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.
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. 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. 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.
