Unit 4: Lecture 23 Muscle Physiology Pt 1

Neuromuscular Junction

ends of the neuron that meet the muscle=synapse

Synaptic Bulbs release NTs that will excite or inhibit the skeletal muscle

Phases Of muscle contraction

1. Excitation of Muscle

2. Excitation and Contraction Coupling

3. Contraction of Muscle

4. Relaxation of muscle

Excitation Of Muscle

Signal to contract

What triggers the release of ACh at the NMJ?

An action potential arriving at the axon terminal.

What happens when the action potential reaches the synaptic terminal?

Voltage-gated Ca²⁺ channels open, allowing Ca²⁺ influx, which triggers ACh release.

Where is ACh released, and what does it bind to?

ACh is released into the synaptic cleft and binds to nicotinic receptors on the motor end plate.

What occurs after ACh binds to receptors?

Na⁺ channels open, causing depolarization (end-plate potential).

How is ACh cleared from the synaptic cleft?

It is broken down by acetylcholinesterase (AChE) or diffuses away.

Excitation and contraction Coupling

Preparing to contract the muscle

How does the action potential spread into the muscle fiber?

It travels along the sarcolemma and down T-tubules.

What structure releases Ca²⁺ in response to T-tubule depolarization?

The sarcoplasmic reticulum (SR) releases Ca²⁺ from terminal cisternae.

What does Ca²⁺ bind to in the thin filament?

Troponin, causing a conformational change that moves tropomyosin.

What is exposed when tropomyosin shifts?

Active sites on actin, allowing myosin to bind.

What provides energy for myosin head movement?

ATP hydrolysis into ADP + Pi (energizes the myosin head).

What is the "cocked" position of the myosin head?

Myosin head is upright, bound to ADP + Pi, ready to bind actin.

What happens during cross-bridge formation?

Myosin head binds to actin’s active site, forming a cross-bridge.

What is the power stroke?

Myosin head pivots, pulling actin toward the M line (ADP + Pi released).

How is the cross-bridge broken?

A new ATP binds to myosin, causing detachment from actin.

Why is ATP essential for muscle relaxation?

Without ATP, myosin remains bound to actin (rigor mortis).

Relaxation of muscle

Return to normal state

What stops muscle contraction?

ACh is broken down, stopping action potentials and Ca²⁺ release.

What happens when Ca²⁺ detaches from troponin?

Tropomyosin reblocks actin’s active sites, preventing myosin binding.

What restores the sarcomere’s resting length?

Elastic forces (tendons) and opposing muscle contractions.

Name three external forces affecting muscle function.

Gravity, elastic force (tendon recoil), and opposing muscles (e.g., dorsiflexion countering plantarflexion).

How do the I band, H zone, and A band change during contraction?

• I band and H zone shorten.

• A band remains the same length.

  • Z lines move closer together.

What are three medical uses of Botox?

Cosmetic (wrinkle reduction), hyperhidrosis (excessive sweating), and urology (bladder control).

What causes rigor mortis?

No ATP → myosin can’t detach from actin → muscles stiffen.

How do organophosphates affect the NMJ?

They inhibit AChE, leading to excessive ACh, causing convulsions and muscle spasms

What is the effect of black widow spider venom on the NMJ?

It causes explosive release of ACh, leading to spastic paralysis.

How does curare affect muscle contraction?

It blocks ACh receptors, causing flaccid paralysis (inability to contract).

What is the mechanism of botulinum toxin?

It blocks ACh release, leading to flaccid paralysis (e.g., Botox).