Thin filament regulation of shortening velocity in rat skinned skeletal muscle: effects of osmotic compression.

J. M. Metzger, R. L. Moss

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Abstract

1. Maximum shortening velocity (Vmax) was examined in skinned single fibres from rat slow‐twitch soleus muscles at various degrees of Ca2+ activation of the thin filament, in the presence and absence of osmotic compression induced by 5% dextran. 2. At maximal levels of Ca2+ activation, Vmax remained constant as the extent of shortening was varied, with values averaging 1.43 +/‐ 0.05 muscle lengths/s (mean + S.E.M., n = 13). When thin filament activation was reduced by lowering the concentration of Ca2+, unloaded shortening consisted of an initial high‐velocity phase for extents of shortening in the range 20‐80 nm/half‐sarcomere, and a subsequent low‐velocity phase for greater extents of shortening. 3. In the absence of dextran, Vmax in the high‐velocity phase of shortening was relatively invariant over a wide range of activation; however, at very low levels of activation, yielding tensions less than 5% of the peak value. Vmax declined precipitously. In contrast, fibres compressed radially with dextran to diameters comparable to those of intact fibres demonstrated a marked decrease in Vmax in the high‐velocity phase when thin filament activation was varied over a wide range. These findings are consistent with the idea that cross‐bridges in the expanded filament lattice of skinned fibres do not bear as great an axial compressive force as in intact fibres (Goldman & Simmons, 1986; Goldman, 1987) but instead buckle as the fibre shortens. 4. The value of Vmax in the low‐velocity phase of shortening decreased as thin filament activation was reduced in both control and osmotically compressed fibres. The low‐velocity phase, which occurred only at reduced levels of thin filament activation, may be a manifestation of a population of slowly dissociating crossbridges which with shortening become negatively strained and oppose contraction.

Original languageEnglish (US)
Pages (from-to)165-175
Number of pages11
JournalThe Journal of Physiology
Volume398
Issue number1
DOIs
StatePublished - Apr 1 1988

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