Muscle Physiology Quiz

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Questions and Answers

What typically initiates the action potential in muscle fibers?

  • Direct electrical stimulation
  • Release of calcium ions
  • Nerve signal from a motor neuron (correct)
  • Exposure to external stimuli

How many muscle fibers does a single nerve fiber typically stimulate?

  • A hundred muscle fibers
  • Only one muscle fiber
  • Over a thousand muscle fibers
  • Several hundred muscle fibers (correct)

Where does the neuromuscular junction typically occur on the muscle fiber?

  • At the muscle fiber's ends
  • Near the muscle fiber's midpoint (correct)
  • At the myofibril interface
  • At the muscle fiber's origin

What is the significance of acetylcholine in the neuromuscular junction?

<p>It transmits nerve impulses to muscle fibers (A)</p> Signup and view all the answers

What happens to the acetylcholine after it is released into the synaptic space?

<p>It binds to receptors on the muscle fiber (B)</p> Signup and view all the answers

What can weaken the end plate potential in muscle tissue?

<p>Botulinum toxin (A), Curare (C)</p> Signup and view all the answers

What is the typical number of vesicles of acetylcholine released upon a nerve impulse reaching the junction?

<p>Approximately 125 vesicles (B)</p> Signup and view all the answers

What is the role of acetylcholinesterase in the neuromuscular junction?

<p>To destroy released acetylcholine (C)</p> Signup and view all the answers

What percentage of muscle fibers have more than one neuromuscular junction?

<p>Approximately 2% (B)</p> Signup and view all the answers

Which part of the neuromuscular junction does the neural membrane interface with?

<p>Subneural clefts on the muscle membrane (D)</p> Signup and view all the answers

Which end plate potential is capable of eliciting a muscle action potential?

<p>Normal end plate potential (C)</p> Signup and view all the answers

What happens to acetylcholine once it is released into the synaptic space?

<p>It persists and continuously activates receptors (A), It gets converted to choline and acetate (C)</p> Signup and view all the answers

Which of the following describes a muscle that cannot contract due to a weak end plate potential?

<p>It is curarized (D)</p> Signup and view all the answers

What condition results from decreased release of acetylcholine at the neuromuscular junction?

<p>Flaccid paralysis (B)</p> Signup and view all the answers

Which component of the neuromuscular junction directly interacts with acetylcholine?

<p>Chemically gated channels (C)</p> Signup and view all the answers

What occurs after acetylcholine detaches from its receptors?

<p>The signal for contraction ceases (D)</p> Signup and view all the answers

What is the primary role of acetylcholine-gated channels in muscle fibers?

<p>To facilitate sodium ion inflow into the fiber (B)</p> Signup and view all the answers

What occurs as a result of the end plate potential at the muscle fiber membrane?

<p>Opening of neighboring voltage-gated sodium channels (A)</p> Signup and view all the answers

Why do end plate potentials A and C not initiate an action potential?

<p>They are too weak to cause sufficient depolarization (D)</p> Signup and view all the answers

What characterizes end plate potential B compared to A and C?

<p>It is much stronger and initiates an action potential (A)</p> Signup and view all the answers

What is the approximate time frame for the sequence of events related to the end plate potential?

<p>5 to 10 milliseconds (B)</p> Signup and view all the answers

What causes the regenerative effect of more sodium ions flowing into the fiber?

<p>Opening of voltage-gated sodium channels (B)</p> Signup and view all the answers

What happens to choline after it is reabsorbed into the neural terminal?

<p>It forms new acetylcholine (B)</p> Signup and view all the answers

What is the overall effect of sodium ion inflow on the muscle fiber membrane?

<p>It leads to depolarization and initiation of action potential (C)</p> Signup and view all the answers

Which drug is mentioned as having effects similar to acetylcholine on the neuromuscular junction?

<p>Methacholine (A)</p> Signup and view all the answers

What is the primary action of the drugs that affect neuromuscular junctions?

<p>Prolonged stimulation of receptors (B)</p> Signup and view all the answers

What phenomenon occurs due to excessive stimulation of synapses in muscle fibers?

<p>Synaptic fatigue (A)</p> Signup and view all the answers

What is the typical duration of effects for the drugs that affect the neuromuscular junction?

<p>Minutes to several hours (A)</p> Signup and view all the answers

Under what conditions does measurable fatigue of the neuromuscular junction occur?

<p>Rarely, at exhausting levels of muscle activity (D)</p> Signup and view all the answers

What is the main difference between the mentioned drugs and acetylcholine?

