At the end of the force transient elicited by a fast stretch applied to an activated frog muscle fiber, the force settles to a steady level exceeding the isometric level prior the stretch. We showed previously that this excess of tension, referred to as "tatic tension" is due to the elongation of some elastic sarcomere structure, outside the cross-bridges. The stiffness of this structure, "tatic stiffness" increased upon stimulation following a time course well distinct from tension and roughly similar to intracellular Ca²⁺ concentration. In the experiments reported here we investigated the possible role of Ca²⁺ on static stiffness by comparing static stiffness measurements in presence of Ca²⁺ release inhibitors (D600, Dantrolene, D₂O) and cross-bridge formation inhibitors (BDM, hypertonicity). Both series of agents inhibited tension, however only D600, Dantrolene and D₂O decreased at the same time static stiffness, while BDM and hypertonicity leaved static stiffness unaltered. These results indicate that Ca²⁺, in addition to promote cross-bridge formation, increases the stiffness of an (unidentified) elastic structure of the sarcomere. This stiffness increase may help in maintaining the sarcomere length uniformity under condition of instability.