Soleus facts - study PDF

Title Soleus facts - study
Author 윤선 최
Course Functional Anatomy
Institution University of Otago
Pages 12
File Size 301.7 KB
File Type PDF
Total Downloads 95
Total Views 135

Summary

study...


Description

 Soleus facts The soleus muscle is a wide flat leg muscle found on the posterior leg. It runs from just below the knee to the heel and lays immediately deep to the gastrocnemius. These two muscles, along with the plantaris muscle, belong to the group of superficial posterior compartment calf muscles. Soleus’ contraction results in strong plantar flexion. It also allows us to maintain an upright posture due to its important role as an antigravity muscle. Together with the gastrocnemius, they form the three-headed group of muscles referred to as the triceps surae. They both insert on the calcaneus via the calcaneal tendon and act in many basic activities, such as walking, running, and leaping. The size and shape of the triceps surae muscle bellies determine the interindividual differences of human calves’ appearance from slim to rather robust. This article will outline the morphology of the soleus muscle, as well as its functional and clinical anatomy. https://www.kenhub.com/en/library/anatomy/soleus-muscle

The soleus muscle, located deep/anterior to the medial and lateral gastrocnemius muscle heads, originates on the posterior aspect of the tibia (middle third of the medial border) and fibula (head and body) and inserts on the calcaneus through the Achilles tendon (see Figure 31.1). One can individualize the soleus muscle into two parts joined by a horizontal arch. A frontal aponeurosis and a sagittal septum divide the muscle into medial and lateral parts (see Figure 31.2). The soleus contributes to walking and static standing. Its association with the gastrocnemius muscle contributes to active plantar flexion of the ankle through the Achilles tendon, which inserts on the posterior calcaneum tuberosity. https://www.sciencedirect.com/sdfe/pdf/download/eid/3-s2.0B9780721605197000319/first-page-pdf

 specific attachment sites, The soleus muscle arises from the soleal line on the dorsal surface of the tibia, medial border of the tibia, head of the fibula, and posterior border of the fibula. Part of the fibers arises from the tendinous arch of the soleus, which spans between the tibia and fibula and arches over the popliteal vessels and tibial nerve. The soleus muscle runs along the gastrocnemius muscle and together they insert onto the posterior surface of the calcaneus via the calcaneal tendon. The calcaneal tendon, commonly called the Achilles tendon, is the strongest tendon of the human body. It is easily visible and palpable at the heel. https://www.kenhub.com/en/library/anatomy/soleus-muscle

The soleus muscle is a large, broad, and rather long muscle located at the posterior aspect of the leg. It is a bipenniform muscle consisting of a lateral and a medial head. The lateral head originates from the fibula head and body and the medial head originates from the medial side of the middle third of the tibia. The lateral and medial soleus muscles are separated in the midline by a septum, which is present in the distal part of the muscle. The two muscle heads join together to form the dorsolateral and dorsomedial component of the Achilles tendon. This tendon, which is formed by the soleus and gastrocnemius muscles, inserts on the calcaneum tuberosity (see Figure 31.4). https://www.sciencedirect.com/sdfe/pdf/download/eid/3-s2.0B9780721605197000319/first-page-pdf

 innervation, The soleus is innervated by the ventral rami of S1 and S2 spinal nerves, carried by the tibial nerve into the posterior compartment of the leg. Blood supply is provided by two main branches. The superior branch arises from the popliteal artery while the inferior branch arises from peroneal artery (fibular artery) or the posterior tibial artery. The peroneal and posterior tibial arteries are direct branches of the popliteal artery and arise in the popliteal fossa. Minor accessory arteries may also branch off the peroneal, posterior tibial and lateral sural arteries. A clinically important venous plexus is present in the soleus muscle belly. Physiologically it contributes to the muscle pump of the lower extremity. In pathological circumstances, such as thrombophilia, it constitutes a common site of onset of deep vein thrombosis (DVT). Veins follow the arteries of the same name into the popliteal vein. https://www.kenhub.com/en/library/anatomy/soleus-muscle Arterial anatomy of the region (see Figures 31.1, 31.2) The soleus muscle is vascularized by the posterior tibial and peroneal arteries, which deliver blood supply through several pedicles described in 1933 by Salmon. Further anatomic studies performed by Baudet et al have demonstrated that some pedicles can also emerge from the popliteal artery or the peroneotibial artery (tibioperoneal trunk). We will discuss these finding in greater detail as we progress through this chapter. Venous anatomy of the region The multiple arterial pedicles supplying the flap are accompanied by small venae comitantes. These veins join the venous system of the posterior tibial vein and peroneal vein at several levels to drain the blood into the popliteal system. Nerves in the region The medial popliteal nerve and the posterior tibial nerve are the main trunks giving off branches to the soleus muscle (see Figure 31.3). They run deep almost medially to the soleus muscle along the entire muscle belly. Main branches enter in the proximal part of the muscle. https://www.sciencedirect.com/sdfe/pdf/download/eid/3-s2.0B9780721605197000319/first-page-pdf

