Sarcomere shortening velocity in pressure overload hypertrophied rabbit right ventricular myocardium at physiological sarcomere lengths.

Earlier we noted the importance of internal loads for sarcomere shortening in heart muscle. Internal loading may change with hypertrophy and influence sarcomere shortening velocity. Therefore, we force clamped trabeculae from normal rabbit right ventricles and those hypertrophied due to pulmonary artery constriction. Diffraction of a laser (lambda = 632.8 nm) by a trabecula was used to measure sarcomere length (SL) in isotonic twitches. Resting SL was set at 2.36 +/- 0.17 microns in the normal (n = 5) and 2.23 +/- 0.08 microns in the hypertrophied (n = 5) (+/- S.E.M.) muscles. The relationship of total stress with log10 sarcomere shortening velocity was linear. In the normals, log(SL/s) = 0.39-1.32 (P(total)/P(isom)), and in hypertrophy, log(SL/s) = -0.16-0.57 (P(total)/P(isom)). SL/s is sarcomere shortening velocity in microns/s divided by SL at the onset of constant force. P(total) is isotonic plus resting stress and P(isom) is peak total isometric stress. The hypertrophy (P(total)/P(isom))-(SL/s) relationship is depressed below normal at low loads (P < 0.001). Estimated unloaded SL/s in the normals was 2.47 and 0.69 in hypertrophy. Paired stimulation had no effect on normal SL/s. In hypertrophy, paired stimulation increased SL/s at low loads to normal levels. Thus, depressed sarcomere shortening velocity at low loads in hypertrophy at physiological sarcomere lengths disappeared when myoplasmic [Ca2+] increased. The results suggested that internal loading was greater than normal during shortening of hypertrophied myocardium. Increased myoplasmic [Ca2+] increased the number of crossbridges and reduced the load per crossbridge. This was a likely mechanism for the increase of sarcomere shortening velocity to normal levels.