Muscle Fiber Contraction Overview

Muscular System Overview

Chapter 9: Muscle Fiber Contraction

9.4 Muscle Fiber Contraction Background and Overview

• Movement initiation:

  • The decision to move is initiated by the brain.

  • Signals are transmitted down the spinal cord to motor neurons.

  • Motor neurons activate muscle fibers.

• Neurons and muscle cells:

  • Both are excitable cells, capable of generating action potentials (APs).

  • Excitable cells can change their resting membrane potential volts.

• Mechanism of action potential transmission:

  • AP crosses from neurons to muscle cells through acetylcholine (ACh).

Ion Channels in Muscle Fiber Contraction

• Role of ion channels:

  • Vital for changing membrane potentials.

• Classes of ion channels:

  • Chemically gated ion channels:

  • Opened by chemical messengers like neurotransmitters (e.g., ACh receptors on muscle cells).

  • Voltage-gated ion channels:

  • Open or close in response to voltage changes in membrane potential.

The Big Picture: Four Steps for Skeletal Muscle Contraction

1. Events at the Neuromuscular Junction (NMJ)

2. Generation and Propagation of Action Potential (AP)

3. Excitation-Contraction Coupling

4. Cross Bridge Cycling

Events at the Neuromuscular Junction (NMJ)

• Mechanism upon arrival of action potential at NMJ:

  1. Action potential arrives at the axon terminal.

  2. Voltage-gated Ca²⁺ channels open.

  3. Ca²⁺ influx causes release of ACh.

  4. ACh crosses synaptic cleft and binds to ACh receptors.

  5. Chemically gated Na⁺ channels open allowing Na⁺ influx.

  6. Na⁺ influx causes end plate potential (EPP).

  7. AChE (acetylcholinesterase) breaks down ACh; channels close.

Action Potential Arrival

• Action potential travels from the neuron cell body down the axon to the axon terminal.

Activation of Voltage-Gated Ca²⁺ Channels

• Depolarization from action potential triggers voltage-gated Ca²⁺ channels, facilitating Ca²⁺ influx along its concentration gradient.

Release of Acetylcholine (ACh)

• Ca²⁺ entry facilitates fusion of synaptic vesicles (containing ACh) to the plasma membrane, releasing ACh into the synaptic cleft.

Binding of Acetylcholine (ACh) to Receptors

• ACh diffuses across the cleft to bind with receptors on the postsynaptic sarcolemma.

Opening of Chemically Gated Channels

• When ACh binds:

  • Opens chemically gated Na⁺ and K⁺ channels.

  • Na⁺ influx is greater than K⁺ efflux.

End Plate Potential (EPP)

• Na⁺ influx depolarizes the sarcolemma, resulting in an end plate potential (EPP).

• EPP elevates the resting membrane potential, signaling potential muscle contraction.

Breakdown of Acetylcholine (ACh)

• ACh is hydrolyzed by AChE into acetate and choline.

• This breakdown closes the ACh receptors and chemically gated channels, stopping Na⁺ influx.

Diseases Affecting the NMJ

• Myasthenia Gravis:

  • Autoimmune disease where antibodies attack ACh receptors at the NMJ.

  • Effects include muscle weakness due to:

  • Reduced Na⁺ channel functionality.

  • Less EPP, potentially failing to reach threshold for action potential.

  • Increased ACh release as compensation, leading to rapid ACh depletion and weakened contractions.

Substances Affecting NMJ Function

• Presynaptic Effects:

  • Botulinum Toxin:

  • Causes flaccid paralysis by blocking ACh release.

  • Latrotoxin: (from black widow spider)

  • Causes massive ACh release and spastic paralysis.

• Postsynaptic Effects:

  • Curare:

  • Binds to ACh receptors, preventing ACh binding, causing flaccid paralysis.

  • Various snake venoms:

  • Similar action to curare, blocking ACh at receptors.

Action Potential Process

1. Generation of EPP:

   • Influenced by Na⁺ influx raising membrane potential.

2. Depolarization:

   • Voltage-gated Na⁺ channels open, leading to further Na⁺ permeability, increasing depolarization.

3. Repolarization:

   • Voltage-gated Na⁺ channels close; K⁺ channels open, leading to K⁺ efflux, restoring resting membrane potential.

Recording of Action Potential (AP)

• Depolarization:

  • Caused by Na⁺ channel opening.

• Repolarization:

  • Caused by K⁺ channel opening.

• Changes in potential:

  • Movement through Na⁺ and K⁺ channels visualized in a graph of AP over time.