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ABSTRACT Recent studies have demonstrated that muscle force is not determined solely by activation under dynamic conditions, and that length history has an important role in determining dynamic muscle force. Yet, the mechanisms for how muscle force is produced under dynamic conditions remain unclear. To explore this, we investigated the effects of muscle stiffness, activation and length perturbations on muscle force. First, submaximal isometric contraction was established for whole soleus muscles. Next, the muscles were actively shortened at three velocities. During active shortening, we measured muscle stiffness at optimal muscle length (L0) and the force response to time-varying activation and length perturbations. We found that muscle stiffness increased with activation but decreased as shortening velocity increased. The slope of the relationship between maximum force and activation amplitude differed significantly among shortening velocities. Also, the intercept and slope of the relationship between length perturbation amplitude and maximum force decreased with shortening velocity. As shortening velocities were related to muscle stiffness, the results suggest that length history determines muscle stiffness and the history-dependent muscle stiffness influences the contribution of activation and length perturbations to muscle force. A two-parameter viscoelastic model including a linear spring and a linear damper in parallel with measured stiffness predicted history-dependent muscle force with high accuracy. The results and simulations support the hypothesis that muscle force under dynamic conditions can be accurately predicted as the force response of a history-dependent viscoelastic material to length perturbations. 

Abstract Although the phenomenon of residual force depression has been known for decades, the mechanisms remain elusive. In the present study, we investigated mechanisms of residual force depression by measuring the stiffness to force ratio during force redevelopment after shortening at different velocities. The results showed that the slope of the relationship between muscle stiffness and force decreased with decreasing shortening velocity, and the y-intercept increased with decreasing shortening velocity. The differing slopes and y-intercepts indicate that the stiffness to force ratio during isometric force redevelopment depends on the active shortening velocity at a given muscle length and activation level. The greater stiffness to force ratio after active shortening can potentially be explained by weakly-bound cross bridges in the new overlap zone. However, weakly-bound cross bridges are insufficient to explain the reduced slope at the slowest shortening velocity because the reduced velocity should increase the proportion of weakly- to strongly-bound cross bridges, thereby increasing the slope. In addition, if actin distortion caused by active shortening recovers during the force redevelopment period, then the resulting slope should be similar to the non-linear slope of force redevelopment over time. Alternatively, we suggest that a tunable elastic element, such as titin, could potentially explain the results.