Mechanism of force potentiation after stretch in intact mammalian muscle

The isometric tension following a stretch applied to an active muscle is greater that the isometric tension at the same sarcomere length. This force potentiation, known as residual force enhancement (RFE), has been extensively studied, nevertheless its mechanism remains debated. In the experiments reported here, unlike RFE studies, 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 on the tetanus rise of FDB mouse muscle at 30°C. The measurements were made between 2.6 and 4.4 µm sarcomere length in normal and BTS-added (10 µM) Tyrode solution. ST increased with sarcomere length, reaching a peak at 3.5 µm and decreasing to zero at ~4.5 µm. At 4 µm, active force was zero but ST was still 50% of maximum. BTS reduced force by ~75% but had almost no effect on ST. Following activation, ST develops faster than force, with a time course similar to intracellular [Ca2+], starting to rise 1 ms after the stimulus, at zero active force, and peaking at 3–4 ms delay after the stimulus. At 2.7 µm, for a stretch of 1% sarcomere length, ST was ~3% of tetanic force, ~7 times greater than the response of resting fibres. All these data indicate that: 1) ST has the same properties and it is equivalent to RFE, 2) it is independent of crossbridges and 3) it is likely due to the Ca2+-induced stiffening of a sarcomeric structure identifiable with titin.