Active fascial contractility: Fascia may be able
to contract in a smooth muscle-like manner
and thereby influence musculoskeletal dynamics
R. Schleip *, W. Klingler, F. Lehmann-Horn, Department of Applied Physiology, Ulm University, Albert-Einstein-Allee 11, 89069 Ulm, Germany, Received 7 March 2005; accepted 9 March 2005. Summary Dense connective tissue sheets, commonly known as fascia, play an important role as force transmitters in human posture and movement regulation. Fascia is usually seen as having a passive role, transmitting mechanical tension which is generated by muscle activity or external forces. However, there is some evidence to suggest that
fascia may be able to actively contract in a smooth muscle-like manner and consequently influence musculoskeletal
dynamics. General support for this hypothesis came with the discovery of contractile cells in fascia, from theoretical
reflections on the biological advantages of such a capacity, and from the existence of pathological fascial contractures.
Further evidence to support this hypothesis is offered by in vitro studies with fascia which have been reported in the
literature: the biomechanical demonstration of an autonomous contraction of the human lumbar fascia, and the
pharmacological induction of temporary contractions in normal fascia from rats. If verified by future research,
the existence of an active fascial contractility could have interesting implications for the understanding of
musculoskeletal pathologies with an increased or decreased myofascial tonus. It may also offer new insights and a
deeper understanding of treatments directed at fascia, such as manual myofascial release therapies or acupuncture.
Further research to test this hypothesis is suggested.
_c 2005 Elsevier Ltd. All rights reserved.
Dense irregular connective tissue sheets in the human
body – such as aponeuroses, joint capsules, or
muscular envelopes like the endo-, peri- and epimysium
– are usually referred to as fascia. Ligaments
and tendons may be regarded anatomically
as local thickenings of fascial sheets, which are
adapting to increased local tension with a denser
and more parallel fiber arrangement. Aside from
ligaments and tendons, several other examples
demonstrate that fascia plays an important role
in musculoskeletal dynamics: stiffness of the plantar
fascia contributes to stability of the foot ;
the lumbar fascia limits spinal mobility ; and
tension transmission across the epimysium contributes
to muscle force [3,4].
0306-9877/$ – see front matter _c 2005 Elsevier Ltd. All rights reserved.
* Corresponding author. Present address: Department of
Applied Physiology, Georgenstrasse 22, 80799 Munich, Germany.
Tel.: +49 89 346016; fax: +49 89 337927.
E-mail address: email@example.com (R. Schleip).
Medical Hypotheses (2005) 65, 273–277
While this is currently accepted medical knowledge,
it is also assumed that fascia is solely a passive
contributor to biomechanical behavior.
Contrary to this common conception, the authors
propose the hypothesis, that human fascia may
be able to spontaneously adjust its stiffness in a
time period ranging from minutes to hours and
thereby contribute more actively to musculoskeletal
dynamics. If verified by future research, the
existence of active fascial contractility could have
implications for the understanding and treatment
of musculoskeletal disorders which are associated
with increased or decreased myofascial tension or
with diminished neuromuscular coordination. The
authors will review here four general indications
as well as two experimental in vitro reports as evidence
for the hypothesis. Finally, the implications
of this new perspective will be discussed and suggestions
will be offered for testing the hypothesis.
The presence of contractile cells in fascia
Recent findings by Spector and others have shown
that fibroblasts, as well as chondro- and osteoblasts,
are ”connective tissue cells with muscle”,
i.e., that they have an innate capacity to express
the gene for a-smooth muscle actin (ASMA) and to
display contractile behavior . Expression can
be triggered by environmental factors, such as increased
mechanical stimulation as well as specific
cytokines. With fascia this expression happens naturally
in wound healing and in several pathological
situations. Additionally, fibroblasts which contain
ASMA stress fibers have been found in normal tendons
 and ligaments [7,8]. Cells containing ASMA
stress fibers are known to be either contractile
smooth muscle cells or to be a contractile phenotype
of fibroblasts with smooth muscle-like features,
now known as myofibroblasts .
Furthermore, the potential contraction force of
myofibroblasts has been shown to be correlated
to the degree of ASMA expression .
