5.4 - Sliding Filaments and Physiology of Muscle Contraction

Sliding filament theory

Thin filaments are pulled and slide past thick filaments within sarcomeres; the sarcomere shortens as the zone of overlap increases, but the actual length of the filaments does not change.

What changes during sarcomere contraction (4 observations)

Z-lines move closer to the M line; H bands and I bands become smaller; zones of overlap become larger; A band width remains constant.

What initiates sliding filament movement

Ca²⁺ entry into the sarcoplasm, which exposes the myosin-binding sites on actin filaments.

Origin (muscle)

The fixed end of a skeletal muscle that does not move during contraction.

Insertion (muscle)

The free end of a skeletal muscle that moves toward the origin during contraction.

Resting membrane potential

The electrical gradient across a cell membrane at rest; inside is approximately -60 to -90 mV relative to the outside.

Excitable cells

Only neurons and muscle cells; they can change their membrane potentials and generate action potentials by controlling ion movement through ion channels.

Action potential

A special electrical signal that travels along a cell membrane as a wave (propagation), allowing signals to be transmitted quickly over long distances.

Propagation

The wave-like travel of an action potential along a cell membrane.

Neuromuscular junction (NMJ)

The synaptic connection between a motor neuron's axon terminal and a skeletal muscle fiber; every skeletal muscle fiber is innervated at an NMJ.

Synaptic cleft

The small space between the motor neuron axon terminal and the muscle fiber at the NMJ; the signal must cross this gap via neurotransmitter.

Motor neuron cell body location

Found within the spinal cord; sends impulses along its axon to the axon terminal at the NMJ.

Axon terminal

The end of a motor neuron axon where neurotransmitter (ACh) is stored and released.

Motor unit

A single motor neuron plus all the skeletal muscle fibers it innervates.

Small motor unit

One motor neuron innervating a small number of muscle fibers; allows precise fine motor control (e.g., extraocular eye muscles, fingers).

Large motor unit

One motor neuron innervating many muscle fibers (up to thousands); used for gross motor movements requiring more force (e.g., thigh and back muscles).

Recruitment

The progressive activation of additional motor units (small first, then larger) to increase muscle contraction strength as more force is needed.

Why motor units alternate during sustained contraction

To prevent complete muscle fatigue; some units rest while others are active, allowing longer contractions with sustained tendon tension.

Acetylcholine (ACh)

The neurotransmitter released from motor neuron axon terminals at the NMJ; crosses the synaptic cleft to bind receptors on the motor end plate.

Motor end plate

The highly folded region of the muscle cell membrane directly across from the motor neuron; contains a high density of ACh receptors (Na⁺/K⁺ ion channels).

Depolarization (muscle)

Movement of positive ions (Na⁺ in, K⁺ out) across the sarcolemma causing the inside to become more positive; more Na⁺ enters than K⁺ leaves; begins at the motor end plate and spreads through the sarcolemma and T-tubules.

Acetylcholinesterase (AChE)

Enzyme that breaks ACh into acetic acid and choline in the synaptic cleft; removal of ACh closes Na⁺/K⁺ channels and ends the contraction signal.

Excitation-contraction coupling

The process linking the action potential (excitation) to the release of Ca²⁺ from the SR (contraction); action potential travels down T-tubules → triggers Ca²⁺ release from terminal cisternae → Ca²⁺ binds troponin → tropomyosin moves → active sites on actin exposed → contraction begins.

How Ca²⁺ triggers contraction

Ca²⁺ binds to troponin, causing tropomyosin to shift and expose the active sites on G-actin, allowing myosin heads to bind and begin the cross-bridge cycle.

Cross-bridge cycle – Step 1: Cocking the myosin head

ATP binds to the myosin head and is hydrolyzed to ADP + Pi; the released energy cocks the head into a high-energy position ready to bind actin.

Cross-bridge cycle – Step 2: Active site exposure

Ca²⁺ binds troponin → tropomyosin shifts → active sites on actin are exposed.

Cross-bridge cycle – Step 3: Cross-bridge formation

The energized (high-energy) myosin head binds to the exposed active site on actin, forming a cross-bridge.

Cross-bridge cycle – Step 4: Power stroke

ADP + Pi detach from myosin; the myosin head pivots toward the M line (power stroke), pulling the actin filament and shortening the sarcomere; myosin is now in a low-energy state.

Cross-bridge cycle – Step 5: Cross-bridge detachment

A new ATP molecule binds to the myosin head, breaking the link between myosin and actin; the active site on actin is now free.

Cross-bridge cycle – Step 6: Myosin reactivation

The newly bound ATP is hydrolyzed to ADP + Pi, recocking the myosin head into the high-energy state; the cycle can repeat as long as Ca²⁺ and ATP are present.

How muscle contraction ends

Motor neuron signaling stops → AChE breaks down ACh → sarcolemma repolarizes → voltage-gated Ca²⁺ channels in SR close → Ca²⁺ pumped back into SR → tropomyosin covers actin active sites → cross-bridge formation stops → muscle relaxes.

Why muscles cannot push

There is no mechanism in the sarcomere to push the Z-lines apart; sarcomeres can only shorten (pull), not lengthen actively.

Three ways a muscle returns to resting length

Gravity (pulls the muscle back), opposing muscle contractions (antagonistic pairs stretch each other), and elastic forces (stretch of tendons and elastic fibers causes recoil).

Antagonistic muscle pairs

Muscles that work in opposition; as one contracts the other is stretched; example: biceps contracts → triceps is stretched, and vice versa.