Studies of skeletal muscle suggest that the ratio of stiffness to tension will increase in the presence of a slower rate of crossbridge head rotation from the attached perpendicular state (non-force generating) to the attached 45 degree angle state (force generating). Maximum shortening velocity is depressed proportionate with adenosinetriphosphatase activity in pressure overload cardiac hypertrophy. The maximum rate of isometric force generation also is less than normal but active isometric force levels are normal. The myosin isoenzymes of hypertrophied heart muscle are shifted to predominantly slower than normal types. Among a number of possibilities, the overall rate of crossbridge cycling may be less than normal and crossbridge head rotation may be slower. We reasoned that a greater than normal ratio of active elastic stiffness to total tension development in hypertrophy would be suggestive of an alteration from normal in crossbridge dynamics. We studied right ventricular septal papillary muscles from normal rabbits and from rabbits with hypertrophy induced by pulmonary artery constriction. A high level of mechanical activation was obtained by tetanizing the muscles in solutions containing caffeine. Small (less than or equal to 2% muscle length) and rapid (0.8 ms) length perturbations were applied to the preparations with a servo-controlled motor. Active elastic stiffness was estimated from the linear relationship of minimum (for releases) or maximum (for stretches) tension reached during a length change with muscle length change (strain). Although total tetanic tension development was normal in the hypertrophied muscles (p greater than 0.1), active elastic stiffness was greater than normal in hypertrophy (p less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)