Do the fasciae of the soleus have a role in plantar fasciitis?

Plantar fasciitis is a chronic, self‐limiting, and painful disabling condition affecting the inferomedial aspect of the heel, usually extending toward the metatarsophalangeal joints. There is compelling evidence for a strong correlation between Achilles tendon (AT) loading and plantar aponeurosis (PA) tension. In line with this, tightness of the AT is found in almost 80% of patients affected by plantar fasciitis. A positive correlation has also been reported between gastrocnemius‐soleus tightness and heel pain severity in this condition. Despite its high prevalence, the exact etiology and pathological mechanisms underlying plantar heel pain remain unclear. Therefore, the aim of the present paper is to discuss the anatomical and biomechanical substrates of plantar fasciitis with special emphasis on the emerging, though largely neglected, fascial system. In particular, the relationship between the fascia, triceps surae muscle, AT, and PA will be analyzed. We then proceed to discuss how structural and biomechanical alterations of the muscle‐tendon‐fascia complex due to muscle overuse or injury can create the conditions for the onset of PA pathology. A deeper knowledge of the possible molecular mechanisms underpinning changes in the mechanical properties of the fascial system in response to altered loading and/or muscle contraction could help healthcare professionals and clinicians refine nonoperative treatment strategies and rehabilitation protocols for plantar fasciitis.


| INTRODUCTION
The plantar aponeurosis (PA) is a broad and thick band of connective tissue that arises from the calcaneus and runs longitudinally to attach to the plantar aspect of the forefoot in three distinct sites, thus creating three distinct components (i.e., medial, central, and lateral bands; Stecco, Corradin, et al., 2013;Wearing et al., 2006).The central aponeurotic band is the thickest component.It divides distally into five longitudinal digitations, which insert at the level of each metatarsophalangeal joint capsule (Figure 1).Even from a biomechanical viewpoint, the central band of the PA is often cited as the key supporter of the longitudinal arch of the foot, acting like a windlass and preventing arch flattening (Hicks, 1954).Furthermore, it assists subtalar joint supination during propulsion (Ward et al., 2003).This band of the PA is therefore the one most often involved in the development of plantar fasciitis.
Plantar fasciitis is the most common cause of adult heel pain, accounting for over 1 million physician visits per year in the United States (Riddle & Schappert, 2004).It primarily affects the PA enthesis and leads to a chronic, painful, and self-limiting condition.It is the most prevalent running-related musculoskeletal disorder among athletes (Lopes et al., 2012), but it also affects both physically active and sedentary middle-aged and older adults (Thomas et al., 2019) as well as workers whose activity impacts the foot strongly (Dyck & Boyajian-O'Neill, 2004;Stecco, Corradin, et al., 2013).
Patients usually complain of persistent inferior heel pain (Riddle & Schappert, 2004).The classic clinical presentation is a sharp stabbing heel pain, usually more intense during the first steps following long non-weight bearing periods (i.e., first standing after rest; typically, the first steps in the morning or after being seated for a long time).The pain tends to reduce gradually once the patient starts walking (Cutts et al., 2012;Siriphorn & Eksakulkla, 2020).However, it can worsen at the end of the day or be exacerbated by prolonged weight-bearing activities (McPoil et al., 2008).
Increased tension on the Achilles tendon (AT) resulting from intense muscle contraction is a major mechanical factor in PA overstraining (Cheung et al., 2006;Porter et al., 2002).Previous studies reported a positive correlation between AT loading and PA tension (Cheung et al., 2006).As a proof of concept, AT tightness is found in almost 80% of patients affected by plantar fasciitis (Singh et al., 1997).There was a strong statistically significant correlation in this condition between isolated gastrocnemius contractures or increased gastrocnemius-soleus complex tightness and heel pain severity (DiGiovanni et al., 2002;Patel & DiGiovanni, 2011;Pearce et al., 2021).Increased tightness in other posterior leg muscles (e.g., hamstring) can also induce prolonged forefoot loading and increase repetitive injury to the PA through the windlass mechanism (Labovitz et al., 2011).
