The main job of the heart is to pump blood all over the body, to our organs and tissues and keep them oxygenated.
It does so by contracting around 70 times per minute.
The physiological basis of cardiac contractility is the synchronous contraction of heart muscle cells, aka cardiomyocytes.
Cardiac contractility is a measure of the strength of cardiomyocytes, to contract.
In order for cardiomyocytes to contract, they first need to depolarize.
Depolarization is when ions move across the membrane of a cell, and the membrane potential becomes less negative or even slightly positive.
Think of a really pessimistic negative cell throwing his hands up and enjoying a moment of joy.
When one cell depolarizes enough - it can cause some ions like calcium to flow into neighboring cells and trigger them to depolarize as well.
If one cell after another depolarizes, then there’s a depolarization wave which you can imagine would look like a wave moving through a crowd at a football stadium.
Each depolarization wave causes a heart muscle contraction, so the rate at which depolarization waves ripple through the heart actually sets the heart rate.
This depolarization wave starts with the sinoatrial node, which sometimes gets called the SA node and then moves through the rest of the heart to cause a contraction.
So if depolarization waves are going through about once per second, that means that your heart beats once per second, or sixty times in a minute.
Now let’s zoom in on a cardiomyocyte.
These hard working cells have branches and intercalated disks along their edges which have small holes called gap junctions that allow ions to flow from one cardiomyocyte to the next.
When ions like calcium move from that cell into a neighboring cell, this triggers depolarization, and cardiomyocytes depolarize one after another.
Another feature of cardiomyocytes are passageways called transverse tubules, or T-tubules.
T-tubules are invaginations or tunnels of the cardiomyocyte membrane that increase the surface area of the cardiomyocyte and they look like the letter T, so it’s easy to remember their name.
One last important element to depolarization and contraction is the sarcoplasmic reticulum, which is an organelle that stores the intracellular calcium.
When a depolarization wavefront hits a cardiomyocyte, a few calcium ions flow through gap junctions,
Looking at the cell membrane, if a threshold membrane potential is reached, then sodium channels start to open up.
If there’s depolarization, then calcium and sodium ions start to move across the cell membrane and into the cell.
That’s where the T-tubules play a key role, by bringing 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.
This process helps to activate two contractile proteins, actin and myosin, which are called myofilaments.
Myosin is able to attach and pull actin with the help to adenosine-triphosphate or ATP to form cross-bridges that result in shortening of the muscle fiber.
Eventually, calcium ions are removed by ion transporters, that rely on ATP or concentration gradients.
Now that we understand how a cardiomyocyte contracts, we can look at the various factors that affect cardiomyocyte contractility.
Contractility is directly related to the concentration of calcium within the cardiomyocyte so any factors that increase intracellular calcium levels will increase cardiac contractility.
Since calcium is stored in the sarcoplasmic reticulum, concentrations of calcium will vary with: how much calcium there is intracellularly and how much calcium is stored within the sarcoplasmic reticulum to be released.
One of the main methods intracellular calcium can be changed is with the autonomic nervous system.
The heart is innervated by both parasympathetic and sympathetic neurons of the autonomic nervous system.
Sympathetic neurons has a positive inotropic effect, where positive means increase, and inotropic refers to contractility.
So sympathetic stimulation increases cardiac contractility, by releasing catecholamines like norepinephrine, which bind to beta 1 receptors on cardiomyocytes.
Activation of the beta 1 receptors leads to downstream phosphorylation of proteins like sarcolemmal calcium channels on the sarcoplasmic reticulum membrane which increases the sarcoplasmic reticulum’s ability to release calcium.