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In order to contract, a WHAT must: 1. Be stimulated by a nerve ending 2. Propagate an electrical current, or action potential, along the sarcolemma 3. Have a rise in intracellular Ca2+ levels. Final trigger for concentration
Linking electrical signal to contraction is called WHAT? It refers to the events that link the action potentials on the sarcolemma myofilaments, thereby preparing them to contract
Axons of WHAT branch profusely as they enter muscles. Each axonal branch forms a neuromuscular junction with a single muscle fiber.
Each terminal branch of the nerve fiber within the NMJ forms a separate synapse with the WHAT? (Each axonal branch forms a neuromuscular junction with a single muscle fiber) Thus, one nerve fiber stimulates the muscle fiber at several points within the NMJ
At each synapse, the nerve fiber ends in a bulbous swelling called a WHAT? The knob doesn't directly touch the muscle fiber but is separated from it by a narrow space called the synaptic cleft.
The synaptic knob doesn't directly touch the muscle fiber but is separated from it by a narrow space called the WHAT?
A third cell, called a WHAT, envelops the entire junction and isolates it from the surrounding tissue fluid.
The synaptic knob contains spheroidal organelles called WHAT, which are filled with a chemical called acetylcholine (ACh).
The synaptic knob contains spheroidal organelles called synaptic vesicles, which are filled with a chemical called WHAT? (ACh).
The electrical signal (nerve impulse) traveling down a nerve fiber causes the synaptic vesicles to undergo WHAT (cellular process of releasing contents to the outside of the cell), releasing ACh into the cleft. ACh thus functions as a chemical messenger from the nerve cell to the muscle cell.
To respond to this chemical (ACh), the muscle fiber has WHAT- proteins incorporated into its plasma membrane. Nearly all these occur directly across from the synaptic knobs
The entire muscle fiber and the Schwann cell of the NMJ are surrounded by a WHAT, which separate them from the surrounding connective tissue. Composed partially of collagen and glycoproteins, the WHAT passes through the synaptic cleft and virtually fills it.
Both the sarcolemma and that part of the basal lamina contain an enzyme called WHAT (AChE). This enzyme breaks down ACh after the ACh has stimulated the muscle cell.
Toxins that interfere with synaptic function can paralyze the muscles. Some pesticides contain cholinesterase inhibitors that bind to AChE and prevent it from degrading ACh. This causes spastic paralysis.
(Neuromuscular toxins) WHAT is a state of continual contraction of the muscle, which poses the danger of suffocation. Tetanus (lockjaw) is a form of spastic paralysis caused by the toxin of a soil bacterium, Clostridium tetani. Therefore must get a tetanus shot every 10 years.
(Neuromuscular toxins) WHAT is a state which the muscles are limp and cannot contract. This can cause respiratory arrest. Flaccid paralysis can be caused by poisons that compete with ACh for receptor sites but do not stimulate the muscle.
(Neuromuscular toxins) WHAT is a type of food poisoning caused by a neuromuscular toxin secreted by the bacterium Clostridium botulinum. Botulinum toxin blocks the release of ACh and causes flaccid muscle paralysis. Botulinum toxin is used for cosmetically treating "frown lines" caused by muscle tautness between the eyebrows. It is injected in small doses into specific facial muscles. The wrinkles gradually disappear as muscle paralysis sets in over the next few hours.
The study of the electrical activity of cells, called WHAT, is a key to understanding nervous activity, muscle contraction, the heartbeat, and other physiological phenomena.
In an unstimulated WHAT, there are more anions (negative ions) on the inside of the plasma membrane than on the outside. Thus, the plasma membrane is electrically POLARIZED, or charged. In a resting muscle cell, there is an excess of sodium ions (Na+) in the extracellular fluid (ECF) outside the cell and an excess of potassium ions (K+) in the intracellular fluid (ICF) within the cell.
A difference in electrical charge from one point to another is called an electrical potential, or WHAT?
resting membrane potential
On the sarcolemma of a muscle cell, the voltage is much smaller, about -90 mV, but important to life. (The negative sign refers to the negative charge on the intracellular side of the membrane). This voltage is called the WHAT (RMP) It is maintained by the sodium-potassium pump.