However, the biomechanical importance of the fascial system cannot be neglected.Indeed, fascial tissue cannot be considered a passive bystander in musculoskeletal dynamics, merely enveloping the muscles.Current literature indicates that the central importance of the fasciae in movement and postural control systems is being recognized (Blottner et al., 2019;Buscemi et al., 2021;DellaGrotte et al., 2008;Findley et al., 2012;Langevin, 2021;Stecco et al., 2023).Increasing amounts of experimental evidence demonstrate that the fascial system provides a pathway for force transmission, transmitting, and receiving mechano-metabolic information and thus influencing movement perception, peripheral motor coordination, and proprioception (Ryskalin et al., 2022;Stecco et al., 2019;Stecco, Macchi, et al., 2011).Thus, one can expect that biomechanical abnormalities within the myofascial unit place excessive stress on the PA and ultimately contribute to heel pain and plantar fasciitis.
F I G U R E 1 (A) Schematic representation of the anatomy of the plantar aponeurosis (PA).(B) Macroscopic view of the PA from an unembalmed human cadaver.LG, length of the PA along the main longitudinal axis; WP, proximal width of the PA near the heel insertion; WD, distal width of the PA.Reprinted with permission from Stecco, Corradin, et al. (2013).Copyright 2013 John Wiley and Sons.
Therefore, in the present review, after a brief overview of the anatomy of the suro-Achilles-calcaneal-plantar complex of the superficial posterior compartment of the leg, we discuss the complex structural and functional coupling between muscles and fascial tissue, and the possible correlation between myofascial abnormalities, muscle/ tendon tightness, and heel pain severity in plantar fasciitis.

| A brief overview of Achilles tendon anatomy
Also termed the calcaneal tendon owing to its attachment to the calcaneus, the AT is one of the thickest, largest, and strongest tendons in the human body (O'Brien, 2005).Nevertheless, because it serves as the primary plantar flexing mechanism of the ankle, it is at the greatest risk of rupture, accounting for nearly 20% of all large tendon injuries (Chen et al., 2009).Indeed, AT injuries are a very common clinical picture in sports medicine (Hess, 2010;Lopes et al., 2012), and they have also become significantly more common within the middle-aged, physically active population (i.e., 40-59 years) during the last decade, probably because of the growing popularity of competitive and recreational sports (Lantto et al., 2015;Lemme et al., 2018).
Both comparative and ex vivo studies demonstrate the architectural complexity of this tendon.For instance, variations in its twisting structure and the degree of rotation near its insertion on the calcaneal tuberosity have been reported (Benjamin et al., 2007;Cummins & Anson, 1946;Edama et al., 2016;Szaro et al., 2009).Reports of the arrangements of the attachments of the AT fascicles to the facets of the calcaneal tuberosity are inconsistent (Ballal et al., 2014;Cummins & Anson, 1946;Edama et al., 2016;Kim et al., 2010;Pękala et al., 2017;Szaro et al., 2009).Also, the relative contributions of the medial and lateral heads of the gastrocnemius and the soleus to the AT can differ among subjects, making the internal AT force distribution even more complicated to understand (Del Buono et al., 2013;Doral et al., 2010;Yin et al., 2021).
Anatomically, the AT represents the conjoined junction of the triceps surae muscle, which is located at the superficial posterior compartment of the leg (i.e., the calf).This complex consists of the soleus and the medial and lateral heads of the gastrocnemius (Figure 2).
The gastrocnemius comprises two heads at its origin, medial, and lateral, which insert proximally in the posterosuperior region of the corresponding femoral condyle (Dalmau-Pastor et al., 2014).The soleus lies deep to the gastrocnemius and superficial to the muscles of the deep posterior compartment of the leg (Olewnik et al., 2020).It originates from two heads, tibial, and fibular, which are united by a tendinous arch from which additional fibers arise (Balius et al., 2014).The tibial origin is at the inferior border of the soleal line, while the fibular origin is on the posterior aspect of the head and about the upper fourth of the diaphysis (Dalmau-Pastor et al., 2014).Besides the posterior margins of the tibia and fibula, the soleus can also arise from the surrounding deep fascia of the leg (Balius et al., 2013).The medial and lateral intramuscular aponeuroses (originating from the tibia and the fibula, respectively) are continuous with the epimysium of the soleus muscle and penetrate distally into the main muscle belly.Distally, from the thickest point of the muscle belly, a central aponeurotic tendon arises within the soleus (Balius et al., 2014).These latter fibers then contribute to the AT, along with those of the gastrocnemius, generally inserting on to the most distal part of the AT while the gastrocnemius fibers insert more proximally (Figure 3).
