Action potentials in skeletal muscle cells
Do you know what’s special about action potentials in skeletal muscle cells?
In part 3 of this Chalk Talk series on action potentials, we’ll focus on the ion transport process
in the skeletal muscle cell.
The generation of action potentials in skeletal muscle cells is similar to that in neurons,
which we looked at in part 2 of this Chalk Talk series:
In the default state, chloride and potassium channels are open in the skeletal muscle cell membrane,
termed the sarcolemma.
Together, the channels generate a resting potential of approximately -85 millivolts,
which is significantly lower than that of neurons.
Therefore, the sarcolemma needs to be depolarized stronger
than the neuron to reach the threshold potential of -55 millivolts.
Generally, this requires the accumulation of multiple stimuli at the motor end plate
termed excitatory postsynaptic potentials, in short, EPSP.
The neuron releases acetylcholine, which binds to ligand-gated
sodium channels in the sarcolemma.
Through these channels, sodium flows down its concentration gradient into the
skeletal muscle cell and the membrane potential increases.
Once the threshold potential is reached, the voltage-gated sodium channels in the
sarcolemma also open.
Even more sodium ions flow into the cell, leading to depolarization with a membrane
potential of around +25 millivolts.
Similar to the neuronal action potential, the sodium channels in muscle cells begin to
close before reaching the theoretical maximum potential, which we explained in part 2.
Additionally, there’s delayed voltage-dependent potassium channel opening.
The efflux of potassium ions down their concentration gradient repolarizes the
sarcolemma.
Because of the highly negative resting potential, repolarization doesn’t lead to afterhyperpolarization, as is the
case in neurons.
Whether repolarization is also shaped by the voltage-gated chloride channels of the
sarcolemma, which play a role in generating the resting potential,
is still subject to research.
But as soon as a chloride channel opens, chloride ions flow down their concentration
gradient into the skeletal muscle cell.
With their negative charge, they reduce the positive excess charge in the cell,
stabilizing the resting potential and reducing skeletal muscle cell excitability.
Conversely, inhibiting voltage-gated chloride channels increases skeletal muscle cell
excitability.
Physiologically, this is important particularly when extracellular potassium levels
increase as a result of muscle activity.
Without a regulatory mechanism, voltage-gated sodium channels in the sarcolemma
could then no longer be easily activated, leading to difficulties in forming action
potentials.
In skeletal muscle cells, the action potential duration is up to 10 milliseconds
and slightly longer than that of a neuron, whereas the refractory period is short.
For most muscles, contraction occurs only at the end of an action potential.
This is because the action potential needs to pass along the sarcolemma, down the
T-tubules.
There, the action potential causes the sarcoplasmic reticulum to release calcium ions,
initiating muscle contraction via the crossbridge cycle.
This time difference explains why skeletal muscles can enter a tetanized state, that
is, they’re under sustained contraction: Because of their short duration,
sequential action potentials can be so close to one another that the intervals between
them are about one-third to one-quarter of the duration of a single muscle twitch.
The resulting tetanic contraction is physiologically important in generating maximum
muscle strength but can also lead to pathological muscle cramps.
Such cramps need to be avoided in cardiac muscle, which we'll delve into in the
next episode.