Abstract
IT is generally agreed that the form of the length–tension relation of a fully activated skeletal muscle is determined by the overlap of actin and myosin filaments within the sarcomere. Figure 1 shows the length–tension curve for tetanised frog skeletal muscle1, which is thought to be fully activated at lengths above 75% Lmax (ref. 2). This is the form of the curve that would be expected from any muscle of similar sarcomere structure to frog muscle, provided that it has a constant degree of activation (either complete or partial) at muscle lengths above 75% Lmax. The sarcomere structure of cardiac muscle is similar to that of frog muscle3, yet the shape of its length–tension curve is strikingly different (Fig. 1). In skeletal muscle deviation from the ‘ideal’ curve shown in Fig. 1 has been attributed to variation in the degree of activation when the muscle is stimulated at different lengths. We have investigated this possibility in cardiac muscle by studying the effect on the length–tension relation of varying the degree of activation produced by electrical stimulation: we have done this by altering the concentration of calcium in the bathing medium and by using paired pulse stimulation4.
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ALLEN, D., JEWELL, B. & MURRAY, J. The contribution of activation processes to the length–tension relation of cardiac muscle. Nature 248, 606–607 (1974). https://doi.org/10.1038/248606a0
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DOI: https://doi.org/10.1038/248606a0
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