Fire an action potential, follow the signal to the calcium stores, and watch myosin heads walk the thin filaments of one sarcomere. Every spike you trigger in Part 1 drives a twitch in Part 3.
The trace is a live membrane-voltage simulation, slowed way down. Give the membrane a 1 ms jolt of current and see whether it crosses threshold.
A Na⁺ channel conducts only when its activation gate is open and its inactivation gate hasn’t closed.
Steps light up in order each time a spike fires (with “Each spike triggers a twitch” on). Tap any step to highlight it.
Neither filament gets shorter. Thin filaments slide past thick ones, so the Z discs move closer together. Watch which bands change and which stay fixed.
Muscle relaxed. Tropomyosin covers the binding sites.
Write a prediction first, run the experiment, then open the explanation.
No. Below threshold you only get a small graded bump that fades. Once threshold is crossed, positive feedback (more depolarization opens more Na⁺ channels) produces a full spike of about the same height every time. This is the all-or-none principle. A stronger stimulus mostly makes the spike start sooner.
Right after a spike, the Na⁺ inactivation gates are closed, and no stimulus can reopen those channels until they reset. That is the absolute refractory period. At a 12 ms gap, 10 µA/cm² still fails but 20 µA/cm² fires a second spike: the membrane can fire again, but only with a stronger push, because some Na⁺ channels are still inactivated and K⁺ gates are still open. That is the relative refractory period. (This squid-axon model runs cold, so its refractory periods are longer than in a human neuron.)
No spike forms, because the rising phase depends on Na⁺ rushing in. Tetrodotoxin (pufferfish toxin) and local anesthetics like lidocaine work by blocking voltage-gated Na⁺ channels, so signals never reach the muscle.
Repolarization. Without K⁺ flowing out, the voltage drifts down slowly as Na⁺ channels inactivate and leak currents act. There is no undershoot below rest.
The I band and H zone shrink. The A band stays 1.60 µm because it is the length of the thick filaments, and filaments don’t change length. That observation in the 1950s is what led to the sliding filament model.
Myosin needs a new ATP to let go of actin. Without ATP, attached heads stay in the bound (rigor) state and the sarcomere can’t relax. SERCA pumps also need ATP, so Ca²⁺ isn’t cleared. This is why muscles stiffen in rigor mortis.
A single spike releases a brief pulse of Ca²⁺, so the sarcomere shortens and then relaxes. When spikes come fast enough, Ca²⁺ never gets pumped away and the contraction is sustained. This is tetanus (the physiology term, not the disease).