Force enhancement after stretch in mammalian muscle fiber: no evidence of cross-bridge involvement

Stretching of activated skeletal muscles induces a force increase above the isometric level persisting after stretch, known as residual force enhancement (RFE). RFE has been extensively studied; nevertheless, its mechanism remains debated. Unlike previous RFE studies, here the excess of force after stretch, termed static tension (ST), was investigated with fast stretches (amplitude: 3-4% sarcomere length; duration: 0.6 ms) applied at low tension during the tetanus rise in fiber bundles from flexor digitorum brevis (FDB) mouse muscle at 30 degrees C. ST was measured at sarcomere length between 2.6 and 4.4 mu m in normal and N-benzyl-p-toluene sulphonamide (BTS)-added (10 mu M) Tyrode solution. The results showed that ST has the same characteristics and it is equivalent to RFE. ST increased with sarcomere length, reached a peak at 3.5 mu m, and decreased to zero at similar to 4.5 mu m. At 4 mu m, where active force was zero, ST was still 50% of maximum. BTS reduced force by similar to 75% but had almost no effect on ST. Following stimulation, ST developed earlier than force, with a time course similar to internal Ca2+ concentration: it was present 1 ms after the stimulus, at zero active force, and peaked at similar to 3-ms delay. At 2.7 mu m, activation increased the passive sarcomere stiffness by a factor of similar to 7 compared with the relaxed state All our data indicate that ST, or RFE, is independent of the cross-bridge presence and it is due to the Ca2+ induced stiffening of a sarcomeric structure identifiable with titin.