Our small research group at Ulm University recently attracted some interest and attention from media and clinicians, as well as from scientific colleagues worldwide. While we are busy with our ongoing laboratory research, it has become increasingly impossible to attend to all incoming inquiries. This section aims at answering some of the questions - and also some of the frequent misconceptions - that we are often approached with.
- Is it true that you discovered that fascia is highly innervated by sensory mechanoreceptors?
- Can fascia contract on its own, independently from adjacent skeletal muscle fibers?
- Why haven't you published your findings on active contractile properties in a peer reviewed journal yet?
- Does fascia contract in response to emotional stress?
- Do you propose that the 'tissue release' which is often experienced by practitioners (in response to their myofascial release treatment techniques, such as in osteopathy or in Rolfing Structural integration) is due to a decrease of active fascial contraction?
- Does an acidic pH level of the ground substance increase fascial contractility
- Does the lumbar fascia play an important function in the biomechanics of human walking?
- Are you claiming that most cases of low back pain originate from micro injuries in the lumbar fascia?
- Can you support /fund our own research (e.g. on the effects of new and promising treatment modalities)?
Last update of this list: January 10th, 2018, by Robert Schleip
Is it true that you discovered that fascia is highly innervated by sensory mechanoreceptors?
No. We never performed any actual laboratory research related to fascial innervation. Several years ago we conducted a literature research related to the sensory innervation of fascia. This suggested that both myelinated nerve endings as well as unmyelinated ones (free nerve endings) can be found in most fascial tissues. For a review see http://fasciaresearch.com/index.php/literatures/sensory-innvervation. While several of those studies suggest a proprioceptive, ergoceptive and/or nociceptive function of some of those nerve endings, further research is needed to clarify their in vivo function in normal as well as pathological conditions. This is a promising area of research, in which we follow with interest and appreciation the spearheading research of Langevin, Mense, Stecco and others.
An interesting sub-aspect is the question whether the sensory innervation of fascial tissues can be modified, e.g. via skillful mechanostimulation over a period of several months/years. We are not aware of any studies in that respect and suggest to refrain from any claims in support (as well as against) that possibility.
Can fascia contract on its own, independently from adjacent skeletal muscle fibers?
If one includes long term tissue contractures (like Morbus Dupuytren, Palmar Fibromatosis, etc.) within the realm of that question, then the answer is a clear yes. The work of Tomasek et al. strongly suggests that incremental summation of active cellular contractions plays a substantial role in such tissue contractures. The suspected contractile cells are fibroblasts or myofibroblasts.
In our own research, we performed an immunohistochemical examination for the presence of myofibroblasts in lumbar fascia, plantar fascia and Fascia lata from human donors. (For this we used the presence of alpha-smooth muscle actin containing stress fiber bundles as a marker for myofibroblasts, after subtracting those bundles which are associated with vascular vessels). We found such cells in all examined fascial tissues. We also observed a large inter-individual as well as intra-individual variance regarding the density of those fiber bundles, as well as indications for an increased density in perimysial tissues.
In addition we conducted mechanographic examinations of rat lumbar fascia in an organ bath environment for a potential contractile reaction in response to stimulation with different pharmacological agents. We were able to induce a clear contractile response in a significant number of fascia specimens in response to either the thromboxane analogue U46619, fetal calf serum (FCS) or high dosages of mepyramine. While not all samples responded to such stimulation, retrospective tissue analysis revealed a higher density of alpha smooth muscle actin containing stress fiber bundles in responder tissues compared with the non responding ones. Samples pretreated with the cell disrupting substance cytochalasin-D showed insignificant responses only. Neither caffeine nor angioetensin II triggered any contractile responses. Subsequently we examined samples pretreated with a specific thromboxane receptor antagonist for their response to U46619, and also samples pretreated with a Rho-kinase inhibitor substance for their responses to U46619, FCS and mepyramine. Here we found either no or very reduced contracile responses.
