Spastic muscles are a common impairment in cerebral palsy and present with an increased stiffness compared to normal. Definitive conclusions regarding the origin of this increased stiffness have not been made.

The purpose of this study was to investigate whether the increased stiffness observed in spastic muscle may be attributed to changes in the mechanical properties of ti tin, a giant myofibrillar protein known to be related to passive force development at the myofibril level and to adapt to altered stimuli and disease.

Single spastic myofibrils were able to generate up to five times the passive stresses seen in cardiac myofibrils while expressing titin isoforms with large molecular weights. It was concluded that titin does play, at least in part, an important role in the increased passive stiffness seen in spastic muscle. However, an alternative mechanism to increase passive stiffness may be recruited by spastic muscles.