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. Author manuscript; available in PMC: 2018 Feb 1.
Published in final edited form as: J Mol Cell Cardiol. 2017 Jan 11;103:65–73. doi: 10.1016/j.yjmcc.2017.01.004

Figure 1.

Figure 1

Load-clamp protocols indicate that relaxation rate depends on the end systolic strain rate, not afterload. Top: Force and length versus time traces; Middle: Relationship between relaxation rate and afterload; Bottom: Relationship between relaxation rate and end systolic strain rate. Left (blue): overlay of 6 twitches that were load-clamped at various afterloads; the muscle was relengthened back to its original length before being allowed to relax. Center (red): overlay of 6 twitches; the muscle relaxed while being held at the minimum attained length. Right: overlay of 9 twitches that were load-clamped at ~50% of the peak isometric force; the load-clamp was stopped with variable amounts of relengthening before being allowed to relax. Muscle relengthening was necessary to obtain an inverse relationship between relaxation rate and afterload. Relengthening alone (without modifying afterload) was sufficient to modify the relaxation rate. All data in this figure measured from the same rat trabecula.