Reduced isotonic sarcomere shortening in rabbit right ventricular pressure overload hypertrophy

Abstract

We found previously that sarcomere shortening was reduced in hypertrophied rabbit right ventricular (RV) trabeculae, even when total isometric force and damaged end compliance were the same as normal. Here we studied isotonic shortening of similar preparations force-clamped with a servomotor. A force clamp holds the length of damaged end compliance constant. Sarcomere length ( SL) was measured with laser diffraction in twitches with single and optimally paired stimuli. δ SL was sarcomere shortening divided by SL at the onset of shortening. Muscle shortening divided by unloaded muscle length ( ML) at the onset of shortening was δ ML. RV hypertrophy was produced with pulmonary artery constriction in 11 rabbits and there were eight normal rabbits. δ SL was smaller than normal in hypertrophy, but δ ML was unchanged from normal. δSL δML in hypertrophy, 0.90 ± 0.02, was significantly less than normal, 2.40 ± 0.07 (mean ± s.e.m.) ( P<0.01). δSL δML did not depend on sarcomere shortening, load, time during shortening or stimulus pattern. Therefore, the reduced δ SL in hypertrophy was independent of contractile state parameters. The ratio was also independent of resting SL (normal = 2.29 ± 0.07 μm; hypertrophy = 2.23 ± 0.03 μm; P>0.05) or where diffraction was sampled along central muscle length. One explanation for the findings includes reduced compliance of series viscoelastic elements within the central undamaged region of a hypertrophied muscle. This explanation is consistent with changes from normal in myocardial mechanics and connective tissue in cardiac hypertrophy. Ventricular function remains adequate in hypertrophy without heart failure perhaps because reduced δSL δML in hypertrophy results in less sarcomere work at any level of muscle work.