 muscle architecture and size (e.g. fascicle length, physiological cross-sectional area, volume), The macroscopic arrangement of muscle fibres in the muscle belly is referred to as muscle architecture. Muscle architecture is often quantified by parameters such as fascicle length, pennation angle and physiological cross-sectional area (PCSA). Muscle architecture differs markedly between muscles and individuals (Ward et al., 2009; Woittiez, 1984), and changes with age (Narici, Maffulli & Maganaris, 2008; Siebert et al., 2017; Weide et al., 2015), exercise (Blazevich, 2006) and disease (Shortland et al., 2002; Foran et al., 2005). To study these processes, quantitative methods to measure muscle- and subject-specific architectural parameters are required. In this study, we use magnetic resonance imaging (MRI) techniques to quantify the architecture of the human soleus muscle in vivo. The human soleus has a complex, three-dimensional (3D) architecture. Studies of cadaver muscles using micro-dissection techniques and magnetic resonance imaging have shown that the soleus is compartmentalised: it consists of a unipennate posterior part wrapped around a radially bipennate anterior part (Agur et al., 2003; Hodgson et al., 2006). The fascicles in each compartment have distinctly different orientations but similar lengths (Agur et al., 2003). The large volume (∼425 cm3 in vivo (Lee et al., 2006)) and short fascicle lengths (3– 4 cm (Agur et al., 2003)) give the soleus the largest physiological cross-sectional area of any human lower limb muscle (Ward et al., 2009). The complexity of the soleus’ architecture is also reflected in the connective tissues, examined in great detail by Hodgson et al. (2006). Distally, the muscle is connected to the calcaneus through the rope-like Achilles tendon, which the soleus shares with the gastrocnemius muscle. Just proximal to its insertion on the calcaneus, the Achilles tendon has an elliptical cross-section in the transverse plane, but more proximally it becomes wider and thinner as it joins the sheet-like posterior aponeurosis of the soleus (Hodgson et al., 2006; Finni et al., 2003b; Balius et al., 2013). The distal ends of muscle fascicles in the posterior compartment of the soleus insert on the posterior aponeurosis and the proximal ends of the muscle fascicles originate from the posterior side of the anterior aponeurosis. The anterior aponeurosis (the origin of the muscle) forms another curved sheet of connective tissue that extends almost the entire length of the muscle belly, connecting the muscle proximally to the tibia and fibula and separating the muscle into posterior and anterior compartments. The anterior aspect of the anterior aponeurosis provides the origin of muscle fascicles in the anterior compartment. Fascicles in the anterior compartment insert on a protrusion of the posterior aponeurosis called the medial septum, which separates the muscle into medial and lateral compartments and presents as a clearly identifiable T-shaped structure on transverse MRI images (Hodgson et al., 2006). The structural partitioning of the human soleus is also evident in the 3D branching of nerves (Loh, Agur & McKee, 2003), indicating that compartments may have functionally different roles (English, Wolf & Segal, 1993). There have been few reports of quantitative measurements of the three-dimensional architecture of the soleus in vivo. Quantification of the 3D architecture of the soleus in vivo is

