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Part 1:
The conscious thought of voluntary muscle movement occurs in the cerebral cortex, in the frontal lobe portion. Once the conscious thought is formed, it transmits the signals via action potential in the appropriate neurons. The signals are transferred to the thalamus, which relays motor information, and cerebellum, which coordinates motor movements. All of which is takes place in the central nervous system. The action potentials are then sent via neurons that control the muscle fibers responsible for the desired movements. The neurons that relay information to the muscles pass through the spinal cord via nerves. The neurons involved in our desired actions belong to radial, axillary, sciatic, and femoral nerves. Subsequently, the information is transmitted to the muscle fibers, which cause the contractions of the appropriate muscles. This latter part of the signaling takes place within the peripheral nervous system.
Part 2:
Whether an action potential would begin in the postsynaptic neuron depends on the strength of the signal from the presynaptic neurons. The signals, which can accumulate via temporal or spatial summation, are transmitted from the synaptic terminal of the presynaptic neuron to the postsynaptic membrane of the dendrites of the postsynaptic neurons. A typical neurotransmitter used between two neurons is acetylcholine. Binding of neurotransmitter at the postsynaptic membrane can cause graded potentials, via either depolarization or repolarization. In case of acetylcholine, binding of acetylcholine causes graded potential via depolarization. If depolarization reaches a threshold, an action potential is generated in the axon hillock. At this point, voltage gated sodium channels open, and sodium ions rush into the cell. The action potential then is transmitted down the axon, further opening voltage gated sodium channels (once enough sodium enters the cell, voltage gated sodium channel closes and potassium channel opens, which allow potassium ions to exit the cell, which allows the cell to return to the resting state). In myelinated neurons, salutatory propagation may occur. In either case, once the action potential reaches the synaptic cleft, calcium ions enter the synaptic cleft, which trigger exocytosis of neurotransmitter (in our case acetylcholine). Acetylcholine, then, can bind to the postsynaptic membrane of the postsynaptic neuron to generate graded potential. If enough graded potential is generated, another action potential results.
When the neuron is connected to a muscle, postsynaptic membrane is replaced with neuromuscular junction. In this case, the neurotransmitter used is always acetylcholine. Acetylcholine, like before, binds to the neuromuscular junction causing a depolarization. Enough depolarization (threshold) causes the sarcoplasmic reticulum to release calcium ions. Then, the calcium ions activate the muscle and cause them the contract.
Part 3:
Sliding filament theory is based on the observation that the muscle fibers are composed of two kinds of filaments: thick filaments and thin filaments. Muscle fibers are composed of repeating units of sarcomere. Each sarcomere contains overlapping thick and thin filaments. In the middle of the sarcomere are thick filaments, which makes up the A band. The length of the A band does not change during contraction. The thin filaments are interlaced between the thick filaments and also overlap with the lateral portion of the thick filaments. The area of overlap is called the zone of overlap. The myosin head of the thin filament can bind to the active site of the thick filament. The contraction of the muscle requires, then, movement of the thin filaments toward the thick filament medially. This is where the calcium ions are required. Calcium ions can bind to troponin, a molecule on the thick filament near the active sites where myosin head of the thin filament can potentially bind. Due to binding of calcium, troponin changes shape and moves the active site so that it can interact with myosin head of the thin filament. Further, ATP is required for the “power stroke” of the myosin head, which can then move toward the center of the sarcomere. When another ATP binds to the myosin head, the active site and myosin head of the thin filament detach. Because of this, the active site is able to form another cross bridge, allowing further muscle contraction. Hence, during the muscle contraction the zone of overlap lengthens while the H zone, the part of sacromere composed of thick filament only shortens.
Part 4:
The iliacus muscle contracts, pulling on the femur distal to lesser trochanter (the insertion point of the iliacus), causing the flexion of the hip joint, which is a type of ball-and-socket diarthrosis joint. Also, contraction of tensor fasciae latae and psosas major pull on the iliotibial tract (the insertion point of tensor fasciae latae) and lesser trochanter (the insertion point of psosas major), respectively, causing the flexion of the hip joint (again, a ball-and-socket joint). Further, Sartorius muscle pulls on the medial surface of the tibia near the tibial tuberosity (the insertion point of Sartorius), causing flexion of the knee joint, which is a hinge type of synovial joint. These muscle contractions are involved in lifting of the leg above the step. Next, the leg needs to extend toward the ground surface of the step to lift the rest of the body above the step. So the contraction of the gluteus maximus, pulling on the iliotibial tract and gluteal tuberosity of femur (the insertion points of gluteus maximus), causes the extension of the hip joint, which is a ball-and-socket type of diarthrosis joint.
Part 5:
The deltoid muscle contracts, pulling on the deltoid tuberosity of humerus (the insertion point of deltoid muscle) to cause extension of the shoulder (glenohumeral) joint which is a ball-and-socket type of diarthrosis joint. Also teres major and latissimus dorsi pull on medial lip of intertubercular groove of humerus (the insertion point of teres major) and the floor of intertubercular groove of the humerus (the insertion point of the latissimus dorsi), respectively, to cause extension of the shoulder joint (again, ball-and-socket, diarthrosis).
Also, contraction of biceps brachii pulls on the tuberosity of radius (the insertion point of the biceps brachii) to supinate the elbow joint, which is a hinge type of diarthrosis joint. Similarly, Supinator pulls on the anterolateral surface of radius distal (the insertion point of the supinator), to cause a supination of the elbow joint (hinge type of diarthrosis).
Please mark this as solved if you have no further questions.
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