We know that an action potential is produced by an active cell membrane when the stimulus reaches a certain threshold. When it does, an action potential fires, and when it doesn't, nothing happens.

There are dozens of videos online painstakingly illustrating this point, using examples going from plumbing to pebbles falling down a paper towel.

But this is such a simple idea. There doesn't need to be analogies. When I push a button, something moves, when I don't push it, nothing moves.

But what is the fundamental principle behind this? What biochemical device causes this all or nothing phenomena?


The fundamental principle behind this is a "sensor" or the excitation-contraction coupling, regardless where you are. Let's consider the striated muscle and the cardiac muscle.

The function of excitation-contraction coupling in skeletal muscle is as voltage sensor to tell the SR, "We have got an action potential; release Ca2+ for contraction". This is a contrast to a heart muscle which works like a Ca2+ channel (i.e. Ca2+ is flowing in cardiac muscle continuously). Similarly, xcitation-contraction coupling in cardiac muscle translates the action potential into the production of tension. There are individual steps in this process of cardiac muscle:

    1. The cardiac action potential is initiated in the myocardial cell membrane, and the depolarization spreads to the interior of the cell via the T tubules. Recall that a unique feature of the cardiac action potential is its plateau (phase 2), which results from an increase in Ca and an inward Ca2+ current in which Ca2+ flows through L-type Ca2+ channels (dihydropyridine receptors) from extracellular fluid (ECF) to intracellular fluid (ICF).
    1. Entry of Ca2+ into the myocardial cell produces an increase in intracellular Ca2+ concentration. This increase in intracellular Ca2+ concentration is not sufficient alone to initiate contraction, but it triggers the release of more Ca2+ from stores in the sarcoplasmic reticulum through Ca2+ release channels (ryanodine receptors). This process is called Ca2+- induced Ca2+ release, and the Ca2+ that enters during the plateau of the action potential is called the trigger Ca2+. Two factors determine how much Ca2+ is released from the sarcoplasmic reticulum in this step: the amount of Ca2+ previously stored and the size of the inward Ca2+ current during the plateau of the action potential.
    1. and 4. Ca2+ release from the sarcoplasmic reticulum causes the intracellular Ca2+ concentration to increase even further. Ca2+ now binds to troponin C, tropomyosin is moved out of the way, and the interaction of actin and myosin can occur. Actin and myosin bind, cross-bridges form and then break, the thin and thick filaments move past each other, and tension is produced. Cross-bridge cycling continues as long as intracellular Ca2+ concentration is high enough to occupy the Ca2+-binding sites on troponin C.
    1. A critically important concept is that the magnitude of the tension developed by myocardial cells is proportional to the intracellular Ca2+ concentration. Therefore, it is reasonable that hormones, neurotransmitters, and drugs that alter the inward Ca2+ current during the action potential plateau or that alter sarcoplasmic reticulum Ca2+ stores would be expected to change the amount of tension produced by myocardial cells.

I like this figure about the topic in summarising stimuli in the smooth muscle:

enter image description here

In heart

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In the gastrointestinal tract, we have then again special cells, Cajal cells, that work as "pacemakers" of the GI tract. Myenteric Interstitial cells of Cajal [ICC-MY] serve as a pacemaker which creates the bioelectrical slow wave potential that leads to contraction of the smooth muscle. This activity differs along the length of the system

  • 3 per minute in the stomach
  • 11-12 per minute in the duodenum
  • 9-10 per minute in the ileum
  • 3-4 per minute in the colon

You can see them as to work analogously through the "all-or-none" principle.


  • Costanzo, Physiology
  • Pocock, Physiology
  • My notes during during years 2011-2014 (in three Physiology courses and research)

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