Anatomical dissection studies show that the AT comprises three distinct bundles of tendon fascicles (i.e., subtendons), which are distinguishable at the level of the proximal end of the AT, where the distal aponeuroses of the muscles can be separated from each other (Ballal et al., 2014;Edama et al., 2016;Szaro et al., 2009;Winnicki et al., F I G U R E 2 Schematic representation of a cross-section of the lower leg showing all four compartments: anterior, lateral, deep posterior, and superficial posterior.Blue lines indicate the fascial network.Triceps surae muscle components (i.e., medial and lateral heads of the gastrocnemius and the soleus), located within the superficial posterior compartment of the leg, are highlighted in a more intense red.2020).One subtendon arises from the soleus and lies deep, and two independent subtendons, which lie superficial, originate from each of the two heads of the gastrocnemius (Handsfield et al., 2017).The full incorporation of the tendinous portions of the gastrocnemius and soleus is evident almost 10 cm above the AT calcaneal insertion (Benjamin et al., 2007).However, it has been reported that the soleus can remain separated from the gastrocnemius as far down as the calcaneal insertion (Mellado et al., 1998).Sometimes there is also a small contribution from the tendon of the plantaris muscle (PM; Ballal et al., 2014).Often dismissed as a vestigial (accessory) muscle, the PM consists of a small thin muscle belly and originates from the popliteal surface of the femur.A close connection between the PM tendon and the mid-portion of the calcaneal tendon has been reported in 65% of the adult population (Olewnik et al., 2017;van Sterkenburg et al., 2011).
Unlike other tendons such as those of the wrist and the hand, the AT lacks a true synovial sheath, but is surrounded by a thin sheath of dense connective tissue called a "paratenon" (Maffulli & Almekinders, 2007).Besides providing a certain degree of tendon gliding, the paratenon is an important source of blood supply and nutrition to the tendon (Zantop et al., 2003).Histologically, Golgi tendon organs, free nerve endings, and Pacinian-like corpuscles were identified in AT tissue samples from healthy pigs, suggesting a role for the tendon in proprioception (Kapetanakis et al., 2017).
The paratenon is a thick fibrous layer with few elastic fibers, continuous with the crural fascia, as evidenced by an anatomical study of non-embalmed legs from cadavers (Stecco et al., 2014).The deep investing crural fascia is a layer of connective tissue enclosing the posterior structures of the calf and connected to the paratenon and AT (Webborn et al., 2015).However, another magnetic resonance imaging (MRI) study suggested that the fascia cruris and the paratenon exist as two separate layers around the AT, though they appear less demarcated toward the AT calcaneal insertion, where they seem to fuse with the posterior subcutaneous structures (Soila et al., 1999).
Another anatomical and radiological study revealed that the mean distance to the confluence of the AT paratenon and the fascia cruris from the postero-superior calcaneal tubercle is 37.3 mm (Carmont et al., 2011).

| Achilles tendon pathophysiology
As part of Achilles tendinopathy, tendinosis and tendonitis are defined as clinical pictures of tissue degeneration and inflammation, respectively.Although the term tendinosis is universally accepted since the disease has commonly been described as "degenerative," the role of inflammation in tendinopathy is controversial and is still much debated.Some authors argue that the term "tendinitis" could be inaccurate and misleading because infiltration and inflammatory cells (such as neutrophils and macrophages) are not found in chronic tendon disorders (Maffulli et al., 1998).In contrast, other studies have demonstrated macrophages, T and B lymphocytes, and increased levels of inflammatory markers such as interleukin-1 (IL-1), IL-6, cyclooxygenase-1 (COX-1), COX-2, and TGF-β in chronic Achilles tendinopathy (Dean et al., 2016;Kragsnaes et al., 2014;Rees et al., 2014;Schubert, 2005).Tissue biopsies from AT patient cohorts show a complex inflammation signature, expressing target molecules from the interferon, NF-κB, STAT-6, and GCR activation pathways, which suggests established (chronic) inflammation and ongoing tissue repair (Dakin et al., 2018).Recent data suggest that excessive/pathological levels of force can constitute the mechanical stress that triggers tissue microinjury and a local immune system-mediated tendon repair response (Gracey et al., 2020).This mechanotransduction-mediated dysregulation of the immune response, which ultimately leads to failed healing, is typical of chronic tendinopathic lesions (Chisari et al., 2020).
