Cardiac excitation-contraction coupling

Definitions & Key takeaways

Cardiac excitation-contraction coupling is the process by which an electrical signal generated by the sinoatrial node (the heart's natural pacemaker) is converted into a mechanical force that makes the heart contract. It occurs in a series of events that include:

Excitation: The process by which an electrical signal causes calcium ions to enter the cell.

Calcium is released from the sarcoplasmic reticulum.

Myofilament activation: The released calcium ions bind to troponin C, which causes tropomyosin to move out of the way and expose binding sites on actin for myosin heads. With the help of ATP, the myosin heads then attach to the actin filaments and slide them past each other, shortening the sarcomere (the basic unit of muscle contraction) and leading to cardiac muscle contraction.

Relaxation: The calcium ions are removed from the cytosol by the sarcoplasmic reticulum, and tropomyosin returns to its position blocking the binding sites on actin. This prevents further interaction between myosin and actin, and the muscle relaxes.

Chapters:

Watch video only

Introduction0:00–0:17

Cardiac excitation-contraction coupling is the relationship between electrical signals in the form of action potentials, and mechanical changes in the heart muscle cells, called cardiomyocytes, that causes them to contract.

Cardiomyocytes0:17–1:41

Let’s start by looking at the structure of a cardiomyocyte. Cardiomyocytes have branches, and have intercalated disks along their edges which have small holes called gap junctions that allow ions to flow from one cardiomyocyte to the next.
When a cardiomyocyte depolarizes, ions like calcium move from that cell into a neighboring cell, and these ions trigger depolarization to happen in that cell.
This is what makes cardiomyocytes part of a “functional syncytium,” they’re like a little community of cells intimately working together.
In addition, cardiomyocytes stay physically attached to one another through proteins called desmosomes, which are like staples that hold the cells together when they’re contracting.
Another feature of cardiomyocytes are passageways called transverse tubules, or T-tubules. T-tubules are extensions of the outside environment.
They increase the surface area of the cardiomyocyte and they look like the letter T, so it’s easy to remember their name.
Think of a large walk-through aquarium: you can walk through tunnels and look at the sea creatures all around you, but you’re not in the water with them.
Finally, there’s the sarcoplasmic reticulum, which is an organelle that stores intracellular calcium, the calcium that is sequestered inside the cell.
When a depolarization wavefront hits a cardiomyocyte, a few calcium ions flow through gap junctions, and if a threshold membrane potential is reached, then sodium channels start to open up.

Calcium-induced Calcium Release1:41–2:40

If there’s a depolarization, then ions start to move across the cell membrane, and that’s where the T-tubules play a key role.
During the part of the cardiomyocyte action potential when calcium ions flow into the cell, the presence of T-tubules helps bring calcium deep into the cell.
Once this extracellular calcium gets inside, it binds to the ryanodine receptors on the sarcoplasmic reticulum, which releases even more calcium into the cell - a process called calcium-induced calcium release.
The calcium helps activate two contractile proteins, actin and myosin, which are called myofilaments, and are ultimately responsible for cell contraction, and that’s the key moment when the chemical signal is converted into a mechanical signal.
When calcium ions enter the cardiomyocyte, they bind to troponin C, which is attached to a long thin protein called tropomyosin.
Tropomyosin is draped around yet another protein filament called actin, and it covers up binding sites on the actin, so that it cannot be bound by myosin heads which are lurking nearby.

Troponin C and Tropomyosin2:40–4:24

A bit like a protective parent not wanting a child to go out on a date. The calcium ions bind to Troponin C and that causes tropomyosin to slide off of the actin filament, exposing the actin binding sites.
At that point, myosin heads bind to actin forming a cross-bridge - when the parent’s away, the children will play. The myosin head pushes past the actin with a “power stroke”, effectively pulling the actin and myosin filaments past one another and shortening the muscle.
The myosin does this a few times with actin - binding, sliding past, reattaching, and then repeating this process and using up ATP along the way.
The myosin head looks a bit like an oar in a boat, it hits the water, shifts, and comes out, and this only works in the presence of calcium ions.
Eventually, calcium ions are removed by ion transporters, that rely on ATP or concentration gradients. Most of the calcium gets moved back into the sarcoplasmic reticulum or the extracellular environment, and some also moves into the mitochondria.
Once that calcium is gone, the troponin goes back to its original shape, which blocks the binding sites on the actin and prevents more cross-bridges from forming.
###SUMMARYAll right, as a quick recap: cardiac excitation-contraction coupling is when an action potential is converted into mechanical energy.
Calcium ions move into the cell via T-tubules and bind to troponin. The troponin changes conformation and exposes more of the actin filament, which has binding sites for myosin.

Review4:24–4:52

Myosin-actin bridges form using ATP and are part of the power stroke that pulls actin and myosin closer together - forming the basis for muscle contraction.
exposes more of the actin filament which has binding sites for myosin myosin actin bridges form using ATP and are part of the power stroke that pulls actin and myosin close together forming the basis for