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

Abstract

SUMMARYFor 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 ʻresidual force enhancementʼ (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.

An Effect of the Elastic Energy Stored in the Muscle-Tendon Complex at Two Different Coupling-Time Conditions during Vertical Jump

“…In agreement with the previous studies (Ettema et al, 1990;Lee & Herzog, 2002;Bullimore et al, 2008;Cavagna et al, 1985) peak ground reaction forces (i.e. concentric contraction) before take-off and vertical displacement in the present study were higher in CMJ than in SJ.…”

“…These large stretches are used to gain optimal mechanical energy in muscles and elastic fibers. The enhancement of performance during concentric contraction followed by eccentric contraction can be explained by these stretching (Voigt et al, 1995;Komi, 2000;Lee & Herzog, 2002;Morgan et al, 2000;Bullimore et al, 2008;Hodson-Tole & Wakeling, 2010). In the present study, the initial height and relative knee angle of each individual right before the take-off for vertical jump was set to a fixed height for both trials (CMJ and SJ) by utilizing the photo cell.…”

“…If not controlled, greater force could be produced in one case resulting in higher jump displacement (Voigt et al, 1995). Active muscle resists stretching with a force greater than the isometric force (Lee & Herzog, 2002;Bosco et al, 1987;Bullimore et al, 2008;Cavagna et al, 1985;Herzog & Leonard, 1997;Meijer et al, 1997). The force attained after large, fast stretches was due to 1) a greater force developed by each bridge (Hodson-Tole & Wakeling, 2010); or 2) an increased number of cross-bridge attachments (Lee & Herzog, 2002;Proske & Morgan, 1999).…”

Both the elongation of attached crossbridges and residual force enhancement contribute to joint torque enhancement by the stretch-shortening cycle

“…A significant difference in joint torque was found between the ECC and TRAN conditions at the onset of concentric contraction even though a similar magnitude of active lengthening, which determines the magnitude of residual force enhancement [21,36], was included in preactivation. This difference should be caused by an elongation of attached crossbridges induced by the eccentric contraction conducted just before the concentric contraction.…”

Reduced activation in isometric muscle action after lengthening contractions is not accompanied by reduced performance fatigability

“…Research working with animal models and isolated fiber preparations in combination with histological examinations focuses on decoding the mechanisms generating RFE11121314. Underlying mechanisms are still not fully understood and a combination of active and passive components are discussed in literature, including half sarcomere non-uniformities, increase in the number of attached cross-bridges or in the average cross-bridge force, and CA 2+ -dependent titin stiffness modulation2151617.…”