The Fascial (Connective) Tissue System

Fascial tissue research in sports medicine: from molecules to tissue adaptation, injury and diagnostics: consensus statement – free full-text /PMC6241620/ – Dec 2018

The fascial system builds a three-dimensional continuum of soft, collagen-containing, loose and dense fibrous connective tissue that permeates the body and enables all body systems to operate in an integrated manner.

Injuries to the fascial system cause a significant loss of performance in recreational exercise as well as high-performance sports, and could have a potential role in the development and perpetuation of musculoskeletal disorders, including lower back pain.  

This consensus statement reflects the state of knowledge regarding the role of fascial tissues in the discipline of sports medicine. It aims to

(1) provide an overview of the contemporary state of knowledge regarding the fascial system from the microlevel (molecular and cellular responses) to the macrolevel (mechanical properties),

(2) summarise the responses of the fascial system to altered loading (physical exercise), to injury and other physiological challenges including ageing,

(3) outline the methods available to study the fascial system, and

(4) highlight the contemporary view of interventions that target fascial tissue in sport and exercise medicine.

Terminology and definitions

The term fascia was originally used to describe a sheet or band of soft connective tissue that attaches, surrounds and separates internal organs and skeletal muscles.

Advancing research on the physiological and pathophysiological behaviours of a range of connective tissues has revealed that this definition is too restrictive.

Understanding of mechanical aspects of connective tissue function depends on consideration of a host of interconnected and interwoven connective tissues beyond these sheets or bands, and there is enormous potential gain from understanding the convergence of biology underpinning adaptation, function and pathology.

The fascial system includes

  • adipose tissue,
  • adventitia,
  • neurovascular sheaths,
  • aponeuroses, deep and superficial fasciae,
  • dermis, epineurium, joint capsules,
  • ligaments,
  • membranes,
  • meninges,
  • myofascial expansions,
  • periostea,
  • retinacula,
  • septa,
  • tendons (including endotendon/peritendon/epitendon/paratendon),
  • visceral fasciae, and
  • all the intramuscular and intermuscular connective tissues, including endomysium/perimysium/epimysium

Most people only think about the loose joints and slack ligaments of EDS, but this list shows that literally every system in the body is structured by our defective collagen.

With its diverse components, the fascial system builds a three-dimensional continuum of soft, collagen-containing, loose and dense fibrous connective tissue that permeates the body and enables all body systems to operate in an integrated manner (figure 1).

In contrast, the morphological/histological definition describes fasciaas ‘a sheet, or any other dissectible aggregations of connective tissue that forms beneath the skin to attach, enclose, and separate muscles and other internal organs’.

The proposed terminology distinguishing the terms ‘fascia’ and ‘fascial system’ allows for the precise identification of individual structures as well as grouping them for functional purposes.

Figure 1 Components of the fascial system.

The fascial system includes large aponeuroses like the first layer of the thoracolumbar fascia (A), but also a myriad of enveloping containers around and within skeletal muscles (B) and most other organs of the body. The internal structure of fascial tissues is dominated by collagen fibres which are embedded in a semiliquid ground substance (C). 

Consensus meeting

This document was developed for scientists and clinicians to highlight common traps and truths of fascial tissue screening and imaging techniques and intervention methods, and to present a multidisciplinary perspective of future research in the field.

Molecular adaptation of fascial tissues: effects of physical exercise, ageing, sex hormones and inflammation

Molecular crosstalk between extracellular matrix (ECM) molecules and cellular components is an important determinant of fascial tissue physiology and pathophysiology.

fascial tissue homeostasis is the result of a complex interplay and dynamic crosstalk between cellular components and the ECM.

Especially under dynamic conditions such as growth and regeneration, strong alterations of the local ECM microenvironments are necessary to allow cellular adaptation and rebuilding of fascial tissues. All factors influencing cell or ECM behaviour can result in changes in the structure and homeostasis of tissues and organs.

The ECM also works as a molecular store, catching and releasing biologically active molecules to regulate tissue and organ function, growth and regeneration

In fascial tissues such as tendons, acute and chronic loading stimulates collagen remodelling.

As the exercise-induced increase in collagen synthesis is lower in women than in men, and as injury frequency and the expression of oestrogen receptors in human fascial tissue are sex-dependent, oestrogens may play an important regulatory role in ECM remodelling.

The effects of oestrogens on collagen synthesis appear to differ between rest and response to exercise. While oestrogen replacement in elderly, postmenopausal women impairs collagen synthesis in response to exercise, oestrogen has a stimulating effect on collagen synthesis at rest. Oral contraceptives, on the other hand, have an overall depressing effect on collagen synthesis.

