In order to understand how rigor mortis comes about, one must know about how the muscle functions.
1 Muscle Structure
Before learning how the process works, one needs to have a basic idea of how a unit of muscle works. A unit of muscle is made up of the sarcomere, which is referred to as the basic unit of muscle. The sarcomere is made up of a thin filament, also known as actin, and a thick filament, also known as myosin.
Tropomyosin is a long protein strand that surrounds the thick filaments, or actin. Normally, tropomyosin covers binding sites on actin. You can think of it as rubber bands keeping actin in place and covering the binding sites.
Along the tropomyosin are special protein complexes called troponin. Calcium needs to bind to the complexes to allow binding of myosin heads to the actin binding sites, which are otherwise hidden without calcium. Here is a visual representation of the sarcomere.
2. Nerve Impulses
The brain receives an input to begin muscle contraction. It sends this signal down the spinal cord and to something called the neuromuscular junction (NMJ). The NMJ releases a chemical substance called acetylcholine when it reaches the nerve signal. This substance binds to the receptors onto a muscle fiber’s surface.
After acetylcholine binds to the receptor on the surface of the muscle fiber, sodium ions are released, triggering an action potential. An action potential occurs when the electrochemical characteristic of an individual cell changes. The influx of the sodium ions changes the muscle cell’s electrical potential, causing an action potential to be fired. This action potential is a very quick and short-lasting electrical event that can be considered as fast traveling nerve information.
4. Calcium Binding
This action potential served to release calcium into the muscle fiber. These calcium ions now bind to the troponin complex on the tropomyosin. This reveals the troponin complex. In other words, calcium binding causes the troponin complex structure to change shape, allowing binding of myosin heads. The tropomyosin also moves away from the binding sites on actin, allowing myosin to bind to the binding sites now revealed on actin.
5. Crossbridge Cycle
Now that all of the events prior to muscle contraction has happened, the crossbridge cycle can happen. If you have checked out the visual representation of the sarcomere from step one, you should have noticed that the thin filaments are on the outer part of the sarcomere and the thick filament is in the middle. The goal of the crossbridge cycle is for the thick filament (myosin) to pull the thin filament (actin) to the middle of the sarcomere. This is referred to as a muscle contraction. It is also referred to as sarcomere shortening.
6. Crossbridge Initiation
When a myosin head, which looks like a tail, binds to the binding site on actin, it forms a crossbridge. In order for this to happen, it needs to be activated. Normally, activated myosin heads have one molecule of adenosine diphosphate (ADP) and one molecule of inorganic phosphate attached to it. This causes the myosin head to bind to the actin, forming the crossbridge.
7. Release of Inorganic Phosphate
After the initial binding between actin and the myosin head, the inorganic phosphate is released. After it is released, the binding between the two filaments becomes even stronger.
8. Power Stroke
The next step involves the release of the ADP molecule. This causes the myosin head to pivot, which results in pulling the actin towards the middle of the sarcomere causing sarcomere shortening, or muscle contraction.
The high energy containing molecule adenosine triphosphate (ATP) next binds to the myosin head. It provides the energy to liberate the myosin head from the actin binding site. Now, the myosin head is released, detaching the crossbridge. Soon after, the ATP is hydrolyzed to inorganic phosphate and ADP, which as you recall, activates the myosin head to repeat the crossbridge cycle. As long as there is sufficient ATP, the crossbridge cycle can continue.
10. Rigor Mortis
After death, all bodily processes stop. This means the body will no longer produce the ATP that is necessary to release the myosin head from the actin. This causes the myosin head and actin to remain bound together. When this takes place for a long time, rigor mortis results.
Muscle contraction is a relatively complicated process. There are two types of filaments within the basic unit of a muscle fiber known as thick and thin filaments. A muscle contraction causes binding of a myosin head from the thick filament onto a binding site on the thin filament. This leads to the pulling of the thin filament to the center of the muscle unit. Upon death, there is no more ATP to dissociate the thick filament from the thin filament, slowly leading to brittleness and muscle stiffness, which is otherwise known as rigor mortis.