Force enhancement in lengthening contractions of cat soleus muscle in situ: transient and steady-state aspects

Force enhancement (FE) associated with lengthening is a well-accepted phenomenon of active skeletal muscle, but the underlying mechanism(s) remain unknown. Similar to force depression (FD) following active shortening, the mechanism of FE may be attributed, at least in part, to cross-bridge kinetics. To examine this relationship, a post hoc analysis was performed on the transient force relaxation phase of previous in-situ FE experiments in soleus muscle-tendon units of anesthetized cats. For each muscle (n = 8), nine eccentric lengthenings (3 amplitudes, 3 velocities) were performed while tetanically stimulated (3T at 30 Hz, 3× α motorneuron, 35 ± 1°C). To determine transient aspects of FE, the period immediately following stretching was fit with an exponential decay function (R(2) > 0.95). Statistical analyses revealed that total steady-state FE (FE(SS)) increased with stretching amplitude and applied mechanical work. A positive relationship was observed between the active FE(SS) and rate of force decay (k), indicating that a kinetic mechanism may explain active FE. However, for all muscles and stretch conditions, there was no correlation between the total amount of FE(SS) and rate of decay. Therefore, FE cannot be explained solely by an active FE mechanism involving the interaction of actin and myosin. Rather, these findings suggest a combination of underlying mechanisms, including a kinetic mechanism for active FE, contributions of a passive elastic element, and possibly an activatable passive component operating outside of actin–myosin cross-bridging. Moreover, this transient analysis identifies that FE is not simply the opposite of FD, and its underlying mechanism(s) cannot simply be the opposite in nature.