capsule with a high
density of myofibroblasts) we could demonstrate contractile responses to the
smooth muscle agonist adenosine as well as to the hormone oxytocine. Repeating
the in vitro test with mepyramine on fresh human surgical fascia at our own
laboratory at Ulm university, we were also able to confirm the existence of an
active fascial contractility for human fascia.
What does fascia have in common with sea
shells?
Based on a very
early suggestion by Prof. Gabbiani, original co-discoverer of myofibroblast
cells, we recently explored whether the slow and sustained contraction of
fascial myofibroblasts may have some similarity with the catch musculature of
ocean mussles which are known for their ability to sustain contractions for
very long times. When members of our team together with Dr. Naylor applied this
ocean muscle tissue to our in vitro contraction tests with mepyramine, we got
an almost identical response curve as we usually got with our fascia tissues.
This suggests that the contractility of fascial myofibroblasts may not only
include some smooth muscle features, yet it may also include strong
similarities with the kinetics of molluscan catch muscles. This would explain,
how fascial myofibroblasts can hold a particular tension for very long times, while
using only a fraction of the energy for that compared with skeletal or smooth
muscle cells.
Fig. 9: Members of the
European Fascia Research Group working together with Dr. Ian Naylor.
(Left to right: Dr. Ian
Naylor, Birgit Frank, Robert Schleip, Adjo Zorn Ph.D.)
Implications for passive muscle tone
Some of our histological tissue sections
did not only include the proper fascia but also small pieces of related
skeletal muscle tissue. When we started to look at these portions more
carefully, we discovered much to our surprise, that the intramuscular
connective tissue often had a higher relative density of contractile cells than
the proper extramuscular fascia. Quite often the intramuscular fascial layer of
the perimysium, which envelopes bundles of muscle fibers, was particularly
packed with myofibroblasts. We speculate that this may be related to the
spatial proximity of intramuscular blood vessels (and probably also nerves)
which tend to travel along this layer. It is known that tonic muscles such as
the soleus or the upper trapezius generally include a thicker perimysium; which
also makes them the tougher meat nutritionally. Interestingly these are the
same muscles which are more prone for chronic shortening or stiffening as
compared with phasic muscles. E.g. persons with spastic myopathies often show
increased problems in motor performance, particularly in locomotion, due to
chronic shortening of the soleus or other tonic muscles.
Based on these condiderations, we treated
rat soleus muscle tissue in our organ bath with a ‘knock out protocol’ of high
caffeine additions into the bath until it was clear that the myocells in the
tissue were depleted and no more able to contract. At that point we added our
usual myofibrblast contractile agent mepyramine, which triggered nevertheless a
clear and long lasting contractile tissue response. Since the tissue had
previously shown to be unable to contract to electrical stimulation as well as
to additional dosages of caffeine, we tend to assume that this subsequent
response is due to an active intramuscular connective tissue contraction.
Since recent research by a group around
Prof. Huijng’s in Amsterdam[xiii],
[xiv]
indicates that intramuscular connective tissue significantly influences passive
muscle elasticity, we now speculate that an active shortening of the
intramuscular perimysium may contribute to chronic stiffness of tonic muscles
which is so often found in pathological conditions as well as in many of us
‘normal people’[xv].
Potential strength of fascial contractility
To calculate the
potential in vivo contraction force of the lumbar fascia, we chose the data
from the experiments with human lumbar fascia by Yahia et al., reported
earlier. With a tissue strip of 1.5 mm x 1.0 mm x 30 mm the maximal measured force
increase was 4.2 N. If we hypothetically apply the same force ratio to whole
fascial sheets in the human body, it seems clear that such fascial contractions
could have substantial biomechanical influences. As an example, the superficial
lamina of the lumbar fascia, with a reported horizontal cross sectional area of
71 mm x 0.53 mm at the level of the
third lumbar vertebra (plus adjusting for the 45 degrees oblique fiber
angulation in this fascial layer) would have a theoretical contraction force of
51 N (equal to 5.1 kg).
This would put the
force of active fascial contractions within a biomechanically significant
range, at which it could cause a lumbar paraspinal compartment syndrome ([xvi]). It is also in a range where a decreased
fascial tonus can contribute to spinal segmental instability, which is
frequently associated with the onset of low back pain ([xvii],
[xviii]). Similarly a loss of fascial tone could
also be responsible for sacroiliac pain, which is often caused by a lack of
force closure of the sacroiliac joint ([xix]) and resulting hypermobility (an example of this is the high incidence of
pelvic pain during pregnancy due to hormonal changes).
Interim conclusions
To summarize our conclusions to date:
·
Chronic
contractures of frequently loaded tissues are common adaptations, driven by
cellular contraction within fascia.
·
Fascia is capable
of performing smooth muscle-like, slow contractions, through a surprising
regulation of its water content. Since dehydration is an intrinsic aspect of
aging, specific stretching routines or manual therapies may be worthwhile study
projects in anti-aging.
·
Our in vitro
contraction results as well as those of Dr. Naylor give evidence that a short
term fascial contractility, happening over minutes, does exist. This may have important implications for the understanding
of back stability as well as deep tissue therapies such as Structural
Integration.
·
Certainly, fascia proves to be a truly fascinating
tissue, and warrants further investigation
Practical applications
Already at this
point, this research has changed our Rolfing work. Our insights about the scrub-like water binding nature of the
semi-fluid matrix, now bring up images and a more detailed caring for the
sponge-squeezing and refilling effects of our work. It suddenly makes new
sense, why a repeated slow-draining stroke followed by appropriate rest
sometimes makes all the difference. And why such treatment often works wonders
in rejuvenating dried-out tissues. On the other hand, having observed thousands
of spindle shaped cells floating in the collagenous matrix in our microscopes,
our working fingers now frequently feel like they are contacting similar
fish-like creatures under our hands. Future results of this project may help us
to understand more specifically, which of our effects are due to dynamic
changes in the water content, and which may be due to cellular contractile
changes. These insights may also help
us to find out how different durations and amounts of manual pressure may
results in different short tem or long term fascial effects.
Acknowledgment
This research project has been supported by grants
from the Rolf Institute of Structural Integration, the International
Biomechanical Society, and the European Rolfing Association, which is
appreciated very much by the authors. While the majority of expenses are still
supplied by involved European Rolfing Practitioners, additional organizational
backup support continues to come from the European Rolfing Association, the
University of Ulm (Germany), and from the University of Bradford (U.K.). If
you, dear reader, know of any private person or a foundation willing to support
such a unique research project, please do connect them with us[xx]. And
yes, we love to have more people join in our efforts and network with us in
what feels like an important and exciting journey of discovery.