Functional Structure Of Skeletal Muscle
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Muscle makes up the largest group of tissues within the body, roughly half the body's weight (Sherwood). Skeletal muscle is attached to the bones of the skeleton and through its highly developed ability contract, produces movement at joints. A controlled contraction of the muscle enables purposeful movements of the body and manipulation of objects (Sherwood).
First it is important to understand the structure of the muscle and how it functions. We will then discuss the factors that control normal growth and repair in the muscle, and lastly explore how muscle atrophy results from not using a muscle.
A skeletal muscle is made up of muscle and connective tissues, which both play a role in the contracting and function of the muscle. A single cell of a skeletal muscle is called a muscle fiber, the muscle is made up of groups /bundles of these muscle fibers bound together by fibrous connective tissue, and each bundle is called a fasciculus (muscles nerves movement). Another layer of connective tissue binds the fascicule together and the whole muscle is surrounded by an outer layer of connective tissue. (M<N<M).
Muscle fibers are long and cylindrical in shape, usually extending the whole length of a muscle. They contain multiple nuclei, which come from the fusion of smaller cells during development and formation (ezeilo and Sherwood). These nuclei lie beneath a cell membrane called the sacrolemma (ezeilo). The cytoplasm, which is known as sarcoplasm, is filled with numerous bundles of contractile proteins called myofibrils. The myofibrils contain many mitochondria, energy generating cells (ezeilo and Sherwood). Each myofibril consists of two types of myofilaments - namely, the thick filaments (containing the protein myosin) and the thin filaments (containing predominantly the protein actin, but also tropinin and tropomyosin).
Summary of the levels of organization in a skeletal muscle (Sherwood)
Whole muscle - muscle fiber - myofibril - thick and thin filaments - myosin and actin
A and I bands
When viewed under a light microscope, a myofibril shows dark (the A bands) and light (the I bands) bands alternating along its length. All the bands lie parallel to each other and together lead to the muscle fiber's striated appearance (ezeilo Sherwood). The thick and thin filaments are stacked in an alternating pattern which slightly overlaps each other, and this arrangement is responsible for the A and I bands (Sherwood).
An A band is made up of thick filaments and the sections of thin filament that overlap on both ends of the thick filaments. The thick filaments cover the width of the A band and are only found there. There is a lighter section in the centre of the A band, where there are no thin filaments, which is called the H zone. The middle portions of the thick filaments are found in this area and a network of supporting proteins holds the thick filaments together vertically. The supporting proteins are form the M line which is found in the centre of the A band within the middle of the H zone (Sherwood).
An I band consists of the section of thin filament that does not enter the A band, this means that an I band contains only thin filaments, but not the whole length of the filament (Sherwood). The Z line is the dense vertical section that's located in the centre of each I band. The portion in between two Z lines is called the sarcomere. A sarcomere is the functional unit of the muscle. "A functional unit of any organ is the smallest component that can perform all the functions of that organ" (Sherwood). Thus the sarcomere is the muscle fiber's smallest component that can perform a contraction. The Z line forms the connection between the thin filaments of two adjacent sarcomeres. A sarcomere is made up of the entire A band and the end portion of the I band on both ends.
Diagram A myofibril divided into two sarcomeres (sport-fitness-advisor.com)
The cross bridges are the section where the thick and thin filaments overlap. The thick filaments are surrounded by the thin filaments in a hexagonal pattern. In all six direction, the cross bridges extend from the thick filaments to the surrounding thin filaments. In addition, each thin filament then has 3 thick filaments around it. The cross bridges are significant in that the binding of the actin of the thin filaments and myosin of the thick filaments happens at the cross bridges, which produces a contraction of the muscle fiber (Sherwood).
Muscle contraction and cross bridges
Actin and myosin are sometimes referred to as contractile proteins but neither of them actually contract during a muscle contraction. In a relaxed fiber, muscle contraction cannot take place because of the position of the proteins, tropomyosin and tropinin of the thin filament (Sherwood).
Tropomysosin and tropinin are called regulatory proteins because they both play a role in stopping contraction from occurring or allowing contraction to take place by exposing the actin binding sites (Sherwood). Tropomyosin covers the sctin binding sites on the cross bridges thus blocking the interaction between myosin and actin which results in muscle contraction. Tropin is made up of 3 polypeptide units which bind to tropomyosin, actin and calcium. When troponin is not bound calcium, it stabilizes tropomyosin in the blocking of the actin sites on the cross bridges. When it is bound with calcium, the shape of the protein changes allowing tropomyosin to slide away, exposing the binding sites, and myosin and actin can bind at the cross bridges, resulting in a muscle contraction (Sherwood). Below is a diagram illustrating the position of the cross bridges, in a relaxed muscle and a contracted muscle.
+, power stroke, action potential- calcium link between excitation and contraction
Diagram 2: The sliding action of the cross bridges of a relaxed and contracted muscle respectively (www. teachpe.com)
Adaptation of muscles to functional use
One of the factors that determines the performance of a muscle is the type of muscle fibers within the muscle (N<M<M). The two main types are slow fibers and fast fibers.
