Why is Cardiac Muscle Contraction more delayed than Skeletal Muscle Contraction (on average)?

[manohman]

Granted Skeletal muscle can come in 3 different forms, Slow Oxidative, Fast Oxidative, and Fast Glycolytic, in order of decreasing speed and increasing rate of fatigue.

Skeletal muscle is presented as contracting sooner after an action potential reaches it than in cardiac muscle. Why is this?

Is it because in Skeletal muscle, the action potential goes through the cell directly causing contraction of that cell, while in cardiac muscle/the heart, the action potential must spread from cell to cell (from SA (atria contract) to AV to Bundle to Purkinje (Ventricle) contract?

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[Czarcasm]

Granted Skeletal muscle can come in 3 different forms, Slow Oxidative, Fast Oxidative, and Fast Glycolytic, in order of decreasing speed and increasing rate of fatigue.

Skeletal muscle is presented as contracting sooner after an action potential reaches it than in cardiac muscle. Why is this?

Is it because in Skeletal muscle, the action potential goes through the cell directly causing contraction of that cell, while in cardiac muscle/the heart, the action potential must spread from cell to cell (from SA (atria contract) to AV to Bundle to Purkinje (Ventricle) contract?

Gap junctions, which relies on diffusion are part of the reason. But I believe a more significant reason is because cardiac muscle have a less developed sarcoplasmic reticulum than skeletal muscle fibers do and therefore relies largely on extracellular Ca2+ for contraction (as well propagation of the action potential itself). If you recall, calcium is stored in the SR for release and upon binding to troponin, triggers a series of conformational changes that allow muscle to contract.

Also, it's probably worth noting the differences between the action potentials themselves. Cardiac Muscle AP has a longer refractory period because of the associated plateau (a brief period where Ca2+ influx and K+ efflux balance). One of the consequences of this is that cardiac muscles can never lock up (ie. reach tetany) as skeletal muscles do. In skeletal muscles, another AP can be generated while contraction is still occuring, allowing a stronger contraction to occur with the ultimate possibility of achieving tetany but in cardiac muscles, one full contraction must be completed before a new contraction can be generated.

 

[manohman]

Gap junctions, which relies on diffusion are part of the reason. But I believe a more significant reason is because cardiac muscle have a less developed sarcoplasmic reticulum than skeletal muscle fibers do and therefore relies largely on extracellular Ca2+ for contraction (as well propagation of the action potential itself). If you recall, calcium is stored in the SR for release and upon binding to troponin, triggers a series of conformational changes that allow muscle to contract.

Also, it's probably worth noting the differences between the action potentials themselves. Cardiac Muscle AP has a longer refractory period because of the associated plateau (a brief period where Ca2+ influx and K+ efflux balance). One of the consequences of this is that cardiac muscles can never lock up (ie. reach tetany) as skeletal muscles do. In skeletal muscles, another AP can be generated while contraction is still occuring, allowing a stronger contraction to occur with the ultimate possibility of achieving tetany but in cardiac muscles, one full contraction must be completed before a new contraction can be generated.

I see that makes sense. In skeletal muscle the action potential causes VG channels to open up in the Plasma Membrane letting Extracellular Ca in to the cell, and it also causes the Sarcoplasmic Reticulum to "unplug" to let more calcium out.

In the cardiac contracile cells, these calcium channels are mostly in the membrane? So we pump out calcium into our heart ECF as well (im guessing on the side opposite from the lumen/where blood comes in).

Regarding the differences in the action potentials themselves, it makes sense that the long refractory period in the cardiac contractile cells is to ensure that tetanus doesnt occur, but doesnt the SA Node (along with the vagus nerve regulating it) set the pace? Is the long refractory period in the contracile cells a secondary measure in case the SA node goes wack, in addition to the AV node already there as well?).

And the AV node cannot contract on its own right?

Thanks for this man, really opening me up to a better understanding.

 

[Czarcasm]

I see that makes sense. In skeletal muscle the action potential causes VG channels to open up in the Plasma Membrane letting Extracellular Ca in to the cell, and it also causes the Sarcoplasmic Reticulum to "unplug" to let more calcium out.

In the cardiac contracile cells, these calcium channels are mostly in the membrane? So we pump out calcium into our heart ECF as well (im guessing on the side opposite from the lumen/where blood comes in).

Regarding the differences in the action potentials themselves, it makes sense that the long refractory period in the cardiac contractile cells is to ensure that tetanus doesnt occur, but doesnt the SA Node (along with the vagus nerve regulating it) set the pace? Is the long refractory period in the contracile cells a secondary measure in case the SA node goes wack, in addition to the AV node already there as well?).

And the AV node cannot contract on its own right?

Thanks for this man, really opening me up to a better understanding.

You basically got it. Just a few things to clarify. Because of skeletal muscle's well developed SR, they rely entirely on intracellular Ca2+ (no extracellular Ca2+ is involved here). The stimulus for their release is via a voltage-gated protein (DHPr) which upon receiving the AP as it propagates along the sarcolemma, tugs on a channel of the SR (to which it's attached; the SR RyR Ca2+ channel) to release those stored intracellular calcium ions. In cardiac muscle, SR is involved to a lesser degree but they also have Ca2+ pumps to pump out Ca2+ during relaxation periods. This calcium is pumped into the interstitium, the fluid between cells and so is still in the same localized area for reuse.

Also, recall that cardiac muscle contraction exhibits automaticity because of the specialized nodal cells (which themselves, have their own unique action potential triggered spontaneously). That is to say, no special stimulus is needed to trigger cardiac muscle cells to contract (as skeletal muscles require), since they instead do so on their own via nodal cells. There are 3 generalized types of nodal cells: SA, AV, and Purkinjee fibers. Of the 3, SA nodes trigger AP's at the largest rate and have the potential to cause a heartbeat of 100 bpm. However, vagal tone inhibits some of this stimulation and reduces the heart rate to about 75 bpm. We also have sympathetic input that can do just the opposite, increasing the heart rate, even beyond 100 bpm in some instances. If the SA node fails, the AV node takes over. If both SA and AV nodes fail, Purkinje fibers take over (lowest AP's generated per unit time) which triggers about 20 bpm, unfortunately, not enough to sustain life.

The whole thing is really intricate and I can go on and on about all those intricacies but it's highly unlikely you'll be tested on all those random facts. I think if you understand the major differences, you'll be okay, so don't sweat it.