Everyday Q&A: What causes rigor mortis?

Rigor mortis, the stiffening of a body several hours after death, arises from a combination of two of the oldest definitions of death – cessation of the heartbeat and cessation of breathing. Once either of these essential functions stops, the cells of the body lose their oxygen supply and can no longer perform aerobic respiration.

Immediately after death, the muscles of the body contract in the same manner as they do when the person is alive. Muscle is formed of bundles of long and narrow cells that can span the entire muscle’s length.

In the resting state, these cells build up the electric potential across their membrane by actively pumping out calcium ions. Upon receiving a signal from a neuron, the muscle cells open the calcium channels in their cell membrane, and the calcium ions rush in due to the voltage difference between the inside and outside of the cell.

These ions then interact with actin and myosin filaments to cause muscle contraction. The muscles remain in the contracted state until adenosine triphosphate (ATP) binds to myosin, releasing the myosin and actin filaments from one another.

Additionally, muscle cell membrane proteins use ATP to actively pump the calcium ions back out of the cell, restoring the membrane potential and preventing the calcium ions from re-stimulating contraction.

ATP consists of three phosphate groups, ribose, and adenine.

When breathing and circulation stop, muscle cells lack oxygen and therefore cannot use aerobic respiration to efficiently produce ATP. Respiration continues anaerobically at first, but the muscle cells eventually become so short on ATP that the myosin and actin filaments cannot release from the contracted state and the calcium ions cannot be pumped back out of the muscle cell.

Unable to release contraction, all the muscles of the body remain tense, causing rigor mortis.