The process of concentric contraction within skeletal muscle
Skeletal muscle is highly important for the body’s support and mobility. It regulates the internal environment and externally brings about movement, typically via voluntary contractions (Marieb ; Hoehn, 2016). A total of 660 skeletal muscles are attached to the bones via tendons formed at the myotendinous junctions, complex specialized regions situated at the muscle-tendon crossing points, to bring about movement (Charvet, Ruggiero ; Le-Guellec, 2012). They account for approximately 40% of overall body weight (Frontera ; Ochala, 2014).
The process of concentric contraction
With almost any action conducted by the body, the brain is the starting point. It sends a signal for contraction to the central nervous system via electrical impulses which then travel along the motor neurons, towards the muscles. As the axon (a thread-like impulse conductor) of a motor neuron reach a muscle that it innervates, they branch off forming synapses known as neuromuscular junctions, connecting to individual muscle fibres (Arrowsmith, 2007). The synapse consists of a pre-synaptic end (where neurotransmitters are made), post-synaptic end (contains neuroreceptors) and a synaptic cleft (a minute space). When the action potential, a transfer of electrical signal from the nerves to the muscle, propagates down the branches of one axon, it forms a motor unit; the multiple fibres connected to a single motor neuron, that contracts in response to action potential. The neuromuscular junction then receives this action potential, causing the axon terminal to release a neurotransmitter (acetylcholine (ACh)). This causes the voltage-gated calcium channels to open and release calcium ions to increase intracellular calcium levels. Thereafter synaptic vesicles fuse with the cell membrane and release neurotransmitter chemicals via exocytosis (Südhof, 2012). These molecules then diffuse through the synaptic cleft and bind to ACh receptors located within the motor end-plate of the sarcolemma (a binding sheath forming the plasma membrane). A channel is opened to allow positive ions to enter the fibres and causing them to depolarise. This leads to the membrane potential decreasing in negativity. As this occurs, voltage-gated sodium channels are stimulated to open, allowing sodium ions to enter and spread the action potential quickly across the sarcolemma which initiates excitation-contraction coupling. The membrane repolarises to regain a negative potential via excitability which is a property of muscle in which the electrical state of plasma membrane is altered between polarised and depolarised (Lieber, 2002). ACh within the synaptic cleft is then degraded via an enzyme called acetylcholinesterase to prevent them from rebinding to receptors and causing unnecessary excitation (OpenStax College, 2013). Action potential is then sent down the transverse tubules (t-tubules), which are narrow tubes that extend at ninety degrees into the sarcoplasm to the muscle fibre itself. The action potentials travel along extracellular fluid within the T-tubules which form passageways deep into the muscle fibres. The electrical signal is converted to a contraction signal known as excitation-contraction coupling (Jones, Round ; Haan, 2004). Thereafter, the t-tubular system signals the sarcoplasmic reticulum (SR) – a calcium storage bag that encloses myofibrils – that the fibre has been activated thus releases calcium, initiating the interaction of actin and myosin filaments (Davies, Blakeley ; Kidd, 2001).
These filaments are found in the sarcomere (myofibrils crucial for contraction) where the action potential is sent for this to occur. The sarcomere is a striated structure formed by the thick (a dark ‘A-band’) and thin (a light ‘I-band’) filaments as a result of their size, density and distribution, separated by the ‘M-line’. The I band consists of thin actin filaments, extending from the A-band of one sarcomere to the A-band of another. The boundary between 2 adjacent sarcomeres are marked by a ‘Z-line’. Thick filaments are formed by 2 protein strands twisted together with a globular head found at each end (Lieber, 2002).
After the release of calcium, it binds to troponin which is one of three proteins found within the thin filament along with actin and tropomyosin. Troponin is split into three sub units; Tn-I, Tn-C and TN-T. It holds the tropomyosin in place to cover the binding sites for myosin cross-bridges on actin. Tn-t is saturated by calcium thus causing the troponin to alter the shape of tropomyosin. When the shape is altered, ultimately the tropmyosin molecules penetrate deeper into the groove between two actin chains allowing the biding sites to open. This results in a strong bond between actin and myosin as myosin attaches to the exposed actin forming a crossbridge which penetrates the contraction cycle (Davies, Blakeley ; Kidd, 2001).
This interaction of filaments is further discussed via the sliding filament theory. For the actin and myosin to attach at the opened site, Adenosine triphosphate (ATP) hydrolysis takes place. This is the process by which ATP, in the myosin head, splits by combining with water thus forming Adenosine diphosphate (ADP) and phosphate (P) as a result. Energy is produced by this, allowing the myosin head to become reoriented and twist, stretching the elastic component of the shaft (Chalovich, 2002). Thereafter, the actual crossbridge is formed as the myosin heads bind to the actin, as they now have energy to do so, via the opened binding site created by the increase of calcium. The power-stroke is the next step which involves the myosin cross-bridges formed to move towards the centre of the sarcomere. The myosin heads are responsible for this as the elastic component retracts to pull the actin filament and drag them to create an overlapping of filaments. The thin filament slides past the thick filament generating tension by which the Z-line and M-line are forced to come closer together hence creating a shortening in length of the muscle fibres, producing concentric contraction (Krans, 2010). ADP and P are released through this, which causes detachment between the actin and myosin filaments and free the inactivating site for another molecule of ATP. Arrival of the new ATP within the crossbridge head releases the bond with the actin filament which leads to two pathways, dependant on calcium stores and ATP stores. If there is still a high level of calcium and ATP, the binding sites are still exposed to attachment and so the cycle continues. If, however, the Calcium is reabsorbed into the SR, the ATP is inefficiently hydrolysed thus preventing strong bindings preventing contraction (Krans, 2010).
From the process we can see the importance of calcium in allowing the contraction to occur. Calcium stores are released through the stimulations within excitation-contraction coupling while the crossbridge cycle is reliant on its presence to initiate and produce the actual contraction. Ultimately contraction is required for movement and stability which are the primary functions of skeletal muscle.