The muscle is placed under an initial tension or preload. If the muscle strip is anchored at both ends and stimulated it undergoes isometric contraction. The tension generated during isometric contraction increases with increasing initial length Fig. Alteration in initial fibre length is analogous to preload. Increasing venous return to the heart results in an increased left ventricular end diastolic volume, thereby increasing fibre length.
This produces an increase in the force of contraction and an increased stroke volume resulting in the familiar Starling curve. The conventional explanation for this is that at normal resting length, the overlap of actin and myosin is not optimal. Increasing the initial length improves the degree of overlap and therefore increases the tension developed.
It has become clear in recent years that this mechanism is unlikely to account for the shape of the Starling curve under physiological conditions. Several other possible mechanisms have been implicated. Lengthening the muscle increases the sensitivity of troponin to calcium length-dependent calcium sensitivity and can also lead to enhanced intracellular free calcium.
Contractile properties of myocardial muscle. Left: Simplified arrangement to study contraction of isolated cat papillary muscle. The weight labelled preload sets the resting length.
If the preload is clamped in place contraction becomes isometric. Right: Three fundamental relations: a isometric contraction at increasing lengths, b and c isotonic contractions beginning from two different resting lengths 8 and 10 mm.
Contractile force, velocity, and shortening are all increased by stretching the relaxed muscle. If the muscle is able to shorten, but has to lift a weight, this is known as isotonic contraction. The weight moved by the muscle strip represents afterload. As afterload increases, both the amount and velocity of shortening decreases Fig. Conversely, reducing the afterload enhances shortening, a fact of considerable importance in the management of the failing heart.
If the preload is increased by stretching the muscle and the experiment repeated, both velocity and shortening are enhanced. In vivo , the initial phase of cardiac contraction, from the closure of the mitral and tricuspid valves to the opening of the aortic and pulmonary valves, is isotonic.
Tension is developed, but the ventricle does not eject blood, as there is no muscle fibre shortening. After the opening of the aortic and pulmonary valves, contraction becomes isotonic, tension is maintained, but blood is ejected and tonic shortening occurs. In vitro , perfusing papillary muscles with norepinephrine increases the strength and rapidity of the isometric contraction. This increased contractility i. As mentioned earlier, catecholamines may augment both contraction and relaxation of cardiac muscle.
However, as catecholamines increase the intracellular calcium load, more energy is required to fuel the pumps that sequester the calcium in diastole. In a failing myocardium, energy demand may outstrip supply e. Levosimendan is a new drug that increases the sensitivity of troponin to calcium such that the heart performs better with lower intracellular calcium concentrations.
Less energy is then required in diastole to reduce intracellular calcium concentrations. Google Scholar. Google Preview.
Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account.
Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation.
Volume 7. This article was originally published in. Article Contents Structure of the cardiac myocyte. Resting membrane and action potentials. Excitation contraction coupling. Metabolism and energetics. Contraction of the isolated muscle strip. Cardiac muscle physiology. Oxford Academic. Tel: Fax: Select Format Select format. Structure of the cardiac myocyte Each cardiac myocyte is surrounded by a cell membrane called the sarcolemma and contains one nucleus.
Open in new tab Download slide. Google Scholar Crossref. Specialized conducting cells found within the His-Purkinje system of the ventricles are a third type of action potential that are fast response type action potentials, but in contrast to normal atrial and ventricular myocytes fast response, non-pacemaker cells , these His-Purkinje cells exhibit spontaneous depolarization.
Cardiac action potentials in the heart differ considerably from action potentials found in neural and skeletal muscle cells. One major difference is in the duration of the action potentials. In a typical nerve, the action potential duration is about 1 ms. In skeletal muscle cells, the action potential duration is approximately ms. In contrast, the duration of cardiac action potentials ranges from to ms. Another difference between cardiac and nerve and muscle action potentials is the role of calcium ions in depolarization.
In the SA node, three ions are particularly important in generating the pacemaker action potential. The role of these ions in the different action potential phases are illustrated in the above figure and described below:. It is important to note that action potentials described for SA nodal cells are very similar to those found in the atrioventrcular AV node.
AV nodal action potentials also have intrinsic pacemaker activity produced by the same ion currents as described above for SA nodal cells. Cardiovascular Physiology Concepts Richard E. Klabunde, PhD. Klabunde, all rights reserved Web Design by Jimp Studio.
0コメント