There are a range of theories to account for the increase in range of movement that occurs with stretching.

Lengthening contractile units

One theory is that stretching lengthens the actual contractile units within muscles.

These units are called sarcomeres, and are made up of two types of protein molecules called myosin and actin. These molecules are very long and come in pairs. The myosin can attach to actin and through a series of specific chemical reactions involving calcium, ATP and magnesium, ratchet itself along.

This causes the sarcomere to shorten, which is the basis for muscle contraction.

At one time the primary theory to explain the increase in range of motion from stretching was that the body responded to stretching by increasing the length of the myosin and actin molecules, meaning that at rest the sarcomere was actually longer.

Lengthening fascia

Another theory relates to the connective tissue surrounding muscle.

All organs in the body, including muscles, sit within a matrix of connective tissue or fascia, that helps support these organs and connect them to the surrounding body.

The fascia is not able to contract like sarcomeres, but some forms of connective tissue can be elastic to allow for movement of the underlying organ.

There has been speculation that stretching alters the structure of the fascia, allowing it to lengthen more under force, and that this accounts for the lengthening of muscle with stretching.

Neurological changes

The current best theory is that stretching doesn’t actually introduce any structural change to the muscle or connective tissue.

Stretching alters the brain’s perception of discomfort or pain at the end-ranges of movement.

We know that pain can cause inhibition of muscle activation, so reducing perceived pain at the end range allows you to more effectively contract your muscles throughout the full range of your movement.

The thinking is that this is why it increases functional range of movement.