Fascia Is Able to Actively Contract and May Thereby Influence Musculoskeletal Dynamics: A Histochemical and Mechanographic Investigation.

Fascial tissues form a ubiquitous network throughout the whole body, which is usually regarded as a passive contributor to biomechanical behavior. We aimed to answer the question, whether fascia may possess the capacity for cellular contraction which, in turn, could play an active role in musculoskeletal mechanics. Human and rat fascial specimens from different body sites were investigated for the presence of myofibroblasts using immunohistochemical staining for α-smooth muscle actin (n = 31 donors, n = 20 animals). In addition, mechanographic force registrations were performed on isolated rat fascial tissues (n = 8 to n = 18), which had been exposed to pharmacological stimulants. The density of myofibroblasts was increased in the human lumbar fascia in comparison to fasciae from the two other regions examined in this study: fascia lata and plantar fascia [H(2) = 14.0, p < 0.01]. Mechanographic force measurements revealed contractions in response to stimulation by fetal bovine serum, the thromboxane A2 analog U46619, TGF-ß1, and mepyramine, while challenge by botulinum toxin type C3-used as a Rho kinase inhibitor- provoked relaxation (p < 0.05). In contrast, fascial tissues were insensitive to angiotensin II and caffeine (p < 0.05). A positive correlation between myofibroblast density and contractile response was found (r s = 0.83, p < 0.001). The hypothetical application of the registered forces to human lumbar tissues predicts a potential impact below the threshold for mechanical spinal stability but strong enough to possibly alter motoneuronal coordination in the lumbar region. It is concluded that tension of myofascial tissue is actively regulated by myofibroblasts with the potential to impact active musculoskeletal dynamics.

Strain hardening of fascia: static stretching of dense fibrous connective tissues can induce a temporary stiffness increase accompanied by enhanced matrix hydration.

This study examined a potential cellular basis for strain hardening of fascial tissues: an increase in stiffness induced by stretch and subsequent rest. Mice lumbodorsal fascia were isometrically stretched for 15 min followed by 30 min rest (n=16). An increase in stiffness was observed in the majority of samples, including the nonviable control samples. Investigations with porcine lumbar fascia explored hydration changes as an explanation (n=24). Subject to similar loading procedures, tissues showed decreases in fluid content immediately post-stretch and increases during rest phases. When allowed sufficient resting time, a super-compensation phenomenon was observed, characterised by matrix hydration higher than initial levels and increases in tissue stiffness. Therefore, fascial strain hardening does not seem to rely on cellular contraction, but rather on this super-compensation. Given a comparable occurrence of this behaviour in vivo, clinical application of routines for injury prevention merit exploration.

Passive muscle stiffness may be influenced by active contractility of intramuscular connective tissue.

The article introduces the hypothesis that intramuscular connective tissue, in particular the fascial layer known as the perimysium, may be capable of active contraction and consequently influence passive muscle stiffness, especially in tonic muscles. Passive muscle stiffness is also referred to as passive elasticity, passive muscular compliance, passive extensibility, resting tension, or passive muscle tone. Evidence for the hypothesis is based on five indications: (1) tonic muscles contain more perimysium and are therefore stiffer than phasic muscles; (2) the specific collagen arrangement of the perimysium is designed to fit a load-bearing function; (3) morphological considerations as well as histological observations in our laboratory suggest that the perimysium is characterized by a high density of myofibroblasts, a class of fibroblasts with smooth muscle-like contractile kinetics; (4) in vitro contraction tests with fascia have demonstrated that fascia, due to the presence of myofibroblasts, is able to actively contract, and that the resulting contraction forces may be strong enough to influence musculoskeletal dynamics; (5) the pronounced increase of the perimysium in muscle immobilization and in the surgical treatment of distraction osteogenesis indicates that perimysial stiffness adapts to mechanical stimulation and hence influences passive muscle stiffness. In conclusion, the perimysium seems capable of response to mechanostimulation with a myofibroblast facilitated active tissue contraction, thereby adapting passive muscle stiffness to increased tensional demands, especially in tonic musculature. If verified, this new concept may lead to novel pharmaceutical or mechanical approaches to complement existing treatments of pathologies which are accompanied by an increase or decrease of passive muscle stiffness (e.g., muscle fibroses such as torticollis, peri-partum pelvic pain due to pelvic instability, and many others). Methods for testing this new concept are suggested, including histological examinations and specific in vitro contraction tests.