The effect of shortening on crossbridge dynamics in cardiac muscle

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Landesberg and Sideman have proposed a model for cross-bridge cycling where the rate constant for crossbridge weakening, G, is a function of the sarcomere shortening velocity such that G = G0 + G1 • V , where G0 is the rate constant in the isometric state and G\ is the mechanical feedback. The effect of myosin heavy chain isoform on G1 is unknown. Methods: Rats were made to express either pure α-MHC, by treatment with thyroid hormone (T3), or pure ß-MHC, by treatment with PTU. Force-velocity curves were obtained from cardiac trabeculae (Ca2+ = 1.5 mM, 25°C). To determine G1, ~FN the instantaneous force difference between a shortening and isometric contraction was measured. Results: The sarcomere shortening velocity of T3 rats were twice that of PTU treated rats at all levels of relative load (VMAX= 15.99 µm/s - T3, 8.95 µm/s - PTU). There was no difference in the curvature of the force-velocity relationship between the two groups. G1 as measured from slow ( ≤ 4 µm/s) releases was 4.76 /µm (STD DEV = 1.43) for T3 rats and 4.88 /µm (STD DEV = 1.29) for PTU rats.
Bibliography: p. 96-105
Deis, N. P. (2004). The effect of shortening on crossbridge dynamics in cardiac muscle (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from doi:10.11575/PRISM/22878