Muscle Contraction Essay

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Studying the human body is an intimate academic exercise – my fingers move in response to messages sent through my nervous system and words appear on the page.
Either side of the divide - the neuromuscular junction
In order for motor neurons to communicate with the skeletal muscle fibres of my fingers, a synapse is formed between them, known as a neuromuscular junction.
The neural and muscular sides of the NMJ have different roles to play. The motor neuron’s axon terminal, along which nerve impulses travel, ends in a series of synaptic end bulbs, full of synaptic vesicles, floating in cytosol. Within these vesicles are the precious messengers, molecules of the neurotransmittor, acetycholine (ACh).
Across the synaptic cleft, we find the motor
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They are made of different proteins. The proteins involved in excitation-coupling are myosin and actin. They are known as contractile proteins as they are the powerhouse of muscle contraction. Myosin is further known as a motor protein due to its role in the generation of force by conversion of ATP, a chemical, into mechanical energy. Structurally it differs from actin, being thicker and therefore forming the thick muscle filaments. Each molecule is described as being “shaped like two golf clubs twisted together” (Tortora and Derrickon, 2011), with the tail facing the M line that appears at the centre of the sarcomere. Actin is thinner and its molecules come together in a twisted helix shape to form the thin filaments that come from the Z disc of the sarcomere. What is important to note here is that every actin molecule has its own myosin binding site. This means that the myosin heads, the “golf club” like structures depicted earlier, can attach themselves to the actin – it is this action that causes muscle contraction as we shall see.
As well as contractile proteins, muscles also have structural proteins which give stability and elasticity. Regulatory proteins are involved in the control of muscle action. These form part of the thin filament with actin. Another regulatory protein, troponin, holds the tropomyosin in place. When a muscle contracts, troponin pulls the tropomyosin away from the myosin binding site
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ATP hydrolysis energises the myosin, allowing it to form a crossbridge with the actin. During this process, the phosphate group is detached. The myosin crossbridge swivels and pulls towards the centre of the sarcomere. This powerstroke powerstroke causes the eponymous sliding filament mechanism. As this is happening, the site that binds the ADP on the myosin opens and releases the ADP. It is not until an ATP molecule binds again to the myosin that it releases itself from the actin. The ATPase once more hydrolyzes the ATP and the cycle continues as long as it has sufficient ATP to drive it and a sufficiently high level of Ca2+ around the thin filament.

As the muscle cell shortens, the Z discs are drawn together by the sliding filaments. This in turn pulls on surrounding sarcomeres and generates a larger contraction across the whole muscle fibre.
The force potential of a muscle is determined by the number of action potentials that arrive at the NMJ. To maximise this, oxygen and nutrients are needed. Force potential is also increased when the initial overlap of filaments is optimal, and “extends from the edge of the H zone to one end of a thick filament”.
The axon of a motor neuron can form NMJs with different muscle fibres. These multiple motor units may be recruited, depending on the size and nature of the muscle action needed. The weakest motor units are

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