Physiological ageing is a highly individual process characterised by a progressive degeneration of tissues and organ systems.

Age-related alterations in fascial tissues include densification (alterations of loose connective tissue) and fibrosis (alterations of collagen fibrous bundles).

Functionally, these pathological changes can modify the mechanical properties of fascial tissues and skeletal muscle, thereby contributing to pain-related and age-related reductions in muscle force or range of motion, which cannot be solely explained by the loss of muscle mass.

Interestingly, ageing is characterised by chronic, low-grade inflammation—the so-called inflammaging.

In addition, ECM plays an important role as a barrier to transmigration of immune cells in and out of the tissue. Although early inflammation after tissue damage due to physical exercise or injury is crucial for tissue remodelling and adaptation, stem cell activity and collagen synthesis may be inhibited by the chronic intake of non-steroidal anti-inflammatory drugs prior to exercise.

However, limiting the magnitude of inflammation might be beneficial for tissue regeneration and gains in muscle mass and strength, depending on the nature of the injury, and in elderly people.

Myofascial force transmission

Conventionally, skeletal muscles have been considered as primarily transmitting force to their osseous insertions through the myotendinous junction.

However, in situ experiments in animals and imaging studies in humans have shown that intermuscular and extramuscular fascial tissues also provide a pathway for force transmission.

Figure 3
Factors influencing the mechanical stiffness of fascial tissues and their hypothesised impact.

Up arrows symbolise a positive effect (eg, increased cellular contractility increases stiffness), down arrows symbolise a negative effect (eg, increased use of corticosteroids decreases stiffness) and double arrows symbolise an ambiguous association (eg, hyaluronan decreases stiffness if mobilised by mechanical stimuli, but leads to increased stiffness if no stimuli are applied). ECM, extracellular matrix

Although scarce, initial in vivo evidence points towards a significant role of myofascial force transmission for the locomotor system.

Injury of fascial tissues: cellular and mechanical responses to damage

Excessive or prolonged loading or direct trauma to fascial tissues initiates micro and macro changes necessary for tissue repair.

These effects may also contribute to pathological changes that modify tissue function and mechanics, leading to compromised function of the healthy tissue. Effects may become systemic, and thus not limited to the injured/loaded tissues.

Regardless of the underlying mechanism, fibrotic changes in the muscle have a substantial potential impact on tissue dynamics and force generation capacity.

Figure 4Proposed timeline and mechanisms for fascial, adipose and muscle changes in the multifidus muscle after intervertebral disc lesion. Three phases, acute (top), subacute-early chronic (middle) and chronic (bottom), are characterised by different structural and inflammatory changes. IL-1β, interleukin-1β; TNF, tumour necrosis factor.

Exercise, physical modalities and pharmacological interventions have all been shown to reduce the inflammatory processes associated with fascial tissue injury and fibrosis. For example, early treatment with anti-inflammatory drugs can prevent/reverse pain behaviours induced by TNF signalling and reduce downstream collagen production in animal models

Imaging and non-imaging tools for diagnosis and assessment

Pathological changes in the mechanical properties of fascial tissues have been hypothesised to play an essential role in musculoskeletal disorders such as chronic pain conditions and overuse injuries.

Mechanobiology of fascial tissues: effects of exercise and disuse

findings convincingly show that human tendons respond to the application of

  • chronic overloading by increasing their stiffness and to
  • chronic unloading by decreasing their stiffness

One common finding among studies is that tendon adaptations occur quickly, within weeks of mechanical loading/unloading application. Importantly, however, some studies report adaptations in tendon size but not tendon material, and others in tendon material but not size, while some report adaptations in both tendon size and material

In combination, these findings indicate that stiffening of the tendon through alteration of its material requires ‘supra-physiological’ loading features (eg, in terms of loading magnitude, frequency and/or duration). Once this rapid adaptation occurs and the exercise becomes a habitual daily activity, alterations in tendon size might mediate any further changes in tendon stiffness.

Interventions for fascial tissue pathologies in sports medicine

Fascial tissue dysfunction in the field of sports medicine is rarely treated surgically. Anti-inflammatory drugs are used for sports-related overuse pathologies; however, they may impair regeneration and diminish tissue adaptation.

foam rolling (tool-assisted massage of myofascial tissues) seems to improve short-term flexibility and recovery from muscle soreness and decrease latent trigger point sensitivity.

Nevertheless, the physiological mechanisms of these reported effects remain unclear, although initial evidence suggests increases in arterial perfusion, enhanced fascial layer sliding and modified corticospinal excitability following treatment.

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