Is a parallel elastic element responsible for the enhancement of steady-state muscle force following active stretch?

For over 50 years, it has been recognised that muscles from many different species of animals are able to generate a higher steady-state isometric force after active stretch than during a purely isometric contraction at the same length. This is known as ;residual force enhancement' (rFE). The mechanism underlying this phenomenon remains controversial. One proposal is that an elastic element parallel to the cross-bridges becomes stiffer, or is engaged, when the muscle is activated and generates force when stretched. If this is indeed the sole mechanism, then rFE should be eliminated by subsequently shortening the muscle by a distance equal to or greater than the initial stretch. We tested this hypothesis using six intact single fibres from frog lumbrical muscle. The fibres were activated and stretched to generate rFE and then rapidly shortened by between 25% and 700% of the initial stretch distance. In contrast to previous reports, we found that rapid shortening induced a depression of subsequent isometric force. We used two methods to account for this force depression when calculating rFE, thereby obtaining upper and lower bounds for the true rFE. With both methods of calculation, rFE was significantly greater than zero when shortening distance was equal to stretch distance (P=0.0004 and P=0.03, respectively). Therefore, our hypothesis was not supported. We conclude that rFE is unlikely to be generated solely by a parallel elastic element.