When a nerve or muscle cell is stimulated, WHAT? Ion gates open and Na+ instantly diffuses down its concentration gradient into the cell. These cations override the negative charges in the ICF, so the inside of the plasma membrane briefly becomes positive. This change is called DEPOLARIZATION of the membrane. Immediately, Na+ gates close and K+ gates open. K+ rushes out of the cell. The loss of positive potassium ions from the cell turns the inside of the membrane negative again (REPOLARIZATION). This quick up-and-down voltage shift, from the negative RMP to a positive value and then back to a negative value again. is called an action potential.
WHAT is the controlled conduction of electrical messages in neurons and muscle by depolarization of cell membrane. Polarization to Depolarization to Repolarization.
WHAT have a way of perpetuating themselves- at one point on a plasma membrane causes another one to happen immediately in front of it, which triggers another one a little farther along, and so forth. A wave of action potentials spreading along a nerve fiber like this is called a nerve impulse.
The process of muscular contraction and relaxation has four major PHASES: 1. excitation 2. excitation-contraction coupling 3. contraction 4. relaxation
WHAT is the process in which action potentials in the nerve fiber lead to action potentials in the muscle fiber.
Steps of Excitation
Steps of Excitation: 1.) A nerve signal arrives at the synpatic knob and stimulates volage-regualted calcium gates to open. Calcium ions enter the synaptic knob. 2.) Calcium stimulates exocytosis of the synaptic vesicles, which release acetylcholine (ACh) into the synaptic cleft. 3.) ACh diffuses across the synaptic cleft and binds to receptor proteins on the sarcolemma. 4.) Na+ diffuses quickly into the cell and K+ diffuses out. As a result of these ion movements, the sarcolemma reverses polarity- its voltage quickly jumps from the RMP of -90 mV to a peak of +75 mV then falls back to -90 mV as k+ diffuses out. This rapid fluctation in membrane voltage is called end-plate potential (EPP) 5.) Voltage change in end-plate region opens nearby. Voltage-gated channels producing an action potential that spreads over muscle surface
WHAT refers to the events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract.
(Excitation-contraction coupling) WHAT refers to the activation of myosin's cross bridge (force-generating sites)
(Excitation-contraction coupling) WHAT occurs when the tension generated by the cross bridge exceeds forces opposing shortening
(Excitation-contraction coupling) When cross bridges become inactive, the tension generated declines, and relaxation is induced.
excitation-contraction coupling steps
excitation-contraction coupling steps: 6.) A wave of action potentials spreads. When this wave reaches the T tubules, it continues down the T tubules into the sarcoplasm. 7.) Calcium is released from terminal cisternae. 8.) Calcium binds to the troponin of the thin filaments. 9.) The troponin-tropomyosin complex changes shape. This exposes the active sites on the actin filaments and makes them available for binding to myosin heads.
contraction steps: 10.) Myosin ATPase, an enzyme in the head, hydrolyzes this ATP to ADP + P. This activates the head, which "cocks" into an extended, high-energy position. The head keeps the ADP and phosphate group bound to it. 11.) The cocked myosin binds to an exposed active site on the thin filament, forming a cross-bridge between the myosin and actin. 12.) Myosin releases the ADP and phosphate and flexes into a bent, low-energy position, tugging the thin filament along with it. This is called the power stroke. The head remains bound to actin until it binds a new ATP 13.) Upon binding more ATP, myosin releases the actin. Process is repeated- it will hydrolyze ATP, recock (the recovery stroke), attach to a new active site farther down the thin filament, and produce another power stroke.
In this step, when its work is done, a muscle fiber relaxes and returns to its resting length.
relaxation steps: 14.) Nerve signals stop arriving at the neuromuscular junction, so the synaptic knob stops releasing ACh. 15.) As ACh separates from its receptor, AChE breaks it down into fragments that cannot stimulate the muscle. The synaptic knob reabsorbs these fragments for recycling. Therefore, stimulation of the muscle fiber by ACh ceases 16.) SR begin to pump Ca2+ from the cytosol back into the cisternae. Here, the calcium binds to a protein called calsequitrin and is stored until the fiber is stimulated again. 17.) As calcium ions dissociate from troponin, they are pumped into the SR and are not replaced. 18.) Muscle fibers return to its resting length
A muscle returns to its resting length with the aid of TWO FORCES: 1.) its intracellular and extracelular elastic components stretch it (lie recoiling rubber band) 2.) since muscles occur in antagonistic pairs, the contraction of an antagonist lengthens the relaxed muscle. Ex.) Contraction of the triceps brachii extends the elbow and lengthens the biceps brachii.
