Excitation-Contraction Coupling, Crossbridge Cycle & Relaxation

Excitation-contraction coupling

Phase that links the muscle fiber action potential to contraction by causing Ca2+ release from the sarcoplasmic reticulum.

Excitation-contraction coupling — Step 1

The end-plate potential stimulates an action potential by causing nearby voltage-gated Na+ channels to open.

Excitation-contraction coupling — Step 2

The action potential propagates along the sarcolemma and down the T-tubules.

Excitation-contraction coupling — Step 3

T-tubule depolarization causes Ca2+ channels in the sarcoplasmic reticulum to open, releasing Ca2+ into the cytosol.

Role of the terminal cisternae during contraction

Terminal cisternae of the sarcoplasmic reticulum release stored Ca2+ into the cytosol when the T-tubules depolarize.

Excitation-contraction coupling sequence

End-plate potential → muscle action potential → action potential travels down T-tubules → SR Ca2+ channels open → Ca2+ enters cytosol.

How does Ca2+ prepare the muscle for contraction?

Ca2+ binds to troponin, causing tropomyosin to move away from the active sites on actin so myosin can bind.

Troponin during contraction

Ca2+ binds to troponin, causing a change that moves tropomyosin and exposes the active sites on actin.

Tropomyosin at rest vs. during contraction

At rest, tropomyosin blocks the active sites on actin. When Ca2+ binds troponin, tropomyosin moves and exposes the active sites.

Crossbridge

Connection formed when a myosin head binds to an exposed active site on actin.

Crossbridge cycle

Repeated sequence in which myosin heads bind to actin, perform power strokes, detach, and are recocked to pull thin filaments toward the center of the sarcomere.

Crossbridge cycle — Step 1: ATP hydrolysis

ATP binds to the myosin head and is hydrolyzed to ADP + phosphate; the released energy cocks the myosin head into its high-energy position.

Crossbridge cycle — Step 2: Crossbridge formation

The energized myosin head binds to an exposed active site on actin, forming a crossbridge at about a 90° angle.

Crossbridge cycle — Step 3: Power stroke

The phosphate detaches from myosin, causing the myosin head to pivot and pull actin toward the center of the sarcomere; ADP leaves at the end of the power stroke.

Crossbridge cycle — Step 4: Detachment

A new ATP binds to the myosin head and breaks the attachment between myosin and actin.

Crossbridge cycle sequence

ATP hydrolysis cocks myosin head → myosin binds actin → phosphate release triggers power stroke → ADP leaves → new ATP binds and detaches myosin from actin → cycle repeats.

Power stroke

Pivoting movement of a myosin head that pulls the thin filament toward the center of the sarcomere.

What are the roles of ATP in the crossbridge cycle?

ATP binding allows myosin to detach from actin; ATP hydrolysis provides the energy to recock the myosin head for another cycle.

What happens if Ca2+ remains available and ATP is present?

Crossbridge cycles continue repeatedly, generating tension and pulling thin filaments progressively toward the M line.

Why don't thin filaments slide backward between crossbridge cycles?

Many myosin heads work at different times; while some detach and recock, others remain attached and continue pulling the thin filament.

Muscle relaxation

Occurs when ACh release stops, remaining ACh is broken down, and the Ca2+ concentration in the cytosol returns to its resting level.

Relaxation — Step 1

Acetylcholinesterase breaks down the remaining ACh, ligand-gated cation channels close, and the final depolarization occurs.

Relaxation — Step 2

The sarcolemma returns to its resting membrane potential and Ca2+ channels in the sarcoplasmic reticulum close.

Relaxation — Step 3

ATP-powered pumps actively transport Ca2+ from the cytosol back into the sarcoplasmic reticulum.

Relaxation — Step 4

As cytosolic Ca2+ decreases, troponin shifts and tropomyosin returns to its resting position, blocking the active sites on actin and ending contraction.

Relaxation sequence

ACh release stops → AChE breaks down remaining ACh → sarcolemma returns to resting potential → SR Ca2+ channels close → Ca2+ is pumped back into SR → tropomyosin blocks actin → muscle relaxes.

Muscle spasm

A muscle that is unable to relax; spasms may result from dehydration, electrolyte imbalances, muscle injury, or muscle overload.

Rigor mortis

Progressive stiffening of skeletal muscles beginning about 3–4 hours after death because ATP is no longer available to pump Ca2+ into the SR or detach myosin heads from actin; stiffness ends as myofilament proteins degenerate about 48–72 hours after death.

Why does lack of ATP cause rigor mortis?

Without ATP, Ca2+ remains in the cytosol and myosin heads cannot detach from actin, leaving the muscles in a contracted state.