difficult using conventional techniques such as ultrasound. With ultrasound, measurements from the deeper (anterior and proximal) compartment of the soleus muscle is difficult because image quality is often poor, although this depends on the system (Barber et al., 2017; Rana, Hamarneh & Wakeling, 2013; Lai et al., 2015; Chow et al., 2000; Martin et al., 2001). Also, in the soleus it is difficult to orient the transducer in the plane of fascicles and perpendicular to the aponeurosis (Rana, Hamarneh & Wakeling, 2013), as is required for accurate measurements of muscle architecture (Bolsterlee, Gandevia & Herbert, 2016; Lee et al., 2015). Three-dimensional imaging techniques such as magnetic resonance imaging (MRI) overcome some of the limitations of ultrasound (Finni et al., 2003a; Balius et al., 2013; Hodgson et al., 2006). MRI has been used to quantify lengths of the whole muscle belly and the structure of connective tissues, and to map intramuscular velocities during isometric contractions (Finni et al., 2003a; Hodgson et al., 2006). However, anatomical MRI scans lack the resolution to discern individual muscle fibres, precluding measurement of key indices of muscle architecture such as fascicle lengths and pennation angles. For this reason, there are limited data on fascicle lengths and pennation angles in the human soleus in vivo (see Agur et al. (2003) for an overview of the available data). Also, it is largely unknown whether architectural parameters are uniform or differ between compartments. Non-uniformities could indicate as yet unrevealed functional differences between the soleus compartments. Here, we use diffusion tensor imaging (DTI) to quantify the three-dimensional architecture of the human soleus muscle in vivo (Damon et al., 2017; Van Donkelaar et al., 1999; Bolsterlee et al., 2017; Oudeman et al., 2015). DTI is a magnetic resonance imaging (MRI) technique which exploits the principle that longitudinally arranged microstructures in muscles (such as cell membranes) hinder the diffusion of water molecules more in the plane perpendicular to the muscle fibre’s long axis than along that axis. This principle can be used to measure fibre orientation (Damon et al., 2002) and—most interestingly for anatomical studies—to quantify the 3D muscle architecture using DTI fibre tractography algorithms (Damon et al., 2017; Yeh et al., 2013; Mori et al., 1999). We have recently extended DTI tractography techniques by constraining the fibre tracts to terminate at the surface of the muscle (Bolsterlee et al., 2017). The muscle surface is located using MRI. Here, we apply these novel techniques that combine anatomical MRI with DTI data to quantify the complex architecture of the human soleus in vivo at two different muscle lengths. We provide the most detailed data to date of soleus muscle architecture, and changes in soleus muscle architecture with passive lengthening. Go to:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5910694/ #:~:text=Average%20fascicle%20lengths%20in %20the,51%20mm%20between%20individuals%20(Fig.

 tendon architecture (e.g. cross-sectional area, tendon and/or musculotendinous junction length), The Achilles is the strongest and largest tendinous structure in the body. It is defined anatomically as the distal confluence of the gastrocnemius and soleus muscles and may also include the plantaris longus1 (Fig. 1). During activity, the Achilles tendon can bear loads in excess of 3500 N2,3, yet despite its tremendous strength, is frequently injured. Acute and chronic Achilles tendon pathology is estimated to be responsible for as much as 50% of all sports-related injuries4. 75% of Achilles tendon ruptures occur in middle-aged men between the ages of 30 and 49 while participating in sport4–7 and the incidence is rising4, 6–8. The association of Achilles rupture with obesity, amongst a number of similarly trending parameters, may also play a role7. Chronic Achilles tendon injuries are generally defined by activity associated Achilles pain (e.g. swelling and tenderness) in conjunction with impaired performance during sporting activity4, and asymptomatic degeneration may occur in 4% of active adults9,10. Rare causes of Achilles tendon rupture include fluoroquinalone-induced ruptures (0.02–2.0%) and those associated with systemic disease (2.0%)4,7,11.

Defining baseline compositional properties for normal tendon is necessary to set appropriate benchmarks for healing and to determine appropriate strategies for successful functional tissue engineering. Unfortunately, basic Achilles tendon compositional data is currently lacking, with the most thorough compositional studies performed using flexor tendons. As an extrapolation from data in other systems, Achilles tendons are thought to be composed of approximately 90% type I collagen that forms a hierarchical structure of fibrils, fibers, and fascicles bound together by small matrix molecules, such as proteoglycans29. The Achilles tendon insertion is composed of types II, IX, and X collagen, with type X collagen localized in the mineralized zone and type IX distributed throughout30. Although elastin only accounts for up to 2% of the tendon’s dry mass, recent studies have shown it makes important contributions to the mechanical properties of tendons31. Digestion of glycosaminoglycans has been shown to decrease tendon modulus and ultimate load specifically at the tendon insertion site, suggesting a regional variance in composition that may mirror regional differences in structure and mechanical performance32. Alterations in tendon structure and loading elicit biochemical changes that are exacerbated in cases of injury and healing. The structure of tendon directly relates to its mechanical function33. Baseline characterization of normal Achilles tendon structure is necessary to identify the mechanisms governing tendon injury and failure. Generally, tendon is an inhomogeneous, anisotropic, nonlinear34, fiber-reinforced, biocomposite material35 primarily composed of a collagen extracellular matrix36 and non-collagenous molecules. The dry weight of tendon is primarily composed of longitudinal collagen fibers that are believed to be the primary load bearing components in mature tissue37. At the most basic level, the collagen fibers in tendon are highly organized structures that demonstrate high strength in the direction of fiber

