Myotatic Muscle Contraction

Actin and myosin filaments can be found in skeletal muscle and are the smallest units that form a sarcomere, which is the smallest contractile unit in muscle (Baechle, 2008). The Sliding Filament Theory states that the actin filaments slide inward on the myosin filaments, pulling on the boundaries of the sarcomere, causing it to shorten the muscle fiber, also known as a concentric muscular contraction (Baechle, 2008). The Sliding Filament Theory is composed of five steps: the “Resting Phase”, the “Excitation-Contraction Coupling Phase”, the “Contraction Phase”, the “Recharge Phase”, and the “Relaxation Phase” (Baechle, 2008). During the Resting Phase, the actin and myosin filaments are lined up with no cross-bridge binding of the two filaments. During the Excitation-Contraction Coupling Phase, Calcium is released from the sarcoplasmic reticulum and binds to troponin, causing a shift in tropomyosin where the binding cites are exposed (Baechle, 2008). When the binding cites are exposed, the myosin cross-bridge head attaches to actin. During the Contraction Phase, ATP bonds break, releasing energy that is used to allow the myosin head to flex, causing the actin filaments to move toward the M-bridge. During the Recharge Phase, there is a continuous repetition of the Excitation-Contraction Coupling Phase and the Contraction Phase in order to produce muscular

A simple spinal reflex is a reflex—involuntary, graded, patterned response to a stimulus—that is produced via a single synapse between sensory axons and motor neurons and confined to the spinal cord. In this experiment, two simple spinal reflexes—the myotactic reflex and the H-reflex—were stimulated. We compared a) the latency period—the amount of time between a stimulus and the effector response— and the amplitude—magnitude of an electrical signal—of each reflex; then, b) the effect of the Jendrassik Maneuver (JM) upon the latency period and amplitude of each respective reflex. For the myotactic response, a mechanical stimulus, a sharp strike of the patellar tendon, was utilized to elicit a signal in stretch receptors; however, to trigger the H-reflex, an electrical impulse was applied. These reflexes originate from an action potential produced by a sensory neuron when a stimulus is applied. Sensory neurons transmit the action potentials to an integrating center—the spinal cord—where a response is determined. Then, this response is taken back to the effector organ via motor neurons. The reflex occurs while the brain is becoming aware of the stimulus. Furthermore, the myotactic reflex is

Muscle contraction can be understood as the consequence of a process of transmission of action potentials from one neuron to another. A chemical called acetylcholine is the neurotransmitter released from the presynaptic neuron. As the postsynaptic cells on the muscle cell membrane receive the acetylcholine, the channels for the cations sodium and potassium are opened. These cations produce a net depolarization of the cell membrane and this electrical signal travels along the muscle fibers. Through the movement of calcium ions, the muscle action potential is taken into actual muscle contraction with the interaction of two types of proteins, actin and myosin.

Afferent muscle stretch reflexes are initiated from muscle spindles9. Other afferent receptors such as joint receptors and skin sensors can generate further input8. The sum of these inputs results in reflexive movement in the absence of efferent signals from higher cortical centers7. Afferent neural input from the muscle spindle stretch receptors connected to the muslces intrafusal fibers enters the spinal cord through the dorsal horn9. They are then capable of diverging in order to take different paths and elicit several coordinated responses to a single stimulus9. The patellar reflex is a monosynaptic stretch reflex because the afferent signals synapse directly onto a motor neuron in the spinal cord9. Tapping the tendon pushes on the tissue, which activates stretch receptors within the muscle9. These afferent neural inputs from the receptors send excitatory action potentials to motor neurons in the spinal cord which, elicit the contraction of the quadriceps, extending the lower leg outwards to compensate for the stretch stimulus experienced9. In contrast, in a polysynaptic pathway, the stretch stimuli send afferent signals to the spinal cord that synapse onto inhibitory interneurons, eliciting the inhibition the antagonist (the hamstrings)9. This reciprocal innervation of the agonist and antagonist allows for the appropriate levels of tension to be developed in both muscles to elicit a smooth coordinated

As Lyn D. Weiss et al. (2016) states in Easy EMG: A Guide to Performing Nerve Conduction Studies and Electromyography, the neuromuscular junction is the relay between the nerve terminal and the skeletal muscle fiber. The neuromuscular junction as a whole is the site where the neurons activate the muscle to actually contract. The steps of the neuromuscular junction are supposed to happen quickly and accurately while ensuring voluntary movement of the muscles. The reliability of transmission is aided by specialized architecture (multiple active zones, junctional folds), which has been all studied more closely throughout the last century (Hong and Etherington, 2011). According to “Annual Review of Neuroscience,” the NMJ forms in a series of steps that involve the exchange of signals amid its three important cellular components—nerve terminal, muscle fiber, and Schwann cell (Cowan, 1999). All three cells of the neuromuscular junction travel long distances to meet at the synapse(Cowan,

Facilitation occurs when postsynaptic potentials evoked by a stimulus are increased when that stimulus closely follows a pervious stimulus. Five stimulus pulses were given at decreasing interpulse intervals. The data for this experimenet displays that when the interpulse interval changes from 10msec to 8 msec, the number of pulses needed to reach the maximum MAP increases rather than the expexted outcome. This is most likely due to movement of the muscle in the chamber, causing the recordings to be reading different areas of the muscle. Different neuromuscular junctions in the muscle require different amounts of Ach in order for muscle action potentials to reach threshold.

