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1973). The interaction of the actin (thin) and myosin (thick) filaments govern muscle contraction and primarily establish the sarcomere complex, which is a collection of myofibrils that constitute the muscle fibre cell. These muscle fibre cells are the singular components contained in the fascicle, which together make up the muscle (Lieber, 2002). The skeletal muscle is connected to the rest of the bony skeletal system by tendons and co-ordinates with somatic nerve system stimuli. This hierarchical muscle structure is shown in detail in Figure 2.1 and Figure 2.2.
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Figure 2.1: Higher muscle organ to muscle fibre cell anatomical structure. Image adapted from: Myofibril complex physiology of a skeletal muscle fibre: PP 288-294. (2014)
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Figure 2.2: Lower skeletal muscle macro structure muscle fibril to myofilament anatomical structure. Image adapted from: Myofibril complex physiology of a skeletal muscle fibre: PP 288-294. (2014)
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From the above illustrations we can deduce that muscle tends to be a collaborated collection of tissue structures that allow for neural interaction and stimulation. This stimulation occurs at the neuro-muscular junction therefore allowing for the excitation of the ‘motor unit’. As muscle is generally orientated with its antagonistic counterpart, skeletal muscle is known to only actively ‘contract’ rather than extend; unless passively through its antagonistic partner.
The muscle contracts through a phenomenon called excitation-contraction coupling. The first stage of this cascade of events occurs from the arrival of an action potential from motor neurons and dendrite ends. This stimulates the detachment of a myosin head to actin fibril, which therefore allows for the myosin to bind to a new actin molecule forming a new cross-bridge (Widmaier, et al., 2010). Once the new cross-bridge is formed, the Adenosine Triphosphate (ATP) is hydrolysed by myosin, the process of which releases energy to allow for a partial bond with the actin. The hydrolysed myosin head contains Adenosine Diphosphate (ADP), an extra phosphate group and two Ca+2 ions. The remainder of the acting binding sight is blocked by tropomyosin, which leaves the troponin C to bind to the Ca+2 heads and the exposed ADP and Phosphate group. This troponin - Ca+2 complex causes the tropomyosin to slide over and release the rest of the actin binding site, which allows for the myosin heads to close and strongly bind to actin. This phenomenon results in the shortening of the actin-myosin complex (sarcomere); hence these cyclic occurrences result in further contraction of the sarcomere (Roger & Pearson, 2013). Due to the hierarchical architecture of muscle tissue, this contraction results in the shortening of the muscle fibres, and finally cascades to the contraction of muscle fibres – hence resulting in the contraction of the entire muscle that has been activated.
The macroscopic arrangement of muscles in this context is referred to as the muscle’s architecture (Ganz & Bock, 1965), and it is this that is the primary determinant of muscle function. Elucidating the structure-function relationship of muscle is therefore of great importance since it provides the physiological basis of force production and movement. Although much focus has been placed on factors such as fibre-type distribution in determining muscle function there is no question that muscle function is also strongly determined by its architecture and morphology (Burkholder et al., 1994). Skeletal muscle architecture can therefore be defined as “the arrangement of muscle fibres within a muscle relative to the axis of force generation” (Lieber, 2002).
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The next section discusses the physical processes that occur within muscle mechanics.
There are four types of contraction phenomenon, depending on the behaviour of the muscle when it contracts: concentric, eccentric, isometric and isotonic contraction. In concentric contraction, the length of the muscle shortens as it contracts, which follows the conventional belief of muscle contraction (Faulkner, 2003). In eccentric contraction the force generated is not enough to overcome external loads on muscles, which results in the muscle fibres lengthening as their antagonistic pairs contract (Colliander & Tesch, 1990; Nikolaidis et al., 2012). This type of contraction typically happens when the muscle is trying to decelerate a moving body (for example placing a body gently down rather than letting it fall). In this type of contraction, the muscle is thought to be resisting extension against an external force through contraction.
During isometric contraction, the muscle remains the same length, which is characteristic during passive exercise (for example when someone is simply holding up an object but not moving it through space). In this type of contraction, the muscular force generated is equal to the load therefore no movement/strain results from it. Conversely, in isotonic contraction the tension in the muscle remains constant despite a change in muscle length (Maton, 1981), which occurs when the muscle reaches its maximal plateau of force generated for contraction (Scherrer & Monod, 1960). A less common contraction phenomenon occurs when the contraction velocity of the muscle remains constant, whilst the force in the muscle varies (Guilhem et al., 2010). This contraction phenomenon is known as iso-velocity or isokinetic contraction. Tetanic contraction is the phenomenon of contraction where the muscle produces its maximum force at an optimal stretch range. Consequently, tetanic contraction applies to all the contraction phenomena described above, as it is a region within the operational force- length range of the muscle during contraction. Isokinetic muscle phenomena will be considered in this thesis, in order to limit viscous-elastic effects that are often observed
in vivo.
The active mechanics of the muscle originate from the action potential triggered event of muscle contraction, where a force is generated by the muscle. This has been studied by others but will not be covered comprehensively in this thesis - as this study