Smooth muscles experience cross-bridge cycling when they contract but it has some differences from the sliding filament model. Smooth muscles are not made of sarcomeres but have actin and myosin filaments which are less organised than those in skeletal and cardiac muscles. Ca²⁺ binds to calmodulin (instead of troponin C) which activates myosin light chain kinase (MLCK). This complex catalyses a change in conformation of myosin heads with an increase in its ATPase activity that allow them to bind with actins. Calponin and caldesmon block the ATPase activity of myosin heads but are released with Ca²⁺ binding. Cross-bridge cycling also occurs less frequently in smooth muscle.

The many nuclei can coordinate simultaneous contraction of actin and myosin filaments along the whole length of the muscle fibre. If muscle cells are separate and have only one nuclei, there is a need to communicate with each other via cell signalling. This would slow down contraction unnecessarily.

Muscles become more resistant to stretch after death because of the accumulation of Ca²⁺ that is no longer taken up into the sarcoplasmic reticulum (no active transport mechanism). The cross-bridges are permanently formed. This causes muscle to become stiff and it is difficulty to induce forced movement of muscles externally.

This is to induce treppe so that muscle contraction will be more efficient and stronger when the exercise regime begins.