Summary… A condition which is characterized by an inability of the muscles to function at their full strength; a vague complaint of debility, fatigue, or exhaustion attributable to weakness of various muscles. The weakness can be characterized as subacute or chronic, often progressive, and is a manifestation of many muscle and neuromuscular diseases.

This reflex has a short delay between the actual stretching of the muscles and when the reflex contraction occurs because of the monosynaptic pathway (Kam and Power, 2015). The monosynaptic pathway is the simplest reflex where there is only a single synapse between two different neurons (Alters, 2000). There is a sensory afferent neuron and an efferent somatic motor neuron present (Alters, 2000). When a receptor detects an internal or external stimuli from a receptor cell, this information will be sent to the sensory neuron which will convey the information to the brain or spinal cord (Alters, 2000). Then, it will move on to the motor neuron which will conduct the motor output and send it to the effector, which would be the muscle (Alters, 2000). When it reaches the muscle, a response will occur producing a

The neuromuscular junction is where the nerve meets our muscles. To be able to move, we would need an impulse sent from our brain to our muscles. The nerve impulse gets sent to our muscles from the CNS, which leads to our muscles contracting. The nervous impulse that’s sent to the CNS is called the action potential, the impulse that sends a signal to our muscles is known as the motor neurones. For our muscles to contract we need a nervous impulse, the end of our nerves are called the synaptic knob, this hits the vesicles and releases acetylcholine. The acetylcholine then goes through the cleft (the gap between the synaptic knob and the muscle) and tells the muscles to contract, if it doesn’t go through the cleft our muscles will not contract, this is

In order for any sort of action to occur within a human body, or most any living body, neurons must send and receive signals to other cells within the body. Those signals, sent in the form of action potentials down the axon of a neuron, eventually reach their destination and typically cause a chemical or electrical change in the system being reached. In the case of a muscle fiber, a depolarization occurs, otherwise known as an excitation, and this excitation leads to the contraction of the muscle fiber (Hill et al, 2012). From this, physiologists coined the phenomenon excitation-contraction coupling. There are numerous steps involved in the overall process, with many variables that can adapt and change how the contraction occurs. One major aspect of the overall process is the

A nerve impulse travels to the neuromuscular junction on a muscle cell. The neuromuscular junction is the point where the axons of the nerve meet with the muscle cell.

These muscles requires actin filaments and myosin filaments interacting with each other in-order for movement. [1] The myosin are aligned between the actin and muscle contraction is brought through the sliding of the two filaments. The myosin head can tightly bind to the place on the actin molecule but generally there are other proteins which prevent the binding called tropomyosin (form a filament which semi curve around the myosin where the actin would possibly bind) and troponin (variety of different proteins).[2] Naturally ATP has bounded to the myosin head and when this happens the energy is slit into ADP and phosphate, however both would still remain attached to myosin. The tropomyosin is coving the binding place for myosin to attach to

Skeletal muscles are highly complex and heterogeneous tissues, serving a multitude of functions in different organisms. The process of generating muscle myogenesis can be divided into several distinct phases [40]. Ubiquitin-mediated protein degradation is one of the main mechanisms for controlling proteolysis, which is crucial for muscle development and maintenance. Recently notch signaling has appeared as a key player in skeletal muscle development and regeneration. Simply stated, Notch signaling inhibits differentiation. Accordingly, fine-tuning the pathway is essential for proper muscle homeostasis.Less is known regarding the functions of ASB proteins in muscle development, although various ASB proteins are found to be expressed in the skeletal

Muscles; the way we get around. With smooth muscle gripping bones, creating movement with electric current. Electrical signals flow from the brain down the spinal cord to open the calcium floodgates. With the flow of calcium, the muscles contract, and because they’re attached to bones, the flow of calcium leads to muscles pulling on the bones, which cause movement. While the contraction of muscles starts from the brain to get muscles to move from either slightly or greatly, electricity can be used instead of the brain to create movement.

Philosopher Kwame Gyekye defines the human affairs that means the experience of human beings. To distinguish relevant information and to dissect human activities, “essential universalism” and “contingent universalism” are defined its components and purpose with the limited discernment of humans and their undertakings.