The mechanism(s) underlying the effects of varied calcium concentration and of varied sarcomere length on force development and on the velocity of shortening in cardiac muscle were investigated. Sarcomere dynamics were investigated in thin trabeculae from rat heart with laser diffraction techniques; force was measured with silicon strain gauge 10 kHz. The unloaded velocity of sarcomere shortening was measured with the use of the 'isovelocity' technique. After study of intact muscles, superfused with modified Krebs-Henseleit solution at 25 degrees C, preparations were skinned with relaxing solution containing Triton X-100 and investigated at varied free Ca++. Force increased in all intact muscles continually with sarcomere length from 1.6-2.4 microns; the relation between force and sarcomere length was convex toward the ordinate at high Ca++0 and convex toward the abscissa at low Ca++0. Similar relations between force and sarcomere length were found in skinned trabeculae. Unloaded velocity of shortening (V0) was independent of time between 50 ms and 150 ms following onset of the twitch. V0 increased, in this period with increasing sarcomere length from 1.6 to 1.9 microns from 0 to 13 micron/s; above that length the velocity was constant. V0 increased at a sarcomere length of 2.00 microns with increasing Ca++0 to a maximum at Ca++0 = 1.2 mM above which V0 remained constant though force increased by 100%. These results suggest that the force-sarcomere length relation in cardiac muscle can be explained on the basis of length dependent activation of the contractile filaments to Ca++. Whether the different responses of force and of unloaded velocity of shortening to variations in sarcomere length and in Ca++ concentration are consistent with the hypothesis that force development and unloaded velocity of shortening are controlled by different mechanisms is discussed.