A The concentric muscle contraction starts as

A muscular contraction is when either the tension present within the muscle is changed or the length of the muscle changes, exemplifying isometric contractions, as the tension changes but the length does not. Specifically, a concentric muscular contraction is when the muscle contracts, meaning the tension that is generated causes the muscle to shorten. This is important because concentric contractions allow for movement to occur while playing a role in locomotion as well.
The concentric muscle contraction starts as a stimulus that triggers a message to (afferent signal) and from (efferent signal) the brain. Once the brain has received the afferent signal, it sends an efferent signal, in the form of an electrical impulse down the PNS (Peripheral Nervous System) and towards the neuromuscular junction, whereby excitation can occur. The whole dynamic of the efferent motor neurons and the muscles fibres is known as a motor unit – a motor unit consists of an alpha motor neuron alongside all muscle fibres that are invigorated by it (Maughan, 2009).
Once the efferent neuronal signal has reached the neuromuscular junction, excitation occurs. Firstly, the nervous signal would open up the calcium channels on the presynaptic membrane of the synaptic knob, which then triggers the process of exocytosis to occur – a form of active transport that allows for the contents of a cell to be released. Within this instance, the exocytosis would occur to the vesicles of the synaptic knob that encapsulate the neurotransmitter, acetylcholine (ACh), thus allowing ACh to be released into the synaptic cleft. 2 of these ACh molecules would then bind to structures that are known as AChR – acetylcholine receptors (Newsom-Davis, 1991) on the post synaptic membrane, resulting in the opening of voltage-gated sodium (Na+) and voltage-gated potassium (K+) channels as the ACh causes depolarisation to occur at the motor end-plate. The influx of sodium ions that enter the cell causes depolarization of the resting membrane potential because of the imbalance of charges that occurs, consequently, starting off the action potential – the change of electrical potential along a given membrane, in this case, the neuron (presynaptic membrane) and then the action potential is passed to the muscle fibre (postsynaptic membrane) via the neuromuscular junction (motor end-plate). When contact is made with the neuromuscular junction, the voltage change that is present at the end of the neuron would enable the opening of voltage-gated channels, resulting in the propagation of the action potential and the innovation of a muscle fibre.
After excitation occurs, the excitation-contraction coupling would carry on the contraction process, whereby the action potential would continue to propagate from the neuromuscular junction, where the axon terminals attach, down the sarcolemma of the muscle fibre. Due to the structure of the transverse tubules, A.K.A t-tubules, they penetrate from the inside of a myofibril to the sarcolemma, therefore, allowing the action potential to be picked up and carried down, from the muscle fibre to the individual myofibrils. Then voltage-gated ion channels within the t-tubules would open, causing a counter effect and resulting in calcium (Ca2+) gates being opened in the sarcoplasmic reticulum. After being released from the terminal cisternae, these Ca2+ molecules would enter the cytosol, which is the intracellular fluid and they would travel down the t-tubules until they reach the contractile units that are known as the sarcomeres within myofibrils. A structure known as the triad is created by the alignment of 2 cisternae either side of a t-tubule (Frontera and Ochala, 2014). The Ca2+ would then bind to troponin within the thin filament (actin, that attaches to the Z-lines of the sarcomere), thus, causing tropomyosin to undergo a conformational change – change in shape, resulting in the active binding sites on actin becoming exposed (Zhang et al., 2011).
For contraction to occur, there needs to be an energy source and this is where the commonly known, ATP (adenosine tri-phosphate) becomes useful. The ATP within the muscle cells goes through a process of hydrolysis, caused and catalysed by the enzyme myosin ATPase, resulting in the breakdown of ATP to ADP (adenosine di-phosphate) and Pi (phosphate) with the release of energy. This energy then allows the myosin heads to bind to the exposed actin sites, meaning they are ‘cocking’ in an extended position and this process may also be referred to as the cross-bridge formation, specifically myosin-actin cross-bridge. Next, the power stroke occurs, whereby the myosin head pulls the actin filament past the myosin filament, rotating the cross bridge towards the M line of the sarcomere, due to the fact that the I bands on both sides and the H zone in the centre are shortening. simultaneously, the ADP and Pi is release from the myosin heads. As more ATP molecules are bound to the myosin heads, it can then release from actin and the whole process of the sliding filament theory can be repeated, upon a short phase of relaxation. Some of the structures within the sarcomere that help with the concentric contraction of a muscle are nebulin and titin. Nebulin has multiple roles and these include the facts that it stiffens the thin filament, promotes thin filament activation, and enhances cross-bridge recruitment (Kiss et al., 2018), all of which help with the process of the sliding filament theory. Alternatively, titin’s structure can be described as spring-like since the main role of this protein is to deal with the stress that occurs at the sarcomere, while aiding with the shortening and lengthening of the actin and myosin filaments that occurs during contraction and relaxation.
In basic, the sliding filament theory means that the sarcomeres are shortening and because each myofibril is made up of many of these contractile units, it allows for the backwards reaction of muscular contraction to occur, until it reaches the tendon and movement occurs at a joint.
For contraction to occur again, it would be necessary for a short relaxation phase to occur to facilitate the refractoriness nature of neurons, whereby, they are unable to allow another signal to be passed down them again for a millisecond. This refractory period is split up into 2 parts, these are known as the absolute refractory period that occurs during phases of depolarization and repolarization and the relative refractory period that occurs during hyperpolarization. These repeated contractions of muscle fibres would stop being repeated once they are no longer being stimulated by the motor neurons or when the supply of ATP has been depleted.
If any of the stages of muscular contraction, including anything from excitation, excitation-contraction coupling, contraction (sliding filament theory) or relaxation is interrupted, it will inhibit the muscles’ ability to function properly to a variety of degrees depending upon the degree of interruption.