While no quantitative immunohistochemical
examination has yet been published for cells containing
ASMA in normal fascial sheets, the existence
of cells resembling smooth muscle cells was
accidentally discovered by Staubesand in normal
crural fascia and has been documented with electron
microscopy [11,12]. Since the crural fascia
has a similar morphology to the lumbar fascia or
to the muscular epimysial envelopes, it seems reasonable
to extrapolate that the crural fascia is not
the only fascial sheet with this property. It therefore
can be cautiously assumed, that contractile
cells are probably also present in other dense human
fascial sheets, as have already been found in
tendons, ligaments and in the crural fascia. Given
the presence of contractile fibroblasts in normal
fascia, it is postulated that the regular expression
of this cellular phenotype would most likely serve
a functional purpose; i.e., that these cells are at
times used for smooth muscle like contractions.
Improved sturdiness – an evolutionary
Our biological make-up has been shaped through a
Darwinian process of selective survival, including
countless fight and flight reactions. Life-threatening
situations often involve rapid and strenuous
activities. Survival in these situations not only depends
on luck, wit, speed or muscular strength,
but also on the mechanical sturdiness of one’s
limbs; i.e., not breaking a leg or dislocating an ankle
while jumping or running for one’s life can be a
useful advantage. It would make biological sense
that animals equipped with an additional mechanism
to muscular coordination for a temporary increase
in tissue stiffness would have a distinct
When exposed to several hours or even days of
high stress situations, an innate capacity to increase
fascial stiffness may be invaluable. The ability
of fascia to actively contract, mediated by
mechanical strain, plus specific stress related cytokines,
would consequently provide us with a useful
secondary myofascial tonus regulation system. Given
the genetic capacity of fibroblasts to become
contractile, it seems feasible that our bodies now
may contain the ability to activate this advantage
when challenged by periods of high mechanical
and/or emotional stress.
Effect on neuromuscular coordination
In addition to this mechanical advantage, increased
fascial stiffness offers a further benefit.
Ligaments contain mechanoreceptors which provide
sensory feedback for muscular coordination
[13,14]. Without their feedback, motor coordination
is significantly impaired. The same kind of
mechanoreceptors are also found in broad fascial
sheets, and it is assumed that they serve a similar
proprioceptive function [15–17]. This is congruent
with the recent finding, that patients with chronic
low back pain demonstrate fewer mechanoreceptors
in their lumbar fascia as well as impaired
274 Schleip et al.
lumbopelvic proprioception and motor coordination
[18,19]. Interestingly, low threshold mechanoreceptors
apparently influence muscle activity via
the c-muscle spindle system, while high threshold
mechanoreceptors exert effects directly onto the
a-motorneurons . An increased fascial stiffness
would therefore be expected to result in many
muscular responses elicited by fascial mechanoreceptors
in a shift from a low threshold activated
c-system response towards a much quicker highthreshold
activated a-motorneuronal reaction.
A temporary decrease of ligament stiffness in
cats has been shown to result in the stimulation
of fewer ligamentous mechanoreceptors and in decreased
periarticular muscle activation . It
seems likely that this response would be similar
in the fascial tissues found in humans. A temporary
increase in fascial stiffness would consequently improve
fascial proprioception and increase muscular
activation. An animal or person with an enhanced
fascial stiffness would therefore have the advantage
of a generally more precise and more rapid
muscular reflex coordination in response to fascial
proprioception, as well as the increased sturdiness.
While a chronically increased fascial tonus may
over time have metabolic and physiological drawbacks,
the ability to temporarily increase fascial
stiffness may have helped our ancestors to cope
in situations demanding an increased motor
Existence of chronic fascial contractures
The ability of fascia to contract is further demonstrated
by the widespread existence of pathological
fascial contractures. Probably, the most well
known example is Dupuytren disease (palmar fibromatosis),
which is known to be mediated by the
proliferation and contractile activity of myofibroblasts.
Lesser known is the existence of similar contractures
in other fascial tissues which are also
driven by contractile myofibroblasts, e.g., plantar
fibromatosis, Peyronie disease (induratio penis
plastica), club foot, or – much more commonly –
in the frozen shoulder  with its documented
connective tissue contractures . Given the
widespread existence of such strong pathological
chronic contractures, it seems likely that minor degrees
of fascial contractures might exist among
normal, healthy people and have some influence
on biomechanical behavior.