Ultrasonography of subjects complaining of Achillodynia demonstrated that AT symptoms could also be associated with increased the paratenon thickness with no sign of tendon tissue involvement (Stecco et al., 2015).Histological examination of the affected tissue showed that metabolic and inflammatory changes within the Achilles paratenon could precede or parallel those within the tendon tissue itself (Langberg et al., 1999).Acute exercise or excessive loading can result in alterations of AT paratenon structures known as "paratendinitis," featuring edema, swelling, and lymphocyte infiltration (Maffulli et al., 1998).These latter results in increased paratenon thickness, which is clearly detectable as increased signal intensity in both sonography and MRI investigations (Harris & Peduto, 2006;Leung & Griffith, 2008;Stecco et al., 2015).

| Anatomical and structural continuity between the plantar aponeurosis and Achilles paratenon
Functionally, the AT is pivotal in transmitting the contractile forces generated from the triceps surae muscle and producing the ankle plantar flexion torque required for load distribution in the foot.The elastic spring-like properties of the tendon also allow it to store and release energy explosively during walking and running (Fukashiro et al., 2006).These functions are closely tied to the morphological and biomechanical relationship between the AT and PA (Carlson et al., 2000;Cheng et al., 2008;Singh et al., 2021;Stecco, Corradin, et al., 2013;Zwirner et al., 2020).
A number of randomized control trials have revealed that AT-or calf muscle-stretching exercises can reduce plantar heel pain and increase the range of ankle motion (DiGiovanni et al., 2003;Porter et al., 2002;Radford et al., 2006Radford et al., , 2007)).DiGiovanni et al. (2003) reported statistically significant pain relief at 8-week follow-up in patients affected by plantar fasciitis who were managed with a standard AT-stretching protocol.
Another study reported long-term improvement in symptomatic pain following an AT-stretching program in patients with chronic plantar fasciitis (DiGiovanni et al., 2006).Similarly, patients without previous treatments for plantar fasciitis obtained significant short-term pain relief by using night splints, which keep the foot in a neutral or slightly dorsiflexed position at rest (Powell et al., 1998).
Although the effectiveness of AT/calf-stretching exercises and night splints for treating plantar heel pain substantiates a functional link between the AT and PA, anatomical continuity between these structures is still a matter of debate.Milz et al. (2002) demonstrated a conspicuous bundle of highly oriented trabeculae in the postero-inferior part of the calcaneus.
These trabeculae, which were clearly visible in thick resin sections of hindfeet removed from fresh cadavers, appeared as regularly aligned structures oriented along the lines of force transmission from the AT toward the proximal attachment of the PA.Further morphological and histological examination of plastinated slices revealed a band of calcaneal trabeculae running between the AT paratenon and the superficial posterior and inferior calcaneus toward the PA, surrounded by collagens and adipocytes (Singh et al., 2021;Zwirner et al., 2020).Continuity of the PA with the AT paratenon was also confirmed in an anatomical dissection study of unembalmed human leg specimens (Stecco, Corradin, et al., 2013), which revealed a thin layer of periosteal fibers in the heel.
In line with this, MRI data obtained from patients complaining of Achilles tendonitis and from healthy people highlighted a strong correlation between the thickness of the AT paratenon and that of PA, further strengthening the anatomical and structural relationship between those structures (Stecco, Corradin, et al., 2013).There is also evidence of a strong statistically significant correlation between cross-sectional measurements of the AT and PA at their calcaneal insertion (Singh et al., 2021).Other studies have argued instead for partial contiguity between AT and PA fibers (Kim et al., 2010;Snow et al., 1995).This could be because anatomical continuity between these collagenous structures seems to vary with age (Kim et al., 2010); it is particularly evident in neonates and younger adults but diminishes during adulthood (Kim et al., 2010;Maffulli & Almekinders, 2007;Snow et al., 1995).The number of AT superficial fibers that become continuous with PA fibers seems to decrease with increasing age, along with calcaneal ossification of the tendon into the bone, which further separates these two structures (Maffulli & Almekinders, 2007;Snow et al., 1995;Zwirner et al., 2020).
