Tension production and sarcomere length in lobster (Homarus americanus) cardiac muscles: the mechanisms underlying mechanical anisotropy
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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 by artery stretch during systole. Furthermore, the heart is anisotropic, with characteristically different active and passive forces along the transverse and longitudinal axes. We examined the effects of sarcomere 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. Additionally, we determined the length-tension curves for longitudinal and transverse cardiac muscles. Sarcomere length experiments showed that no significant differences in sarcomere length were found between longitudinal and transverse fibers. Length-tension curve experiments, revealed that tension increased with increasing muscle length, indicative of a classic Frank-Starling mechanism. We also found transverse muscles produced greater contractile forces at a given strain compared with longitudinal muscles. In contrast, longitudinal muscles produced greater passive forces at a given strain compared with transverse muscles. These data corroborate past findings that the lobster heart is mechanically anisotropic. Furthermore, we found maximum strain ranges along the transverse and longitudinal axes to be greater in the lobster than in mammals, but smaller than those characterized in fish hearts. Additionally, frequency was found to increase with increasing length in longitudinal muscles; both of which are indicative of Frank-Starling mechanisms. We hypothesize that the lobster heart modulates cardiac output by altering stroke volume and heart rate, but the extent to which is unknown.
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