Скачати 164.43 Kb.
|7.5 Cardiac muscle|
7.6 Smooth muscle
7.6 Smooth muscle
move. The relationship between the load imposed on a muscle and its rate of shortening is known as the force—velocity curve. If a muscle contracts against a load which prevents shortening, the muscle is said to undergo an isometric contraction. When a muscle contracts against a constant load it is said to undergo an isotonic contraction. Isometric contraction and isotonic contraction with no external load represent the extreme positions of the relationship between the force developed by a muscle and the rate at which it shortens.
The work of a muscle is determined by the distance it is able to move a given load, and the power of a muscle is the rate at which it performs work (Box 7.1). Thus:
Power = Force X Velocity
Box 7.1 The efficiency and power of muscles
It is a matter of common experience that it is more difficult to move heavy objects than light ones, but how efficient are muscles in converting chemical energy into useful work? The force exerted on a given load is defined as:
Force = Mass X Acceleration [1}
and is given in newtons (N). One newton is the force that will give a mass of 1 kg an acceleration of 1 m s_1. The work performed on a load is the product of the load and the distance through which the load is moved. Thus:
Work = Force X Distance. 
The unit for work is therefore N.m and one N.m is a. joule (J). Power is defined as the capacity to do work or the work per unit time and is expressed in joules s-, or watts (W).
Power = Work/Time
= Force X Distance/Time
= Force X Velocity. [3}
The key to understanding the power and efficiency of a muscle is its force—velocity curve. For an isometric contraction, maximum force is exerted but the load is not moved so that no work is done and the power is also zero. Similarly, for an isotonic contraction against zero load no useful work is done. Between these two extremes the work is given by Equation 2 above and the power by Equation 3- The power is usually at a maximum when the muscle is shortening at about one-third of the maximum possible rate (Fig. 7.10).
The mechanical efficiency of muscular activity or work is expressed as a percentage of work done relative to the increase in metabolic rate attributable to the activity of the muscles employed in the task:
Efficiency = (Work done/Energy expended in task) X 100. For our examples above, both isometric and isotonic contractions have zero efficiency. The efficiency of muscles during everyday tasks, such as walking up stairs or cycling, is about 20—25 per cent.
From the curve relating the velocity of shorrening to the power developed (Fig. 7.10), it is clear that the power developed by a muscle passes through a definite maximum. When a muscle shortens isometrically it does no work as the load is not moved through a distance and no power is developed. Equally, if it contracts isotonically no work is done as the muscle is nor acring on an external load. Once more no power is developed. In between these two extremes, the muscle performs useful work and develops power. In general, the greatest power is developed when the muscle is shortening at about one-third of its maximum rate.
The effect of muscle length on the development of tension
If the force generated by a muscle during isometric contraction is measured for different initial resting lengths, a characteristic relationship is found. In the absence of stimulation the tension increases progressively as the muscle is stretched beyond its normal resting length. This is known as the passive tension and is due to the stretching of the connective tissue of the muscle and tendons. The extra tension developed as a result of stimulation (called the active tension) is at its maximum when the muscle is close to its resting length (i.e. the length it would have had in its resting state in the body). If the muscle is stimulated when it is shorter than normal, it develops less tension, and if it is stretched beyond normal resting length, the tension developed during contraction is also less than normal. Overall, the relationship between the initial length of a muscle and the active tension is described by a bell-shaped curve, as shown in Fig. 7.11.
In the body the range over which a muscle can shorten is determined by the anatomical arrangement of the joint on which it acts. The length of muscles which are attached to the skeleton range from 0.7 to 1.2 of their equilibrium length. They therefore develop their maximum tension when they first begin to shorten.
Fig. 7.11 Isometric force—tension relarionship ar different muscle lengths. The data is fot human triceps muscle. As rhe muscle is srrerched, passive tension increases. Active tension increases from zero to a maximum and then declines with furthet srrerching. The total tension developed during a contraction is the sum of the active and passive tensions.
7.5 Cardiac muscle
Threshold Pacemaker potential
While the extent to which a muscle can shorten depends on its length, the maximum tension it can develop in response to stimulation depends on the number of active myofibrils which are the tension-developing units of the muscle fibers. This, in turn, depends on the cross-sectional area of the muscle. When muscles hypertrophy (i.e. become larger) in response to training, it is the cross-sectional area of the individual fibers that increases, not the number of fibers. The increase in cross-sectional area can be attributed to an increase in the number of myofibrils.
Skeletal muscle only contracts in response to stimulation of the appropriate motor nerve. In contrast, denervated cardiac muscle continues to contract rhythmically. It is this intrinsic or myogenk activity that is responsible for the steady beating of the heart and enables the organ to be transplanted. This intrinsic rhythm has its origins in the cardiac myocytes found at the junction of the superior cava and the right atrium. Isolated ventricular fibers beat very slowly, while those derived from the atria beat more rapidly. The cardiac myocytes found at the junction between the great veins and the right atrium have the fastest intrinsic rhythm. This region is called the sinoatrial (or SA) node and the cells of the SA node are known as pacemaker cells as it is their activity that sets the basic heart rate. Action potentials spread from the SA node across the whole of the heart so that cardiac muscle behaves as a functional syncytium (see Chapter 15 for further details).
