Observations of contracting muscle fibrils in cultured cells indicate that the force which restores the resting length of the sarcomere comes from the contractile elements themselves and not from external elasticity, as is now generally accepted. In light of biochemical studies on the contraction-relaxation cycle, it is postulated that the elongating force is one of internal elasticity in the sarcomere, which arises during contraction from the distortion of bonds between filaments and/or structural proteins. This mechanism of restoration may serve to establish optimal sarcomere length for production of maximum contractile force, and in cardiac muscle this mechanism may be a factor in ventricular filling.