Key Points
- To evaluate the origin and magnitude of restoring forces responsible for returning cardiac sarcomeres to resting slack length during relaxation.
- Monitored and controlled sarcomere length in isolated rat cardiac trabeculae using laser light diffraction techniques at 25°C.
- Evaluated active and passive tension under hypotonic swelling, caffeine-induced tetani (10 mmol l⁻¹), and rapid length perturbation protocols.
- Active force fell to zero at a sarcomere length of 1.58 µm and peaked at 2.35 µm, while caffeine tetani allowed active shortening down to 1.35 µm.
- Total restoring forces arising primarily from thin filament repulsion accounted for less than a few percent of maximal active tension, with passive elastic elements providing negligible contributions.
- Unloaded sarcomere lengthening velocity measured 3–5 µm s⁻¹, but introducing a load under 1% of maximal tension accelerated relaxation velocity tenfold.
Structured PICO
PPopulationRat cardiac trabeculae
IInterventionExperimental manipulation of sarcomere length and solutions (hypotonic solutions, caffeine 10 mmol/L, rapid length perturbations)
OOutcomeOrigin and magnitude of forces restoring sarcomere length to slack length during relaxationsurrogate
In rat cardiac muscle, restoring forces at short sarcomere lengths are minimal, and relaxation is primarily driven by the deactivating effect of sarcomere motion and external load.