Biomechanically, there is increasing evidence for a strong correlation between the AT and PA (Carlson et al., 2000;Cheung et al., 2006;D'Ambrogi et al., 2005;Hicks, 1954;Stecco, Corradin, et al., 2013;Zwirner et al., 2020).Thus, the AT-calcaneus-PA-complex can be seen as a part of a broader myofascial system, where adjacent structures collaborate to spread and transmit the load force.If we consider each of these structures as representing respectively the proximal, intermediate, and distal parts of the conjoined tendon of the calf muscles (i.e., the gastrocnemius and soleus; Zwirner et al., 2020), then it can assumed that even triceps surae structures are involved in the development of plantar fasciitis.

| THE CRITICAL COORDINATION BETWEEN THE TRICEPS SURAE MUSCLE, ACHILLES TENDON, AND PLANTAR APONEUROSIS: THE EMERGING ROLE OF THE FASCIA
3.1 | The potential role of the suro-Achilleocalcaneal-plantar complex in PA pathology The triceps surae complex represents the main extensor and propulsion system of the foot, and is equipped with a very sophisticated driving belt, namely the AT-posterior part of the calcaneus-PA in continuity with the fibrous skeleton of the triceps surae (Morvan et al., 2007).This suro-Achilleo-calcaneal-plantar system was first described by Arandes andViladot in 1954 (Arandes &Viladot, 1954).
They showed how the triceps surae complex is placed in series with the PA to ensure force transmission from the triceps surae toward the toes during walking, running, and jumping.Also referred to as the Achilleo-calcaneal-plantar complex (ACP), it was intensively investigated by French and Spanish research groups during the 1990s from both anatomical and biomechanical viewpoints (Nguyen et al., 1987;Sanz-Hospital et al., 1997).
The triceps surae muscle contributes differentially to lower limb movements.In detail, the medial and lateral heads of the gastrocnemius cross both the knee and ankle joints, proximally forming the lower boundary of the popliteal fossa.These muscles then connect to each other in the midline of the superficial posterior compartment of the leg, accounting for the characteristic bulge of the calf.In contrast, the soleus is a one-joint muscle.Its fibers originate below the knee, extending more distally along the tibia than those of the gastrocnemius.Thus, the soleus only crosses the ankle joint, having no action on the knee joint.As a result, the gastrocnemius is mostly involved in forward propulsion during walking, running, and jumping, whereas the soleus primarily acts as a foot stabilizer, giving the body vertical support while standing (Del Buono et al., 2013).This is reflected in their muscle fiber type compositions: the gastrocnemius predominantly consists of Type II (or fast twitch) fibers while the soleus contains a high percentage of Type I (or slow twitch) fibers (Edgerton et al., 1975;Gollnick et al., 1974).Consequently, skeletal muscle mass is lost more rapidly in the soleus than in the gastrocnemius, making the soleus a more sensitive indicator of skeletal muscle atrophy in response to muscle "disuse" (Booth, 1977;Del Buono et al., 2013).This is well documented both in rodents and humans, with considerable similarities (Bodine, 2013;Fitts et al., 2010;Paudyal et al., 2018).
The soleus is generally considered at lower risk for strains than the gastrocnemius (Bryan, 2009).However, soleus muscle injury could have been underestimated, owing to misdiagnosis as thrombophlebitis or gastrocnemius strain (Anouchi et al., 1987;Bryan, 2009).Furthermore, soleus muscle strains could be underappreciated owing to the traditional use of sonography (ultrasound) for assessing calf muscle injuries (Balius et al., 2013).Gastrocnemius strains are easier to detect because the muscle has a superficial anatomical location, while the soleus is located much deeper in the calf region.This could explain why sonography reveals fewer soleus injuries than gastrocnemius injuries (Pedret et al., 2015).
