New Insights into Force After Active Stretch in Damaged Skinned Muscle Fibres

Abstract

The steady-state isometric force after active stretching of muscles is higher than the purely isometric force at the corresponding lengths. It has been suggested that the increase in force after active stretch has an active component associated with actin-myosin cross-bridges and a passive component associated with titin. The aim of this study was to gain insight into the contribution of the passive component to the increase in force after active stretching by reducing the active contribution to force. It has been shown that repeat stretching of a muscle causes substantial damage and reduction in the isometric active force. Therefore, we reduced isometric active force by repeatedly (4 times) activating skinned muscle fibres (n=16) at a sarcomere length (SL) of 2.4μm and then stretching them to a SL of 4.0μm. Isometric active force at a SL of 2.4μm was reduced from 200±25N/mm2 in the first test to 50±25N/mm2 for tests 2-4, indicating a stretch-induced loss in isometric cross-bridge force before stretch. However, force at steady-state after active stretch was not different between the tests. The absence of force loss after active stretch in damaged fibres, where cross-bridge force is substantially decreased, indicates that the passive component plays a major role in force production after active stretch. However, this result could also be explained if muscle damage is increasing the proportion of weakly-bound cross-bridges at the expense of strongly-bound cross-bridges. When the fibre is actively stretched, weakly-bound cross-bridges recover their capacity to produce force, and thus the steady-state force after active stretch is not reduced. However, knowing that at a SL of 4.0μm cross-bridge involvement in force production is minimal, it is likely that a passive element is the structure responsible for force after active stretch.