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The mechanisms causing the steady-state force enhancement following active skeletal muscle stretching are not well understood. Recently, we found direct evidence that part of the force enhancement is associated with the engagement of a passive component. In this study, we reproduced the conditions that give consistent passive force enhancement and evaluated the mechanical properties of this passive force enhancement so as to gain insight into its source. The three primary results were that (1). the passive force enhancement is long lasting (>25 s), (2). passive force enhancement was reduced in a dose-dependent manner by the amount of shortening preceding active muscle stretching, and (3). passive force enhancement could be abolished 'instantaneously' by shortening-stretching the passive muscle by an amount equivalent to the active stretch magnitude. Together with the remaining results, we conclude that the source of the passive force enhancement must be arranged in parallel with the contractile force, it must consist of a viscoelastic molecular spring whose stiffness characteristic can be reset by shortening, and it must have a characteristic length that is governed by the length of the contractile components, possibly the sarcomeres. Based on these results, the molecular spring titin emerges as a possible candidate for the passive component of the steady-state force enhancement observed in this and previous studies.
Herzog et al. (Tue,) studied this question.
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