Mechanical properties of myocardium from hypertrophied rat hearts. A comparison between hypertrophy induced by senescence and by aortic banding

Cardiac hypertrophy is a characteristic change that occurs in senescence. Muscles from senescent as compared to mature hearts also demonstrate functional alterations that are similar to the alterations found in muscles from experimentally hypertrophied hearts. Thus, an attractive hypothesis is that functional alterations in senescent muscles are related to the underlying hypertrophy. To test this hypothesis, we used a rat model of aging in which experimental hypertrophy was produced by aortic banding. The time course and extent of cardiac hypertrophy, as well as isometric twitch and viscoelasticity parameters, as a function of age, first were determined in muscles from the rat hearts. Aortic banding then was performed on middle-aged rats to produce the same extent of hypertrophy as seen in the senescent hearts. The resulting functional alterations in muscles from the banded (B) hearts were compared to the senescent (S) and middle-aged (M) muscles. Using tibial length as a reference, we found 14% LV hypertrophy in senescent compared to both young and middle-aged rats, indicating that the hypertrophy occurred during the last quarter of life. The S muscles demonstrated a 25% prolongation in contraction duration (CD) and a 30% increase in slope of the active stiffness-tension line (α(A)) compared to both young adult and middle-aged muscles. Compared to middle-aged muscles, the B muscles demonstrated a similar spectrum of change in mechanical properties as the S muscles (8% increase in CD and 15% increase in α(A)), but the quantitative differences between the B and S muscles were significant. Over the functional range of developed tensions, the B muscles demonstrated the lowest and the S muscles the highest values of stiffness. The findings suggest that a portion of the mechanical property alterations seen in the senescent heart are due to the underlying hypertrophy. However, the hypertrophy produced by mechanical loading of the LV cannot explain all of the senescent changes.