<p>Their resistance to cholinesterase (D)</p> Signup and view all the answers

What is meant by depolarization of the muscle fiber membrane?

<p>Change in the electrical charge across the membrane (D)</p> Signup and view all the answers

What effect do drugs like carbachol, methacholine, and nicotine have on muscle activity?

<p>They can cause muscle spasm (B)</p> Signup and view all the answers

What is the role of the SERCA pump in muscle fibers?

<p>It pumps calcium ions back into the sarcoplasmic reticulum. (D)</p> Signup and view all the answers

How many T tubules are typically found per sarcomere in mammalian skeletal muscle?

<p>Two (D)</p> Signup and view all the answers

Which protein inside the sarcoplasmic reticulum binds calcium ions?

<p>Calsequestrin (C)</p> Signup and view all the answers

During a muscle contraction, which statement is true regarding the calcium pulse duration in heart muscle?

<p>It typically lasts about one-third of a second. (B)</p> Signup and view all the answers

Where are the T tubules located in frog muscle tissue?

<p>At the Z disk of the sarcomere (B)</p> Signup and view all the answers

What happens to the calcium ions during the contraction of muscle fibers?

<p>They are pumped away from the myofibrils. (B)</p> Signup and view all the answers

What structure surrounds the myofibrils that contract in muscle fibers?

<p>Longitudinal sarcoplasmic reticulum tubules (A)</p> Signup and view all the answers

Why might the duration of the calcium pulse vary in different muscle fibers?

<p>Because of variations in action potential duration. (A)</p> Signup and view all the answers

What is a major consequence of excessive muscle contractions due to calcium release?

<p>Depletion of energy stores (A)</p> Signup and view all the answers

Which of the following symptoms is NOT associated with malignant hyperthermia?

<p>Severe fatigue (D)</p> Signup and view all the answers

What treatment is commonly used for malignant hyperthermia?

<p>Cooling and dantrolene (B)</p> Signup and view all the answers

What is rhabdomyolysis primarily caused by in severe cases of malignant hyperthermia?

<p>Muscle fiber injury and breakdown (A)</p> Signup and view all the answers

What role does dantrolene play in the treatment of malignant hyperthermia?

<p>Antagonizes ryanodine receptors (D)</p> Signup and view all the answers

What physiological response occurs due to the release of large amounts of potassium from damaged muscle cells?

<p>High plasma potassium levels (A)</p> Signup and view all the answers

What condition is most closely related to disorders of excitation-contraction coupling in muscle?

<p>Congenital myopathies (B)</p> Signup and view all the answers

Which of the following is a significant effect of increased metabolic rate due to sustained muscle contractions?

<p>Increased respiration (B)</p> Signup and view all the answers

Flashcards

Neuromuscular Junction

A specialized connection between a motor neuron and a muscle fiber, enabling nerve impulses to trigger muscle contraction.

Acetylcholine

A chemical messenger released from the nerve terminal at the neuromuscular junction, triggering muscle contraction.

Vesicles

Small sacs within the nerve terminal that store and release acetylcholine.

Synaptic Space

The space separating the nerve terminal from the muscle fiber at the neuromuscular junction.

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Subneural Clefts

Depressions on the surface of the muscle fiber membrane that increase the surface area for acetylcholine receptors.

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Acetylcholine Receptors

Proteins embedded in the muscle fiber membrane that bind to acetylcholine, initiating muscle contraction.

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Motor Unit

A single motor neuron and all the muscle fibers it innervates.

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Action Potential Propagation

The process by which an action potential travels in both directions along a muscle fiber after stimulation by a nerve impulse.

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End Plate Potential (EPP)

The change in electrical potential across the muscle membrane at the neuromuscular junction caused by the release of acetylcholine.

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Weakened EPP

A weak EPP that is too small to trigger an action potential in the muscle fiber, resulting in no muscle contraction.

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Normal EPP

A strong EPP that successfully triggers an action potential in the muscle fiber, leading to muscle contraction.

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Curare-induced EPP

A weakened EPP caused by the action of curare, a drug that blocks acetylcholine receptors, preventing muscle contraction.

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Botulinum Toxin-induced EPP

A weakened EPP caused by botulinum toxin, a neurotoxin that prevents the release of acetylcholine, hindering muscle contraction.

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Acetylcholinesterase

The enzyme that breaks down acetylcholine in the synaptic cleft, stopping the signal transmission at the neuromuscular junction.

