A chemical synapse between a motor neuron and one muscle fiber. The transmitter is always acetylcholine.

• Axon terminalThe nerve ending; holds vesicles of acetylcholine (ACh).
• Synaptic cleftThe tiny gap the ACh diffuses across.
• Motor end plateThe folded region of sarcolemma packed with nicotinic ACh receptors.
• The hand-offAn action potential opens voltage-gated Ca2+ channels, vesicles fuse, ACh is released, binds receptors, and Na+ enters to start an end-plate potential.
• AcetylcholinesteraseThe enzyme in the cleft that breaks down ACh so the signal stops cleanly.

1. The action potential sweeps along the sarcolemma and down the T-tubules
2. Voltage sensors (DHP receptors) tug open the ryanodine receptors on the SR
3. The SR floods the cytosol with Ca2+
4. Ca2+ binds troponin, which pulls tropomyosin off the actin binding sites
5. The myosin-binding sites are now exposed and contraction can begin

Calcium is the switch. No calcium, no exposed binding sites, no contraction.

1. Formation: an energized myosin head binds the exposed actin site
2. Power stroke: the head pivots, pulling the thin filament toward the M line; ADP and Pi are released
3. Detachment: a fresh ATP binds the myosin head, which lets go of actin
4. Re-cocking: ATP splits to ADP and Pi, re-energizing the head to bind again

As long as calcium and ATP are present, the cycle repeats and the muscle keeps shortening.

• Thin filaments slideToward the M line from both ends of the sarcomere.
• Z discs pulled inThe sarcomere gets shorter, and so does the whole fiber.
• I band narrowsLess thin-only region.
• H zone narrowsMore overlap of thick and thin.
• A band unchangedThick filament length never changes, so the A band stays the same.

The filaments do not shrink. They slide past each other.

• Signal stopsThe motor neuron quiets and acetylcholinesterase clears the ACh.
• SERCA pumpsActive transport (needs ATP) returns Ca2+ to the SR.
• Tropomyosin recoversIt re-covers the actin sites, so cross-bridges can no longer form.
• Rigor mortisAfter death there is no ATP, so myosin cannot release actin; the muscle locks until enzymes break the proteins down.

• TwitchThe response to one action potential: latent, contraction, then relaxation phases.
• Wave summationA second stimulus before relaxation adds onto the first, producing more force.
• Unfused tetanusRapid stimulation with brief partial relaxation; force wobbles but climbs.
• Fused tetanusStimulation so rapid there is no relaxation: smooth, maximal, sustained force.

Real movements use both recruitment (more units) and rate coding (faster firing) at once.

• Optimal lengthMaximum filament overlap gives maximum force.
• Too shortThick filaments hit the Z discs; force falls.
• Too longToo little overlap to form bridges; force falls.
• IsotonicMuscle changes length under a constant load (lifting a weight).
• IsometricForce with no length change (holding a plank).
• Concentric / eccentricConcentric shortens under load; eccentric lengthens under load and causes most soreness.

• Stored ATPOn hand for about 2 seconds.
• Creatine phosphateRegenerates ATP fast for about 10 to 15 seconds.
• Anaerobic glycolysisAbout 30 to 60 seconds; makes ATP quickly but produces lactate.
• Aerobic respirationMinutes to hours; needs oxygen, makes the most ATP.
• Muscle fatigueA decline in force from ion imbalances, low energy, and reduced calcium release, not usually lactate alone.
• Oxygen debtExtra oxygen used after exercise to restore ATP, creatine phosphate, and clear metabolites.

Both use actin, myosin, and calcium, but they are triggered and controlled differently from skeletal muscle.

• Cardiac, the triggerSelf-rhythmic pacemaker cells start each beat; the signal spreads cell to cell through gap junctions in the intercalated discs.
• Cardiac, the calciumCalcium entering from outside the cell triggers the SR to release more (calcium-induced calcium release).
• Cardiac, no tetanusA long refractory period prevents sustained contraction, so the heart always relaxes and refills. The autonomic system and hormones adjust rate and force.
• Smooth, the structureNo sarcomeres or striations; filaments anchor to dense bodies and twist the cell as they pull.
• Smooth, the calciumCalcium binds calmodulin, which activates myosin light chain kinase to switch on myosin; slow, sustained, and energy efficient (latch state).
• Smooth, the controlInvoluntary: driven by the autonomic system, hormones, and stretch. Single-unit sheets in the gut and vessels contract together.

Cardiac conduction and the full heartbeat get their own lecture in the cardiovascular week.