Based on these findings, we are currently convinced that - at least in some samples of rat lumbar fascia, and within the in vitro conditions used in our examinations - fascia can actively contract within a time frame of minutes and that the presence of intrafascial myofibroblasts seems to be responsible for that capacity. We also performed a hypothetical calculation of the potential contractile force (applied to the paraspinal fasciae of the human lumbar area, based on the histological density values of our human fasciae examinations or alternatively on the measured contractile forces in our in vitro examinations with rat fascia). The resulting force values (of approx. 1N for the whole lumbar are) were strong enough to predict a potential impact on normal musculoskeletal behavior, such as in gamma motor regulation. Yet they are far below the force quantities of skeletal musculature (and are not sufficient to e.g. move a limb in space in a matter of several seconds).
Why haven't you published your findings on active contractile properties in a peer reviewed journal yet?
We will! Since we believe that our findings could be of substantial interest to a larger field within musculoskeletal medicine, we decided to add several additional control investigations in order to further substantiate our suggested conclusions (e.g. by using the Rho-kinase inhibitor mentioned above). While w have just completed these additional examinations, are currently in the process of submiting our findings to a respectable peer reviewed medical journal. Our related publications in the past consisted of two peer reviewed articles in Medical Hypotheses (which did not yet contain our own data collection), as well as in several short abstracts presented at international congresses. In addition, we reported about a portion of our contractility investigations (with the substance mepyramine) in these two publications: https://www.ncbi.nlm.nih.gov/pubmed/24909539 and https://www.ncbi.nlm.nih.gov/pubmed/29314236 . We highly believe in the value of peer review process related to original scientific research. Based on this, we suppose that the extra time taken by us for the further substantiation of our reports will contribute to making these findings more acceptable to the wider scientific community.
Does fascia contract in response to emotional stress?
That was the original hypothesis put forward by Staubesand in 1996, which stimulated our research project to a large degree. While we were quite 'convinced' of that assumption during the first two years of our research, our organ bath experiments failed to support them ... no matter how much we tried. Neither adrenaline (epinephrine) nor acetylcholine addition showed any significant effects in our experiments.
Today we tend to believe, that given the migratory character of myofibroblasts (related to their tissue repair function) it seems unlikely that these cells are directly stimulated via synaptic transmission. It is nevertheless possible, that a sympathetic stimulation or other stress related arousal may indirectly lead to expression of stimulatory cytokines (e.g. from mast cells) which may influence myofibroblast behavior. Given the presence of sympathetic nerves in fascia (indicated by Staubesand and very recently also by Tesarz) there could be some support for that possibility. It could be of interest that a link between sympathetic activation and expression of TGF-beta1 has been reported (Bhowmick et al. 2009, J Leucot Biol 86: 197-207). Similarly, for skin fibroblasts a modulation of TGF-beta1 expression by alpha-1 adrenergic receptors - which belong to the sympathetic nervous system and the endocrine system - has been indicated (Liao et al. 2014, Cell Tissue Res 357: 681-93). In a series of organ bath experiments we found that the addition of TGF-beta1 resulted in a clear increase of tissue stiffness over a time frame of 3 hrs publication in submission as of 10.01.2018). Further research is necessary to clarify whether a sympathetically induced change in TGF-beta1 expression may be able to influence fascial stiffness in living people.
Do you propose that a typical 'tissue release' (which is often experienced by practitioners in response to their myofascial release treatment techniques, such as in osteopathy or in Rolfing Structural integration) is due to a decrease of active fascial contraction?
Since we haven't been able to observe any tissue contracton or relaxation changes happening within seconds in our own in vitro contraction experiments, we tend to doubt such an explanatory model. While the potential forces of active fascial contractitlity could be strong enough - based on our measurements and related hypothetical calculations - to result in palpable tissue changes, it seems like the common duration of individual treatment techniques of below 2 minutes would be too short for such a tissue response. Yet we cannot rule out the opposite, as our organ bath experiments may not be reflecting the complete spectrum of fascial contractility in vitro.