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Acetylcholine Release

The process by which acetylcholine is released from the presynaptic neuron, initiating the signaling cascade at the neuromuscular junction.

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Acetylcholine Binding

The binding of acetylcholine to its receptors on the muscle fiber membrane, triggering the opening of ion channels and initiating muscle contraction.

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End Plate Potential

The change in electrical potential across the muscle fiber membrane caused by the influx of sodium ions through acetylcholine-gated channels.

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Acetylcholine-gated Channels

Specialized channels in the muscle fiber membrane that open when acetylcholine binds, allowing sodium ions to flow into the cell.

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Voltage-gated Sodium Channels

Voltage-gated channels that open in response to a change in membrane potential, allowing even more sodium ions to flow into the muscle fiber.

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Action Potential Initiation

The process by which an action potential is generated in a muscle fiber, triggered by the influx of sodium ions.

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Threshold Potential

The minimum amount of depolarization required to trigger an action potential in a muscle fiber.

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Acetylcholine Breakdown

The process by which acetylcholine is broken down by the enzyme acetylcholinesterase, terminating the signal.

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Choline Reabsorption

The process by which choline, a product of acetylcholine breakdown, is reabsorbed by the neural terminal for recycling.

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Acetylcholine Cycle

The time it takes for the entire sequence of events (acetylcholine release, binding, breakdown, reabsorption) to occur.

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Neuromuscular Junction Fatigue

The state where a muscle fiber is unable to contract effectively due to repeated stimulation.

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Cholinergic Agonists

Chemicals that mimic the effects of acetylcholine at the neuromuscular junction.

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Cholinesterase

An enzyme that breaks down acetylcholine in the synapse.

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Motor End Plate

An area on the muscle fiber membrane where acetylcholine receptors are located.

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Prolonged Contraction

Persistent activation of the neuromuscular junction caused by drugs that are not readily broken down by cholinesterase.

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Drugs Mimicking Acetylcholine

Compounds like methacholine, carbachol, and nicotine that act as cholinergic agonists.

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Depolarization

The process of muscle fiber membrane becoming more positive due to the influx of sodium ions.

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Transverse Tubule (T) System

A network of interconnected tubules within a muscle fiber, responsible for transmitting electrical signals and releasing calcium ions to initiate muscle contraction.

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Sarcoplasmic Reticulum (SR)

A specialized type of endoplasmic reticulum in muscle fibers that stores and releases calcium ions, playing a crucial role in muscle contraction.

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T Tubule-SR Junctions

The junctions between the transverse tubules (T tubules) and the sarcoplasmic reticulum (SR).

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SERCA Pumps

The protein pumps located within the sarcoplasmic reticulum (SR) that actively transport calcium ions back into the SR after contraction.

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Calsequestrin

A calcium-binding protein found within the sarcoplasmic reticulum (SR) that can bind a significant number of calcium ions, contributing to their storage.

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Calcium Pulse

The brief spike in calcium ion concentration within the muscle fiber that initiates muscle contraction.

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Duration of Calcium Pulse

The duration of the calcium pulse, which determines the duration of muscle contraction, and varies depending on the type of muscle fiber.

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Calcium Removal from Cytoplasm

The process of returning calcium ions to the sarcoplasmic reticulum (SR) after contraction, which ends the contraction and allows the muscle to relax.

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Malignant Hyperthermia

A rare inherited disorder that causes uncontrolled muscle contractions due to excessive calcium release from the sarcoplasmic reticulum.

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Sarcoplasmic Reticulum

A specialized organelle within muscle cells that stores and releases calcium ions, playing a key role in muscle contraction.

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Rigidity

A state of sustained muscle contraction, triggered by excessive calcium release from the sarcoplasmic reticulum.

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Rhabdomyolysis

The process by which muscle cells break down and release their contents into the bloodstream, often due to injury or stress.

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Dantrolene

A type of drug that blocks the release of calcium from the sarcoplasmic reticulum, preventing muscle contraction.

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Hyperkalemia

A condition characterized by a high level of potassium in the blood.

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Thermogenesis

The process of transferring heat energy from one object to another.

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Study Notes

Neuromuscular Junction and Impulse Transmission

  • Skeletal muscle fibers are innervated by large myelinated nerve fibers originating from motoneurons in the spinal cord's anterior horns.
  • Each nerve fiber typically branches and stimulates multiple skeletal muscle fibers (3-several hundred).
  • Each nerve ending forms a neuromuscular junction (junction) with a muscle fiber near its midpoint.
  • Action potentials initiated in the muscle fiber travel in both directions towards the fiber ends.
  • Most muscle fibers have only one junction.