However, structural alterations in muscle strain injuries or abnormal patterns of skeletal muscle activity are not necessarily restricted to the muscle, but can affect the fascia.Very recently, Otsuka et al. reported changes in the elastic properties and mechanical behavior of the fascia lata associated with underlying quadriceps femoris muscle contractions, measured in vivo by shear wave elastography (Otsuka et al., 2019).The surrounding fasciae of adjacent muscles are intimately connected, creating continuity rather than separation (Wilke et al., 2018).This challenges the classic concept of muscles as independent actuators of movement, the fasciae being merely passive packing of the underlying skeletal muscles (Wilke et al., 2018).Contrary to this common assumption, increasing evidence demonstrates that the fascia performs several important functions in the body beyond architectural/structural ones (Schleip et al., 2022).It is an active player in biomechanical force transmission and tensile load bearing.At the same time, it can change its biomechanical properties in response to musculoskeletal dynamics (Schleip et al., 2019;Stecco et al., 2020;Wilke et al., 2018).This intimate relationship between skeletal muscles and fascia supports the concept of "myofascial continuity," which emphasizes that an endless and extensive tensegrity network runs throughout the human body (Wilke et al., 2016).This has enormous potential implications for both training and therapy.An example of this emerging concept is the superficial back line, a myofascial chain/meridian consisting of the PA, the AT, and the gastrocnemius, which then runs toward the hamstrings, the lumbar fascia, the erector spine, and up to the epicranial fascia (Myers, 2014;Wilke et al., 2016).These latter findings could provide a plausible explanation for the onset of plantar fasciitis symptoms as a consequence of muscle overuse, where tension is transferred from a stiff gastrocnemius to the sole through the AT-calcaneal-plantar complex.As a proof of concept, gastrocnemius tightness has long been considered a risk factor for plantar fasciitis (Bolívar et al., 2013).For instance, Patel and DiGiovanni (2011) found that 83% of a sample of 254 subjects with plantar fasciitis had an isolated contracture of the gastrocnemius and/or gastrocnemius-soleus tightness.At the same time, there is evidence that these muscles do not move totally independently of each other.Percutaneous electrical stimulation of the gastrocnemius can induce simultaneous displacement of the soleus, which suggests force transmission between these muscles (Bojsen-Møller et al., 2010).
Other recent in vivo studies provide evidence for inter-and intramuscular interactions within human calf muscles (Finni et al., 2017;Karakuzu et al., 2017).Therefore, it seems plausible that even soleus muscle dysfunctions can impair force transmission between the calf muscles and the myofascial system, becoming an etiological factor in plantar fasciitis.

| The potential role of the fascial tissue in PA pathology
Over the years, inexact, ambiguous, or confounding definitions have portrayed the human fascial system as something "mostly left to the imagination of the students" (Singer, 1935).The differences in characteristics of the fascia depending on the anatomical region (neck, trunk, or limbs) provide an additional challenge to the definition of this organ (Natale et al., 2014(Natale et al., , 2015;;Stecco, Gesi, et al., 2013).Although the fascia remains largely neglected, new methodological findings and assessment methods, along with changes in anatomical dissection, have greatly clarified the anatomical and biomechanical recognition and definition of this fundamental system of the human body (Schleip et al., 2012).
In recent years, the fascia has received increasing attention as a major contributor to movement perception, coordination, and the pathogenesis of musculoskeletal pain and dysfunction.Contrary to earlier assumptions, it is potentially a force transmitter intimately connected to the underlying skeletal muscle (Wilke et al., 2019).A recent study by Schleip et al. demonstrated that the fascia has inherent contractility, thereby actively influencing musculoskeletal and biomechanical behavior (Schleip et al., 2019).A potential role of fascia stiffness in limiting the maximal range of motion (ROM) of a joint has been also hypothesized (Nordez et al., 2017).However, further efforts are needed to optimize the proposed novel methods for estimating the motion pattern of the fascia in vivo and its adaptability during muscle contraction (Condino et al., 2015;Langevin et al., 2009;Turini et al., 2015).
