Problem:
Question: How does spacing apart sodium and potassium channels allow the action potential to travel faster down the axon?
This is the reason always cited for saltatory conduction and myelination, but my mental model of conduction tells me that the density of ion gates along the axon should not affect the speed of the AP.
To illustrate, consider a myelinated axon. A wave of Na+ from action potential site 1, a node of Ranvier, rushes into and quickly diffuses down the axon. (It travels in both directions, but backwards is still in the refractory period.) It diffuses through the myelinated region, its concentration always diminishing. Before it attenuates too much, however, it happens upon node of Ranvier 2, where it triggers another action potential. A new wave of Na+ rushes in and the cycle repeats. This should be plain so far.
Now imagine that there is actually a node of Ranvier halfway between node 1 and 2, called node 1.5. The wave of Na+, on its way to node 2, happens to trigger an action potential at node 1.5, from which a wave of Na+ pours in and either boosts the original wave or replaces it by taking its momentum. Now the reinforced wave proceeds to node 2 and triggers it just as soon as, perhaps even sooner than, if node 1.5 had not existed. Repeatedly insert nodes at higher densities until the situation is simply lack of myelination, and we conclude that unmyelinated axons can transmit an action-potential-triggering wave of Na+ as fast as or faster than a myelinated one.
In short, my point of confusion is this: I cannot see how a higher density of gated channels can possibly slow down the wavefront of Na+ that triggers action potentials. If anything, the additional influxes of Na+ should speed up the all-important wavefront, assuming that new waves really "either boost the original wave or replace it by taking its momentum", and also assuming that the wavefront of Na+ is really all-important for signal transmission, and also assuming that the mere presence of (voltage?) gated ion channels in the membrane does not significantly retard the wavefront.
But the usual explanation for why saltatory conduction is faster than continuous conduction (a fact I hope is empirically and unambiguously established) relies on the putative slowing effect of ion channels on the signal fore. Please explain this effect in more detail, if it is not a misconception.
Please explain action potential to travel faster down the axon.