Treatment with 1 mM BDM increased the critical force during stretch from 1.62 to 2.35 times the isometric force, suggesting that pre-power stroke cross bridges largely contribute to stretch forces.
Pre-power stroke cross bridges are largely responsible for the increase in force during the first phase of skeletal muscle stretch.
Tasa de eventos absoluta: 2.35% vs 1.62%
When activated skeletal muscle is stretched, force increases in two phases. This study tested the hypothesis that the increase in stretch force during the first phase is produced by pre-power stroke cross bridges. Myofibrils were activated in sarcomere lengths (SLs) between 2.2 and 2.5 microm, and stretched by approximately 5-15 per cent SL. When stretch was performed at 1 microms-1SL-1, the transition between the two phases occurred at a critical stretch (SLc) of 8.4+/-0.85 nm half-sarcomere (hs)-1 and the force (critical force; Fc) was 1.62+/-0.24 times the isometric force (n=23). At stretches performed at a similar velocity (1 microms-1SL-1), 2,3-butanedione monoxime (BDM; 1 mM) that biases cross bridges into pre-power stroke states decreased the isometric force to 21.45+/-9.22 per cent, but increased the relative Fc to 2.35+/-0.34 times the isometric force and increased the SLc to 14.6+/-0.6 nm hs-1 (n=23), suggesting that pre-power stroke cross bridges are largely responsible for stretch forces.
Dilson E. Rassier (Tue,) conducted a other in Skeletal muscle myofibrils (n=40). 2,3-butanedione monoxime (BDM) vs. Control (untreated myofibrils) was evaluated on Critical force (Fc) relative to isometric force during stretch at 1 mm/s/SL. Treatment with 1 mM BDM increased the critical force during stretch from 1.62 to 2.35 times the isometric force, suggesting that pre-power stroke cross bridges largely contribute to stretch forces.