Slow fibers are known as type I fibers. These fibers are specialized in order to sustain a contraction over a longer period of time (MNM). Within these fibers there is an extensive capillary network, which allows it to be oxygen rich. The slow fibers contain myoglobin which carries oxygen, and the fiber is thus red in colour. Energy for contraction is obtained mainly from oxidative reactions. These fibers make use of a slow twitch in response to stimulation and are thus resistant to fatigue. The slow fibers contain numerous mitochrondria which, because of the rich oxygen and blood supplies, can contribute more ATP during contraction. (MARTINI chp10).
Fast fibers are known as type II fibers. These fibers contain no myoglobin and are white in colour (MNM). These fibers are larger in diameter than the slow fibers and contain densely packed myofibrils, significant glycogen supplies and fewer mitochondria than slow fibers. The fast fibers use glycogen to obtain energy for contraction. They make use of a fast twitch and produce a powerful contraction; however they fatigue rapidly (MARTINI chp10). The fast fibers use large amounts of ATP during contraction and thus extended activity is supplemented by anaerobic metabolism.
Skeletal muscle is able to adapt its structure depending on the functional demands required over time (MNM). The quantity of sarcomeres within the myofibrils and the proportions of fast and slow fibers can adapt and change over a period of time. Depending on what is required of a muscle over a period of time, the fibers can adapt. In training for endurance, some of the fast fibers will adapt and become similar slow fibers and function more like them. During strength/resistance training, muscle bulk and strength is increased through increase in number and size of the myofibrils mainly within the fast fibers. In addition, when a muscle is held in a shortened length over a period of time the number of sarcomeres reduces, whereas if its held in a lengthened position the number increases. This is an adaptation to the length of a muscle that helps from a functional perspective (MNM).
Muscle growth and repair
"Muscle performance is influenced by turnover of contractile proteins. Production of new myofibrils and degradation of existing proteins is a delicate balance, which depending on the condition, can promote muscle growth or loss" (signaling atrophy and hypertrophy). The processes of protein synthesis and degradation are controlled by pathways that are affected by factors such as physical activity, mechanical loading, supply of nutrients and growth factors (signaling atrophy and hypertrophy.
Protein turnover and cell turnover are the two processes that play a large role in the growth of skeletal muscle mass. In an embryo, cell turnover is the process which plays the predominant role in muscle growth and development. During postnatal growth, the satellite cells (stem cells) are included into the growing fibers and at the same time protein synthesis increases (atrophy hypertrophy & sherwood). These satellite cells are significant in keeping the quantity of cytoplasm as well as the quantity of nuclei in the cytoplasm stable.
In adults, there is significantly less cellular turnover. An increase in muscle growth is done principally through amplified protein synthesis as well as a reduction in protein breakdown (atrophy hypertrophy).
GH - IGF1 -AKT
++ size fibers - contractile proteins into myofibrils - ++diameter
When a skeletal muscle is injured, it is necessary for specific cellular pathways to be activated in order to repair the injured tissue. Serrano and Munoz-Canoves stated that "activation and restriction of these pathways must be temporarily coordinated in a precise sequence as regeneration progresses if muscle integrity and homeostasis are to be restored" (Regulation and dysregulation).
After a skeletal muscle has been injured, a series of events happens concurrently to repair the muscle, these are initiated by the release of growth factors and cytokines from the damaged blood vessels and the penetrating inflammatory cells (Regulation and dysregulation). The initial phase of muscle regeneration is distinguished by necrosis of the injured tissue and the activation of the inflammatory response (cellular and molecular regeneration). The inflammatory cells that are released phagocytose the cell debris that is present following an injury.
The encouragement of the survival of various cell types, as well as the migration and proliferation of cells, is the role of the cytokines. Following this, there is a phase of regeneration, where there is the activation of myogenic cells which multiply, differentiate and finally fuse together resulting in the formation of new myofibers, as well as the reconstruction of the functional contractile components (cellular and molecular regeneration).. The satellite cells (stem cells) play a key role in this procedure. The satellite cells make use of the necrotic basement membrane as building blocks to guide the new fibers in forming the same pattern and ensuring that they lie in similar positions. The myoblasts fuse to each other as well as the damaged myofiber and thus form the new myofiber.
At the same time as this, matrix metalloproteases (MMPs) are at work. MMPs play a regulatory role with concerns to the extra cellular matrix formation, break down and remodeling (Role of MMP). The MMPs break down the necrotic base membrane components, which allows the satellite cells to migrate and differentiate in the area. In addition, angiogenesis is required to form a new vascular network within the injured muscle (regulation and dysregulation). The final stage of the muscle repair is when growth and maturation of the new muscle fiber takes place.
If any of these stages persist for longer than is necessary, the result may be unsuccessful muscle repair. Unsuccessful muscle repair is characterized by continued myofiber break down, inflammation and fibrosis, ultimately, extreme build up of the extra cellular matrix components (regulation and dysregulation). Elaborate?
Atrophy was defined by Macro Sandri as "a decrease in cell size mainly caused by loss of organelles, cytoplasm and proteins." (signaling in atrophy and dystrophy). If a muscle is immobilsed and not used for a period of time, the amount of actin and myosin within the skeletal muscle decreases, the muscle fibers decrease in size and the muscles mass reduces, along with the muscle's strength (Sherwood).
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