Cross-bridge induced force enhancement?
When a muscle is stretched while activated, its steady-state isometric force following stretch is greater than the corresponding purely isometric force. This so-called residual force enhancement (RFE) has been observed for half a century, yet its mechanism remains unknown. Recent experiments suggest that RFE is not caused by non-uniformities in sarcomere lengths, as had been assumed for a long time, and cannot be explained primarily with increases in passive force, but is directly related to the kinetics of the cross-bridge cycle. Specifically, it has been suggested that stretching an attached cross-bridge increases its dwell time and duty ratio; therefore, the proportion of attached cross-bridges in a muscle would be increased by stretch, thereby causing RFE. A three bead laser trap setup was used for testing single cross-bridge (myosin II) interactions with actin. Upon attachment of a cross-bridge, a stretch or shortening of the cross-bridge was applied with a force of about 1.0 pN. The hypothesis that stretching a single cross-bridge increases its dwell time and duty ratio was rejected. However, stretching caused an increase in the average steady-state force per cross-bridge (3.4+/-0.4 pN; n=433) compared to shortening (1.9+/-0.3 pN; n=689). Therefore, based on the results of this study, RFE cannot be explained by an increased duty ratio and the associated increase in proportion of attached cross-bridges, but might be associated with an increased force per cross-bridge.
Mehta
A
A
Faculty of Kinesiology, Human Performance Laboratory, University of Calgary, Calgary, AB, Canada.
Herzog
W
W
D008841:Actin Cytoskeleton / Q000502:physiology*; D000818:Animals; D007537:Isometric Contraction / Q000502:physiology*; D009126:Muscle Relaxation / Q000502:physiology*; D015879:Myosin Subfragments / Q000502:physiology*; D011817:Rabbits; D012518:Sarcomeres / Q000502:physiology*
D015879:Myosin Subfragments