In smooth muscle isometric force, shortening velocity, the ATP utilization under isometric conditions, and tension cost are all functions of calcium. This suggests that both cross bridge number and cycle rate are dependent on calcium. On the other hand, the series elastic component does not exhibit a significant dependence on calcium under conditions in which Vus can be increased with little change in Fo. And although the data is not as extensive, the efficiency in working producing contractions is not a strong function of calcium. Our challenge is to fit these mechanical and energetic data into a mechanism which fits the ever growing and controversial body of evidence on the biochemical basis for the action of calcium on the contractile apparatus. At present the most striking feature is the observation that calcium can control the velocity in a manner which is independent of isometric force and efficiency. This would appear to favor a mechanism in which calcium directly affected cross bridge cycle rate in the absence of an internal load.