One could argue, that there may be general differences
between long term chronic contractures
and the proposed ability of fascia to temporarily
contract in a smooth muscle like manner. Interestingly,
in the condition ”frozen shoulder” the
fascial contracture sometimes improves spontaneously
within a few days [24,25]. This seems to indicate
a fairly rapid release of cellular contractions,
rather than long term morphological changes in
the collagen architecture. Another supporting
indicator for a similar physiological basis are the
experiments with granulation tissue, in which
myofibroblast driven tissue contractions were significantly
increased by the addition of pharmacological
smooth muscle agonists, with clearly
significant effects during as little as half an hour
While none of these indications are conclusive
on their own, collectively they add considerable
support to the hypothesis, that fascia may be able
to influence biomechanical behavior by an active
temporary contraction of intrafascial myofibroblasts.
As well as these general theoretical indications,
there are two experimental studies, which
offer more concrete evidence for our hypothesis.
Biomechanical in vitro evidence
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. 
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 min, then allowed
to rest for 30 or 60 min, 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
Pharmacological in vitro evidence
The second line of experimental evidence comes
from recent research into the pharmacological
control of wound contraction. In order to understand
more about the contractile behavior of myofibroblasts
in wound healing, several authors
conducted in vitro contraction tests with fascia in
response to pharmacological substances. While
most authors performed their studies with injured
or pathological fascia only, Pipelzadeh and Naylor
Active fascial contractility: Fascia may be able to contract in a smooth muscle-like manner 275
[28–30] included tissue from normal superficial
fascia of rats. Suspending thin strips of this fascia
in a superfusion system, they were able to induce
clear and reversible tissue contractions in response
to mepyramine, calcium chloride, as well as adenosine.
The contractile behavior of this fascia was
found to be similar to that of injured fascia from
rats, which again was fairly congruent with the
contractility of human myofibroblasts reported
elsewhere [31,32]. The rapid onset, the reversibility,
the repeatability and the dose dependency of
the contractile responses in all these tissues suggest
that cellular receptors are responsible for
the observed effects. Given the usual caveats of
extrapolating from in vitro animal data to living humans,
these results appear as congruent with the
hypothesis of a cellular driven active contractility
in normal fascia.
Assuming that human fascia does contract in vivo as
proposed in our hypothesis, how strong would the
resulting force be? For an estimation of this we chose
the data from the in vitro experiments with human
lumbar fascia by Yahia et al., reported earlier. With
a tissue strip of 1.5 mm • 1.0 mm • 30 mm the maximal
measured force increase during an isometric
stretch was 1.5 N. If we hypothetically apply the
sameforce 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 • 0.53 mm at the level of the third
lumbar vertebra (plus adjusting for the 45_ oblique
fiber angulation in this fascial layer) would have a
theoretical bilateral contraction force of 38 N.
This would put the force of active fascial contractions
within a biomechanically significant
range, at which it could cause a lumbar paraspinal
compartment syndrome . 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
[34,35]. 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  and resulting hypermobility (an example
of this is the high incidence of pelvic pain during
pregnancy due to hormonal changes ). Manual
deep tissue therapies, such as Rolfing or myofascial
release, which claim to influence fascial tone ,
may be able to benefit from more specific understanding
(and new questions) from this new perspective.
It is also possible, that acupuncture,
which has been recently shown to be intimately
linked with fascial anatomy [39,40], may be better
understood and its effectiveness improved.
The authors therefore suggest that this hypothesis
be tested with further research. A first step
could be a quantitative immunohistochemical
examination of human fasciae for cells containing
ASMA stress fibers. Additionally a replication of
the pharmacological in vitro contraction experiments
of Pipelzadeh and Naylor could be done with
human surgical fascia. If verified, this might not
only have interesting therapeutic implications,
but the new appreciation of fascia would also pose
new questions: How is fascial contractility related
to microinjuries, to hypoxia, to stress or infection
related cytokines? How does it respond to different
hormonal or pharmacological agents? Why does the
fascial contraction in frozen shoulder often heal
spontaneously, while this is rarely the case with
the palmar fascia in Dupuytren contracture? How
do different types of static and cyclic mechanical
stimulation influence fascial contractility? As
intriguing as these questions may be, before
attempting any clinical research, first an exploration
of the hypothesis through basic research is
The authors acknowledge the support of the International
Society of Biomechanics, the Rolf Institute
for Structural Integration (USA), and the European
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Active fascial contractility: Fascia may be able to contract in a smooth muscle-like manner 277