At the microscopic level, fascial tissue comprises two or three layers of collagen fiber bundles, the fibers being differently oriented in each layer.This contributes to the strong resistance to traction of the fascia itself (Ryskalin et al., 2022).Remarkably, the fascial system is viscoelastic because it contains high levels of hyaluronic acid (HA) in the interfaces between the collagen layers and between the deep fascia and the underlying muscle epimysium (Stecco, Stern, et al., 2011).
This allows gliding to occur between the structures during movement and force transmission.The high concentration of HA also enables the facial tissue to undergo greater viscoelastic deformation than muscles and tendons (Stecco et al., 2020).HA is a linear glycosaminoglycan consisting of regular repeating disaccharide units of N-acetyl-glucosamine and D-glucuronic acid, linked by β1-3 and β1-4 glycosidic bonds, respectively (Matteini et al., 2009;Pratt, 2021).Proper functioning of a healthy fascia requires specific levels of this essential component of the extracellular matrix (Fede et al., 2018).These can differ depending on the anatomical site, so the sliding properties of specific fascia also differ.For instance, Fede et al. reported a significant difference between the amount of HA in the aponeurotic fasciae (fascia lata of the thigh and rectus sheath of the abdomen, about 43 μg/g) and that in the epimysial fascia (or epimysium) of the trapezius and deltoid (about 6 μg/g; Fede et al., 2018).This is not surprising since these structures have totally different functions and mechanical properties.The aponeurotic fascia envelops various muscles and has a high potential for gliding, whereas the epimysium adheres more tightly to the underlying muscles.Alterations in the physiological levels or physicochemical properties of HA have been associated with several myofascial diseases (Ugwoke et al., 2022).
It is well-established that the main phenotypic and biochemical adaptations induced by exercise training involve the skeletal muscles (Bartalucci et al., 2012;Demirel et al., 1999;Powers et al., 1999;Toti et al., 2013).However, evidence that has emerged in recent decades suggests that the fascial tissue can also undergo molecular adaptations and/or alterations in response to muscle exercise (Piehl-Aulin et al., 1991).In particular, muscle overuse, disuse, or misuse can increase HA fascial densification, which results in greater resistance to fascial layer sliding and increased fascial stiffness (Luomala et al., 2014;Pavan et al., 2014;Stecco, Gesi, et al., 2013;Wilke et al., 2022).Muscle contraction-driven changes in loose fascial connective tissue can include increased HA production, aggregation of HA into supramolecular structures, changes in HA viscoelasticity and viscosity, and reduced HA lubrication.The HA content of the fascia lata was significantly reduced in patients with hip osteoarthritis (OA), where altered joint mechanics, distorted hip posture, and altered gait consequent on the disease resulted in altered fascial structure and behavior, further worsening the OA symptoms (Fantoni et al., 2021).Besides overuse syndromes, connective tissue can become tighter after direct traumatic injuries not involving muscle lesions (Stecco, Gesi, et al., 2013).For instance, residual alterations in fascial sensitivity and movability (fascial densifications) were more prevalent in the lower limbs of individuals with a history of ankle sprain than in healthy controls (Kalichman et al., 2016).
Therefore, in recent years, different fascia-directed treatment modalities such as fascial manipulation, increased local temperature, and alkalinization have been proposed to reverse these alterations in HA and thus relieve the pain associated with fascial densification (Pawlukiewicz et al., 2022;Raja et al., 2021;Stecco, Gesi, et al., 2013).Any impairment of proper fascial gliding results in anomalous tension and altered input transmission from the mechanoreceptors and nociceptors embedded within the fascial layers, which can influence musculoskeletal dynamics negatively and create conditions for the onset of myofascial pain.Indeed, if we inject hypertonic saline into the erector spine muscle, the thoracolumbar fascia, and the overlying subcutis, the patient will complain of more intense and unpleasant pain sensations if the fascia rather than muscular or subcutaneous tissue is injected (Schilder et al., 2014).
This means that the fascia can be considered a fully-fledged major pain generator in the musculoskeletal system.As a proof of concept, compelling evidence demonstrates that the fascia is more strongly innervated with multiple myelinated and nonmyelinated sensory nerve fibers, including nociceptive ones, than the adjacent muscle tissue (Ryskalin et al., 2022).
