Slowing of cross-bridge cycling in smooth muscle without evidence of an internal load.

We have tested whether the slowing in velocity of shortening that occurs in mammalian smooth muscle under conditions of high force output and dephosphorylated myosin light chains is due to an internal load presented by non- or slowly cycling cross bridges. The experimental design included stimulation of the rabbit taenia coli for 25 s under isometric conditions followed by 30 s of relaxation prior to the test stimulus. There was a large decrease in maximum velocity of shortening and chemical energy usage as well as a significantly decreased myosin light-chain phosphorylation response during the test stimulus even though active force developed to 90 +/- 4% of the original. The chemical energy cost of active external work production was not significantly different from that of the initial stimulation. There is, therefore, no energetic evidence for the dissipation of work against an internal load under conditions during which most of the force would be expected to be generated by latch bridges. We conclude that force maintenance with a low energy input and a slow velocity of shortening in mammalian smooth muscle represents a general slowing of the cross-bridge cycling rate rather than the appearance of a class of latch bridges that provide an internal load against which other cross bridges must operate.