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Sarcomere length dependence of rat skinned cardiac myocyte mechanical properties: dependence on myosin heavy chain

The effects of sarcomere length (SL) on sarcomeric loaded shortening velocity, power output and rates of force development were examined in rat skinned cardiac myocytes that contained either α‐myosin heavy chain (α‐MyHC) or β‐MyHC at 12 ± 1°C. When SL was decreased from 2.3 μm to 2.0 μm submaximal isometric force decreased ∼40% in both α‐MyHC and β‐MyHC myocytes while peak absolute power output decreased 55% in α‐MyHC myocytes and 70% in β‐MyHC myocytes. After normalization for the fall in force, peak power output decreased about twice as much in β‐MyHC as in α‐MyHC myocytes (41%versus 20%). To determine whether the fall in normalized power was due to the lower force levels, [Ca2+] was increased at short SL to match force at long SL. Surprisingly, this led to a 32% greater peak normalized power output at short SL compared to long SL in α‐MyHC myocytes, whereas in β‐MyHC myocytes peak normalized power output remained depressed at short SL. The role that interfilament spacing plays in determining SL dependence of power was tested by myocyte compression at short SL. Addition of 2% dextran at short SL decreased myocyte width and increased force to levels obtained at long SL, and increased peak normalized power output to values greater than at long SL in both α‐MyHC and β‐MyHC myocytes. The rate constant of force development (ktr) was also measured and was not different between long and short SL at the same [Ca2+] in α‐MyHC myocytes but was greater at short SL in β‐MyHC myocytes. At short SL with matched force by either dextran or [Ca2+], ktr was greater than at long SL in both α‐MyHC and β‐MyHC myocytes. Overall, these results are consistent with the idea that an intrinsic length component increases loaded crossbridge cycling rates at short SL and β‐MyHC myocytes exhibit a greater sarcomere length dependence of power output.