Consistent with this hypothesis, repetitive microtraumas to the gluteus maximus muscle from overuse and misuse led to myofascial pain syndrome (Waldman, 2014).Likewise, a recent report showed that the onset of acute Achilles paratendinopathy could be related to histological and biomechanical changes in the crural fascia resulting from calf muscles injury (Mattiussi et al., 2016).Another recent study described a case series of nine athletes with pain in the Achilles region who had tears in the fascia cruris from the attachment to the paratenon and AT (Webborn et al., 2015).The deep crural fascia has been also implicated in overuse injuries such as medial tibial stress syndrome (MTSS), also known as "shin splints" (Bouché & Johnson, 2007).These authors hypothesized that the tenting effect of the tendons of the deep leg flexors, caused by eccentric muscle contraction, exerts a tensile strain load on the deep fascia directed toward its tibial crest insertion (Bouché & Johnson, 2007).It is therefore not surprising that manual treatment of the crural fascia is emerging as an effective option for relieving pain and restoring exercise tolerance in MTSS patients (Schulze et al., 2014).Concerning the calf muscles, fascial lesions are more prevalent following muscle strain injuries within the soleus than the gastrocnemius or the hamstrings (Koulouris et al., 2007;Prakash et al., 2018;Wilke et al., 2019).Besides muscle contraction-driven changes in the mechanical properties of the fascia, mechanical adaptations at the fascial level after chronic stretching interventions have also been hypothesized (Nordez et al., 2017).
However, how and to what extent fascial tissue properties are affected by muscle overuse, misuse, or trauma still merits further investigation.

| FUTURE DIRECTIONS AND PERSPECTIVES
From the present narrative review, it transpires that clinicians and therapists who are going to treat plantar fasciitis should be more aware of the complex anatomical and biomechanical substrates that can underly the onset and development of PA pathology.In particular, their attention should not be restricted to the plantar aspect of the foot, but rather focused upstream on the myofascial chain consisting of the PA, the AT, and the triceps surae muscle and their fasciae.Evidence reported in the present paper has highlighted that biomechanical abnormalities within the myofascial unit can be crucial since they can place excessive stress on the PA and ultimately contribute to heel pain and plantar fascitiis.At the same time, the fascial tissue should not be neglected since it is potentially a prime contributor to the pathophysiology of several chronic musculoskeletal painful conditions.
Clearly, the structure, function, and biomechanics of the fascial system still deserve more attention.Notwithstanding the decisive involvement of the fascia in the onset of overuse muscle injuries and painful syndromes, fascial injuries and alterations continue to be generally overlooked and are seldom considered.Future research efforts should be focused on the optimization of novel approaches to studying fascial mobility in vivo in both physiological and pathological conditions.This will allow clinicians to optimize treatment strategies and rehabilitation protocols to obtain better outcomes for patients affected by lower-limb musculoskeletal conditions such as plantar fasciitis.
Finally, because of the intimate anatomical and biomechanical relationship between the PA and the triceps surae complex, calfstretching exercises are commonly used in therapeutic and rehabilitation protocols for plantar fasciitis.However, despite their widespread clinical application, their effectiveness in managing this condition has sometimes been questioned and conflicting data are reported in the current literature.This indicates the need for more carefully designed studies within this field.Other conservative treatments should be considered.This is the case, for instance, with eccentric calf-muscle exercises, which are increasingly being used to reduce pain and improve function in patients with Achilles tendinopathy.Thus, future research efforts should focus on evaluating the effectiveness of eccentric loading exercises for calf muscles and also for plantar fasciitis.Additional knowledge of the mechanisms that could underpin their clinical benefit would affect both the management and treatment of plantar fasciitis.
Anterior view of the right soleus muscle.lhGM, lateral head of the gastrocnemius muscle; mhGM, medial head of the gastrocnemius muscle.(B) The figure depicts both the medial and lateral intramuscular aponeuroses and the central tendon, as evident from the panel in (C) showing an anatomical dissection of the anterior view of the left soleus muscle.MiA, medial intramuscular aponeurosis; LiA, lateral intramuscular aponeurosis; CT, central tendon; AT, Achilles tendon.Reprinted with permission from Olewnik et al. (2020).Copyright 2020 Elsevier.