= Solution
In a classical <action potential>, delayed activation of <voltage-gated potassium channels> supplies outward <electric current> that drives <repolarization>. In the <Hodgkin-Huxley model>, for example, $I_K=\bar g_Kn^4(V-E_K)$ and $\dot n=\alpha_n(V)(1-n)-\beta_n(V)n$. Increasing the opening rate at depolarized <membrane potential>, other properties fixed, recruits outward <electric current> earlier: the <action potential> generally becomes narrower and may have a smaller peak. Slower opening delays <repolarization> and broadens the <action potential>.
Slower closing after <repolarization> retains excess <potassium> <electrical conductance>, lengthening the after-<hyperpolarization> and often the interval of reduced excitability. Faster closing shortens this tail and permits earlier recovery. If activation or the available <electrical conductance> is insufficient, normal <repolarization> may fail; changing rates can also change the steady open fraction. Duration is therefore determined by the whole balance of inward and outward <electric currents>, not by a closing rate in isolation.
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