alignment36. Under polarized light, tendons exhibit periodic banding due to its waveform configuration known as “crimp”. This property extends down in a hierarchical fashion from macro- to nano-structural scales38. When initially loaded, the force-displacement curve demonstrates a distinct nonlinearity or “toe region” that arises from uncrimping and an associated increase in collagen alignment39. This concept is supported by the observed decrease in crimp frequency and amplitude in loaded Achilles tendons38. Glycosaminoglycans (GAGs) and structural proteins, such as elastin31, connect adjacent fibrils. Such molecules may play a role in tendon structure-function relationships, though their specific role requires further elucidation31,37. Disruption to any of these load bearing elements may be detrimental to physiologic function, potentially leading to injury and failure. Ultimately, Achilles tendon mechanical properties govern the tendon’s ability to respond and adapt to its loading environment. Achilles tendon mechanical nonlinearity is shown through its stress strain curve at low strains40. At higher strains, Achilles tendons deform linearly prior to yield and rupture. Although the Achilles tendon is commonly referred to as a viscoelastic material containing both elastic (stress and strain occur in phase) and viscous (90 degree phase difference between stress and strain) components that store and release energy during loading to protect soft tissues from being damaged41, recent evidence in humans has suggested that its elastic properties dominate42. These elastic spring-like properties allow the Achilles tendon to deliver explosive propulsion during ambulation as they may bear up to 3500 N before rupture2. Aside from cases of injury, Achilles tendon mechanical properties may be influenced by genetics43, development44, and aging45. Several studies have used conventional quasi-static methods to evaluate tendon mechanical properties46,47. However, given that the Achilles tendon typically performs at high and repetitive loads at or near failure, the clinical relevance of utilizing fatigue testing becomes increasingly important. Cadaveric and animal studies have shown that the response of tendon to fatigue loading is marked by three phases of damage48. In particular, stiffness initially increases, reaches a maximum, and then gradually decreases. This gradual decrease in stiffness is attributed to accumulated sub-rupture damage, which ultimately leads to the dramatic increase in peak deformation and decrease in stiffness prior to failure48–50. Interestingly, measured tendon fatigue in vivo in humans51,52 has been less than that observed in vivo or ex vivo in animals53. Future work is necessary to fully evaluate this mechanism since these studies were not designed to control for the loads evaluated, which affects ex vivo fatigue damage54.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4187594/ #:~:text=As%20an%20extrapolation%20from %20data,molecules%2C%20such%20as%20proteoglycans29.

The Achilles tendon is a tough band of fibrous tissue that connects the calf muscles to the heel bone (calcaneus). The Achilles tendon is also called the calcaneal tendon.

The gastrocnemius and soleus muscles (calf muscles) unite into one band of tissue, which becomes the Achilles tendon at the low end of the calf. The Achilles tendon then inserts into the calcaneus. Small sacs of fluid called bursae cushion the Achilles tendon at the heel. The Achilles tendon is the largest and strongest tendon in the body. When the calf muscles flex, the Achilles tendon pulls on the heel. This movement allows us to stand on our toes when walking, running, or jumping. Despite its strength, the Achilles tendon is also vulnerable to injury, due to its limited blood supply and the high tensions placed on it. https://www.webmd.com/fitness-exercise/picture-of-the-achilles-tendon#1

Tendons are able to adapt their properties to meet the needs placed upon them (7, 15, 20). The Achilles tendon cross sectional area (CSA) has increased in response to an increased load during military training (13). A heavy loaded exercise regimen led to mechanically stronger and hypertrophic tendon in an animal model (20). These examples of tendon remodeling and adaptation indicates a metabolically active tissue, especially during exercise, that enables tendons to interact with muscle and contribute to muscle performance and movement (12). The cause of tendon remodeling in response to running, leading to changes in Achilles cross sectional area (CSA), is still speculated because of conflicting research findings. Running has caused Achilles tendon CSA to increase (12), decrease (14, 19), and remain unchanged (5). However, subject population, running conditions, and running distances varied in these studies. Magnusson et al (12) showed that habitual runners have a larger CSA of the Achilles tendon compared to non-runners. Decreases in Achilles tendon CSA w...


Similar Free PDFs