Neuromuscular Junction Anatomy

  • Composed of branching nerve terminals that invaginate the muscle fiber surface (motor end plate).
  • The nerve terminals are insulated by Schwann cells.
  • The invaginated membrane is called the synaptic gutter/synaptic trough.
  • The space between terminal and fiber membrane is the synaptic space/synaptic cleft (20-30 nanometers wide).
  • Smaller folds (subneural clefts) on the muscle membrane increase surface area for synaptic transmission.
  • Mitochondria are abundant in the axon terminal, supplying energy (ATP) for acetylcholine synthesis.

Acetylcholine Secretion

  • Nerve impulses trigger the release of approximately 125 acetylcholine vesicles into the synaptic space.
  • Neurotransmitter release is calcium-mediated:
    • Action potentials cause the opening of voltage-gated calcium channels in the nerve terminal.
    • Calcium influx activates protein kinases, detaching acetylcholine vesicles from the cytoskeleton.
    • Vesicles fuse with the neural membrane, releasing acetylcholine via exocytosis at the release sites.
  • Acetylcholinesterase rapidly destroys acetylcholine a few milliseconds after release, thus rapidly terminating its effect.

Acetylcholine Receptor Action

  • Acetylcholine receptors are large protein complexes (275,000 molecular weight).
  • Receptors are composed of five subunits (2 alpha, 1 beta, 1 delta, 1 gamma in fetal, 1 epsilon substitutes for gamma in adult).
  • Receptor proteins penetrate the membrane forming a channel.
  • Two acetylcholine molecules binding to alpha subunits trigger conformational change, opening the channel.
  • Channel opening allows Na+, K+, and Ca2+ ions to pass through the channel.
  • Sodium influx is greater than potassium efflux, creating a local positive potential change (end plate potential).
  • End plate potential triggers action potentials in the muscle fiber membrane.

End Plate Potential and Skeletal Muscle Fiber Excitation

  • End plate potential is a local depolarization that increases nerve membrane potential by 50-75 mV.
  • This causes neighboring voltage-gated sodium channels to open, initiating muscle action potentials.
  • Muscle action potentials trigger muscle contraction.
  • Acetylcholine is rapidly destroyed, preventing continuous muscle re-excitation.

Safety Factor and Fatigue

  • The normal neuromuscular junction has a high safety factor, where the end plate potential is several times greater than needed to stimulate the muscle.
  • Prolonged high-frequency stimulation may lead to neuromuscular junction fatigue.
  • Fatigue is due to decreased acetylcholine vesicle numbers, impacting impulse transmission.

Drugs Affecting Neuromuscular Junction

  • Drugs can enhance or block neuromuscular transmission.
    • Drugs like methacholine and carbachol mimic acetylcholine's action leading muscle spasm.
    • Neostigmine, physostigmine and diisopropyl fluorophosphate inhibit acetylcholinesterase prolonging acetylcholine action and causing sustained muscle spasm
    • Curariform drugs, such as d-tubocurarine, block acetylcholine receptor sites, preventing action potential initiation and muscle contraction.

Excitation-Contraction Coupling and Transverse Tubules

  • Transversal tubules (T-tubules) transmit action potentials deep within the muscle fiber.
  • T-tubules communicate with extracellular fluid.
  • Action potentials in T-tubules trigger calcium release from the sarcoplasmic reticulum (SR).
  • Calcium ions initiate muscle contraction.
  • Calcium ions are actively pumped back into the SR, ending muscle contraction.

Myasthenia Gravis

  • Autoimmune disease characterized by muscle weakness.
  • Immune system develops antibodies that block/destroy acetylcholine receptors at the neuromuscular junction.
  • Muscle end plate potentials are too weak to trigger action potentials, thus resulting in muscle weakness and respiratory failure if untreated.
  • Neostigmine or other acetylcholinesterase inhibitors can temporarily improve symptoms.

Malignant Hyperthermia

  • Genetic condition causing uncontrolled muscle contractions when exposed to certain anesthetics or depolarizing muscle relaxants.
  • Mutations affect calcium release channels (ryanodine receptors - RYR) or dihydropyridine receptors (DHP) increasing calcium influx, causing muscle rigidity and high fever.
  • Treatment involves cooling the patient and administering dantrolene, a drug that antagonizes RYR and inhibits calcium release.

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