Residual force enhancement in cardiac myofibrils

There are conflicting observations regarding residual force enhancement (RFE) in cardiac muscle. In this study, we intended to re-examine RFE in cardiac myofibrils. RFE was tested after active stretches from average sarcomere lengths of i) 1.8 to 2.0 µm (n = 8), and ii) 2.0 to 2.2 µm (n = 8). All myofibrils showed RFE, averaging 20.7 ± % and 16.8 ± %, at sarcomere lengths of 2.0 µm (p = 0.008) and 2.2 µm (p = 0.012) respectively. RFE is thought to be caused by a shortening of titin’s free spring length by binding of titin to actin. Since cardiac and skeletal muscles have different titin isoforms, our results suggest that cardiac titin can lead to RFE and that titin-actin binding may occur in skeletal and cardiac titin isoforms.