WHAT is the hardening of the muscles and stiffening of the body that begins 3 to 4 hours after death. It occurs because the deteriorating sarcoplasmic reticulum releases calcium into the cytosol. The calcium activates myosin-actin cross-bridging. Once bound to actin, myosin cannot release it without first binding an ATP molecule, and of course no ATP is produced in a dead body. Thus, the thick and thin filaments remain rigidly cross-linked until the mypfilaments begin to decay. This process peaks about 12 hours after death and then diminishes over the next 48 to 60 hours.
By gradually increasing the voltage and stimulating the muscle again, we can determine the WHAT, or minimum voltage necessary to generate an action potential in the muscle fiber and produce a contraction.
At threshold or higher, a stimulus thus causes a quick cycle of contraction and relaxation called a WHAT?
There is a delay of about 2 milliseconds between the onset of the stimulus and the onset of the twitch. This is the time required for excitation, excitation-contraction coupling (acetycolen is released and t-tubules release Ca2+), and tensing of elastic components of the muscle.
Once the elastic components are taut, the muscle moves a resisting load. This is called the WHAT (cross bridges actively form and the muscle shortens) of the twitch. The load is usually a bone. Ex.) Imagine lifting a weight from a table with a rubber band. At first, internal tension would stretch the rubber band. Then as the rubber band became taut, external tension would lift the weight.
The contraction phase is short-lived, because the SR quickly reabsorbs Ca2+ before the muscle develops maximal force. Myosin releases the thin filaments and muscle tension declines. This phase is called WHAT?
Twitches vary in strength for a variety of REASONS: 1.) Twitch strength varies with stimulation frequency; stimuli arriving close together produces stronger twitches than stimuli arriving at longer time intervals 2.) Twitches vary with the concentration of Ca2+ in the sarcoplasm. 3.) Twitch strength depends on how stretched the muscle was just before it was stimulated. 4.) temperature of the muscle 5.) Twitches are weaker when the pH of the sarcoplasm falls below normal 6.) Vary with the state of hydration of a muscle, which affects the overlap between thick and thin filaments and the ability of myosin to form cross-bridges with actin.
Even when stimulus intensity (voltage) remains constant, twitch strength can vary with stimulus frequency. High-frequency stimulation produces stronger twitches than low-frequency stimulation. We see that when a muscle is stimulated at a low frequency, it produces an identical twitch for each stimulus and fully recovers between twitches.
The muscle still recovers full between twitches, but each twitch develops more tension than the one before
Wave is added upon wave, so each twitch reaches a higher level of tension than the one before, and the muscle relaxes only partially between stimuli. This effect produces a state of sustained fluttering contraction called WHAT?
At a still higher frequency, the muscle has no time to relax at all between stimuli and the twitches fuse into a smooth, prolonged contraction called WHAT?
full recovery and complete tetanus
what two muscle twitch relationships between stimulus frequency and muscle tension rarely occur under natural conditions? Used for experimental conditions.
Muscle contracting at cellular level; produces internal tension while an external resistance causes it to stay the same length. Prelude to movement- this contraction of antagonistic muscles at a single joint is important in maintaining joint stability at rest. Also, the WHAT contraction of postural muscles is what keeps us from sinking in a heap to the floor.
WHAT contraction with a change in length but no change in tension- begins when internal tension builds to the point that it overcomes the resistance. The muscle now shortens, moves the load, and maintains essentially the same tension from then on.
One form of isotonic contraction. A muscle shortens as it maintains tension- ex.) when the biceps brachii contracts and flexes the elbow
One form of isotonic contraction. A muscle lengthens as it maintains tension. If you set a dumbell down, your biceps brachii lengthens as you extend your elbow, but it maintains tension to act as a brake and keep you from simply dropping the weight. A weight lifter uses concentric contraction when lifting a dumbbell and eccentric contraction when lowering it.
summary: During isometric contraction, a muscle develops tension without changing length, and in isotonic contraction, it changes length while maintaining constant tension. In concentric contraction, a muscle maintains tension as it shortens, and in eccentric contraction, it maintains tension while it is lengthening.
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