Several other body processes appear as more appealing explanations to us:
- Changes in matrix hydration, induced by the technique
- Possibly changes in resting tone (Gamma tone?) of skeletal muscle fibers which are capable of transmitting their tension force to the respective fascial tissue
- Ideomotor dynamics (Carpenter effect): Associated with an unconsconscious expentency bias in the practitioner, the palpating hand/body of the practitoner may change their resting tone in an involuntary and subtle manner, thereby creating a palpatory illusion.
Does an acidic pH level of the ground substance increase fascial contractility?
That is possible, yet not yet clear. Since a change in pH occurs in the early stages of wound healing, it has been suggested that the development of myofibroblasts and their contractile activity could be influenced by the pH of their enviroment. Pipelzadeh & Naylor 1998 showed that a low pH level (i.e. an acidic environment) tends to increase the contractile force of rat lumbar fascia in response to pharmacological stimulation in an organ bath environment. Similarly, Kottmann et al. 2012 showed that an acidic pH level increases myofibroblast differentiation in lung fibrosis. In case these findings can be generalized towards non-pathological human fasciae in vivo, it could have interesting implications regarding the potential effects of nutrition, of the presence of chronic silent inflammation, or of chronic breathing pattern disorders on fascial tonicity. However, both studies examined very different conditions and the applicability of their findings to healthy fascia in living human bodies is less than certain. We therefore suggest to wait for further clarifications before making any definite 'claims' regarding the complex physiological dynamics of this field.
Does the lumbar fascia play an important function in the biomechanics of human walking?
Yes, based on our current data analysis we suggest that the spring-like elastic property of the human lumbar fascia could play a more substantial role than is commonly assumed in the field of human gait biomechanics. Our kinematic measurements indicate that there are probably large differences between people as to the usage of those properties during everyday walking. We are currently completing our mathematical modeling project, to estimate the particular contribution of the lumbar fascia to various gait dimensions. For a brief overview, click here.
Are you claiming that most cases of low back pain originate from micro injuries in the lumbar fascia?
We are not the only ones to question the common tendency, to attribute most cases of acute low back pain to spinal disc damage. MRI imaging data indicate that disc bulging and disc protrusions are not significantly more present in back pain patients than in their healthy peers of the same age group. Furthermore it has been shown that MRI imaging data of spinal discs are not predictive of the development or duration of low-back pain. Panjabi in a Eur Spine paper in 2006 suggested an alternate model, in which subfailure injuries in spinal ligamentous tissues can lead to chronic low back via related muscle control dysfunction and resulting tissue changes including subsequent neural inflammation. Based on the positioning of the lumbar fascia and several other indicators we subsequently published a response in the same journal, in which we suggested that micro injuries in the posterior layer of the human lumbar fascia should be included in that model as a potential back pain generator. Since then several other authors have published similar suggestions, such as the very comprehensive paper by Langevin, or the new findings about nociceptive properties of the lumbar fascia in rats by Tesarz et al.
In our own histological analysis of the posterior layer of the lumbar fascia from human donors, we found areas with an exceptional high density of myofibroblasts in some people, comparable to that found in healing wounds. While it is too early to claim a clear causal relationship between such tissue changes and low back pain, we suggest that these indications - together with the exciting reports by Fox, Tesarz, Taguchi, and others - support the notion that micro injuries and related downstream effects could play a significant role in many cases of low back pain. Yet it is far too early to estimate, whether this may apply to the majority of low back pain cases or only to a minor and specific fraction of those cases
Can you support /fund our own research (e.g. on the effects of new and promising treatment modalities)?
Most likely not. While we have fairly good connections with other researchers in the field of fascia research, we are quite busy to perform our own investigations and to look for potential funding for that. With the exception of the limited funds of the Ida P. Rolf Research Foundation we are not aware of any funding institution that is willing to place a high priority on fascia research. However, if you are able to connect us with such funding possibilities, please let us know.