Meeting Abstract
With increased activity, the heart’s blood volume during diastole increases, which consequently increases the stretch on the walls of the heart. As is typical with striated muscles, the ability of the heart to generate tension increases with increasing stretch up to some maximum. This increase in tension-generating ability may be due to sarcomeres generating greater force at longer lengths on the ascending limb of the length-tension curve. However, lobster hearts are suspended by elastic ligaments and arteries within a pericardial space, thus the tension on the heart is influenced both by changes in sarcomere length during diastole and artery stretch during systole. Furthermore, the heart is anisotropic, with characteristically different active forces along the transverse and longitudinal axes. We examine the effects of both sarcomere and artery length changes on tension generation by the heart at different points in the cardiac cycle as well as the potential contribution of differences in sarcomere length to the observed anisotropy. In terms of anisotropy, no significant differences in sarcomere length were found between longitudinal and transverse fibers. In terms of length-tension curves, we found that tension increased with increasing length of the heart plus artery system, but that the initial portion of the whole-heart length-tension curve occurred at lengths where the arteries were responsible for absorbing the imposed changes in length. Thus, whole-heart length-tension curves for lobster heart suggest potential neural stretch receptors in the arteries that anchor the heart in the pericardium.
