Passive force enhancement is not abolished by shortening of single rabbit psoas fibres

Passive force enhancement is defined as the increase in steady-state passive force following deactivation of an actively stretched muscle compared to the corresponding passive force following passive stretching of the muscle. Passive force enhancement has been associated with contributing to the residual force enhancement property, providing stability to sarcomeres, and preventing sarcomeres from over-stretching during eccentric muscle action. Despite its functional importance, the molecular mechanisms underlying passive force enhancement remain unknown. Specifically, it remains unknown how passive force enhancement develops and how it is abolished. Incidental observations on cat soleus muscles led to the speculation that passive force enhancement is abolished when the actively stretched muscle is deactivated and then passively shortened to its pre-stretched length. Here, we tested this hypothesis using skinned fibres from rabbit psoas and rejected it. Rather, we found that passive force enhancement increased following shortening of the fibres to their pre -stretched length (2.4 mu m), and furthermore, that the passive force enhancement increased by 70-106% when the shortening and subsequent stretch to the original length (3.6 mu m) increased in duration (200 ms, 6 s, and 14 s). These results indicate that passive force enhancement increases during a shortening-stretch cycle, and that this increase is time-dependent. We propose that this increase in passive force enhancement is caused by titin; specifically, with a refolding of titin's immunoglobulin domains that were unfolded during the active fibre stretching that produced the residual and passive force enhancement. Molecular level experiments are required to test this proposal.

Automated summary

Passive force enhancement refers to the increase in force generated during passive stretching of a muscle after it has been actively stretched. The mechanism behind this enhancement is still unclear, but it is believed to be related to the stability of sarcomeres and protection against over-stretching. A hypothesis that passive force enhancement is abolished when the actively stretched muscle is deactivated and passively shortened was rejected in experiments with rabbit psoas fibers. Instead, it was found that passive force enhancement increased when the fibers were shortened and then stretched again, and this increase was time-dependent. These findings suggest that titin, a protein involved in muscle contraction, may play a role in passive force enhancement. Molecular level experiments are needed to test this hypothesis.