Muscle Physiology

What is a motor unit?

A motor neuron and all the muscle fibers it innervates.

What is the neuromuscular junction (NMJ)?

A specialized synapse between a motor neuron and a muscle fiber where neural signals are transmitted to initiate contraction.

What are the three main parts of the NMJ?

Presynaptic terminal (ACh vesicles), synaptic cleft (AChE present), and postsynaptic motor end plate (ACh receptors).

What neurotransmitter is released at the NMJ?

Acetylcholine (ACh).

What enzyme breaks down ACh and stops the signal?

Acetylcholinesterase (AChE).

What ion triggers ACh release from the presynaptic terminal?

Calcium (Ca²⁺).

What happens when ACh binds to receptors on the muscle fiber?

Na⁺ rushes in, causing depolarization and triggering a muscle action potential.

What is the resting membrane potential (RMP) for a neuron and muscle fiber?

Neuron ≈ –70 mV; muscle fiber ≈ –90 mV.

What maintains the RMP?

Na⁺/K⁺ pump and K⁺ leak channels.

Why is the inside of the cell negative at rest?

More K⁺ leaks out than Na⁺ enters, leaving inside negative.

What are K⁺ leak channels?

Always-open channels that let K⁺ move out, making the inside negative and setting RMP.

What is an action potential?

A rapid flip in charge (negative → positive → negative) that travels along a nerve or muscle to send a signal.

List the steps of an action potential.

Resting → Threshold → Depolarization → Repolarization → Hyperpolarization → Resting.

What ion causes depolarization?

Sodium (Na⁺) influx.

What ion causes repolarization?

Potassium (K⁺) efflux.

What is excitation–contraction coupling?

The process that converts an electrical signal (AP) into a mechanical response (contraction).

Outline the steps of EC coupling.

AP travels along sarcolemma → T-tubules → DHPR activates RyR on SR → Ca²⁺ released → binds troponin → tropomyosin moves → actin-myosin binding → contraction → Ca²⁺ reuptake → relaxation.

What is the role of the sarcoplasmic reticulum (SR)?

Stores and releases Ca²⁺ for contraction; reabsorbs Ca²⁺ for relaxation.

What is the sliding filament theory?

Muscle contraction occurs when actin and myosin slide past each other, shortening the sarcomere.

Describe the cross-bridge cycle.

ATP binds myosin (detaches), ATP hydrolyzes (cocking), myosin binds actin, power stroke (ADP released), new ATP binds to detach.

List three roles of ATP in muscle contraction.

Powers myosin head movement, allows myosin detachment, fuels Ca²⁺ reuptake by SR pumps.

What happens if there’s no ATP available?

Myosin stays bound to actin → rigor mortis.

What causes muscle relaxation?

ACh broken down by AChE and Ca²⁺ pumped back into SR by SERCA pumps.

How does botulinum toxin affect muscle function?

Blocks ACh release → prevents depolarization → flaccid paralysis.

What happens in Myasthenia Gravis?

Antibodies destroy ACh receptors → weak muscle activation.

How do anti-AChE drugs help Myasthenia Gravis?

Prevent ACh breakdown, increasing ACh at NMJ for stronger signaling.

What is the length–tension relationship?

Force depends on sarcomere length; optimal at resting length with maximal cross-bridge overlap.

What is the force–velocity relationship?

As contraction velocity increases, force decreases (inverse relationship).

Give examples of force–velocity relationships in activity.

Heavy squat = high force/low speed; kettlebell swing = high speed/low force.

What happens when load equals maximum muscle force?

Contraction velocity = 0 → isometric contraction.

What are the phases of a muscle twitch?

Latent (Ca²⁺ release), contraction (cross-bridges active), relaxation (Ca²⁺ reuptake).

What is summation?

Successive stimuli before full relaxation add together to increase total force.

What is tetanus?

Rapid repeated stimulation causing sustained contraction; incomplete = partial relaxation, complete = fused contraction.

What is the maximum strength of tetanic contraction?

~50 pounds per square inch of muscle cross-section.

What causes muscle fatigue?

Glycogen depletion, reduced neurotransmission, and limited oxygen/nutrient supply.

What happens during “training to failure”?

More motor units recruited, greater Ca²⁺ release, improved neuromuscular adaptation, and hypertrophy stimulus.

Which ions are key to muscle function?

Na⁺ (depolarization), K⁺ (repolarization), Ca²⁺ (contraction trigger).

What does the Na⁺/K⁺ pump do?

Pumps 3 Na⁺ out and 2 K⁺ in per ATP → maintains ionic gradient and RMP.

What is the voltage change during an action potential?

About 100 mV (from –70/–90 mV to +30 mV and back).

Difference between voltage-gated and leak K⁺ channels?

Leak: always open for RMP; voltage-gated: open during AP repolarization.

How does EC coupling differ in smooth muscle?

Ca²⁺ binds calmodulin instead of troponin → activates myosin light-chain kinase.

What is the “all-or-none” principle?

Once threshold is reached, the fiber contracts fully; below threshold = no contraction.

Why are summation and tetanus important physiologically?

Allow smooth, sustained force for movement and posture.

What happens to Ca²⁺ during summation/tetanus?

Cytoplasmic Ca²⁺ stays high, allowing continuous cross-bridge cycling.

Why does the refractory period occur after an AP?

Na⁺ channels inactivate and need time to reset.

What is the Nernst potential?

The voltage that balances the diffusion tendency of a specific ion (–94 mV for K⁺, +61 mV for Na⁺).

What factors determine resting membrane potential?

K⁺ permeability, Na⁺/K⁺ pump, and negatively charged intracellular proteins.

How does reduced blood flow cause fatigue?

Limits O₂ and nutrients → less ATP → reduced cross-bridge cycling and Ca²⁺ handling.

What type of feedback is an action potential?

Positive feedback (Na⁺ entry opens more Na⁺ channels).

What complication occurs if respiratory muscles are paralyzed in Myasthenia Gravis?

Respiratory failure, which can be life-threatening.