The action potential of cardiac myocytes
is of long duration and is maintained by a
prolonged inward movement of calcium
Like skeletal muscle, the contractile response of a cardiac muscle fiber is associated with an action potential. The characteristics of
Fig 7.12 The characteristics of the cardiac action potential in the myocytes of the SA node, atria, and ventricles. Note the very different appearance of the action potential in the different cell types and the presence of the pacemaker potential, which is especially prominent in the cells of the SA node.
the action potential depend on the position of the myocyte within the heart. Cardiac action potentials are between 150 and 300 ms in duration. They are therefore of far longer duration than those of nerve and skeletal muscle (which last for 1—2 ms) and this has important consequences for the contractile response of cardiac muscle (see below). The appearance of the action potentials of the cells of the SA node, atria, and ventricles is shown in Fig. 7.12.
The myocytes of the sinoatrial node develop a pacemaker potential
In the cells of the SA node, the membrane potential shows spontaneous fluctuations (Fig. 7.12). It is at its most negative (about —60 mV) immediately after the action potential and slowly falls (becomes less negative) until it reaches a value of about —50 mV which is the threshold for action potential generation. The action potential of the SA node cells has a slow rise time (time to peak is about 50 ms) and the whole action potential lasts for 150—200 ms. The slow depolarization that precedes the action potential is known as the pacemaker potential and the rate at which it falls towards threshold (i.e. its slope) is an important factor in setting the heart rate. Nerves and hormones that alter the heart rate do so both by changing the slope of the pacemaker potential and by altering the membrane potential (Chapter 15). The pacemaker potential arises because the sodium permeability of the membrane of the SA node cells slowly increases relative to that of potassium. This leads to a slow depolarization of the cell until an action potential is triggered. The upstroke of the action potential of SA node cells is caused by a large increase in the permeability of the membrane to calcium (not sodium as
is the case for the myocytes of the atria and ventricles). Since the equilibrium potential for calcium is positive (just as it is for sodium), the rise in calcium permeability leads to a reversal of the membrane potential. Repolarization occurs as the permeability of the membrane to potassium increases while that to calcium falls.
As for other cells, the resting membrane potential of atrial and ventricular myocytes is determined mainly by the permeability of the membrane to potassium. During the upstroke of the action potential there is a short-lived influx of sodium, just as there is during the nerve action potential. This is followed by a sustained increase in calcium permeability that lasts for many tens of milliseconds and this gives rise to the plateau phase so characteristic of the action potential of heart cells. Finally, the calcium permeability falls, the potassium permeability rises, and the membrane repolarizes.
The contractile response of cardiac muscle
The long duration of the cardiac action potential has the important consequence that the mechanical response of the muscle occurs while the muscle membrane remains depolarized (Fig. 7.13). Since a second action potential cannot occur until the first has ended and, since the mechanical response of the cardiac muscle largely coincides with the action potential, cardiac muscle cannot develop tetanic contractures. This is an important adaptation as the heart needs to relax fully between beats if it is to allow time for filling. Fibrillation may occur if the duration of the cardiac action potential (and therefore that of the refractory period) is substantially decreased.
Fig. 7.13 The relationship between the action potential and the development of isometric tension in cardiac muscle.
Calcium activates the contractile machinery of cardiac muscle in much the same way as it does in skeletal muscle but there is one important difference. If heart muscle is placed in a physiological solution lacking calcium, it immediately stops contracting, unlike skeletal muscle which will continue to contract when it is stimulated. In cardiac muscle, the rise in calcium within the myocyte during the plateau phase of the action potential is
Fig. 7.14 The relationship between the resting length of a papillary muscle from the heart and the maximum isometric force generated in response to stimulation. The passive tension increases steeply as the muscle is stretched. Note that cardiac muscle normally operates on the ascending phase of the active tension curve, unlike skeletal muscle which operates around the peak (see Fig. 7.11 for data for a skeletal muscle).
derived both from the sarcoplasmic reticulum and from calcium influx through voltage-gated ion channels. Indeed, this calcium influx is the trigger for the release of the stored calcium. This is known as calcium-dependent calcium release. Relaxation of cardiac muscle occurs as calcium is pumped from the sarcoplasm either into the sarcoplasmic reticulum or out of the cells.
The force of contraction in cardiac muscle is even more closely linked to the initial length of the sarcomeres than that in skeletal muscle. As cardiac muscle is stretched beyond its normal resting length more force is generated until it is about 40 per cent longer than normal. Further stretching of the muscle then leads to a decline in tension development. These characteristics are summarized in Fig. 7.14.
In the normal course of events, the degree to which the muscle fibers of the heart are stretched is determined by the amount of blood returning to the heart (the venous return). If the venous return is increased, the ventricular muscle will be stretched to a greater degree as the ventricle fills with blood and it will respond with a more forceful contraction (see Fig. 7.15). Similarly, if the work of the left ventricle is increased by a rise in blood pressure while the venous return remains constant, the muscle will again be stretched to a greater degree as the ventricle fills and will respond with a more forceful contraction. This principle is enshrined in Starling's law of the heart (Chapter 15). This property of cardiac muscle ensures that, in normal circumstances, the heart will pump all the blood it receives.
The force with which the heart contracts varies according to the needs of the circulation. During exercise the heart beats more strongly and frequently. These changes are mediated by the
Fig. 7.15 Comparison of the intrinsic and extrinsic regulation of the force of contraction in cardiac muscle, (a) The effect of increasing the initial length on the force of contraction is shown. Note the increase in resting tension with each 0.5 mm increment of the muscle above its resting length. As the muscle is stretched, the force developed in response to stimulation increases, (b) The effect of norepinephrine on the force of contraction. In this case the increased force of contraction occurs for the same initial resting length.
sympathetic innervation and by circulating epinephrine secreted by the adrenal medulla (Chapter 15). The change in rate is called a chronotropic effect, while the increased force of contraction (or contractility) is called an inotropic effect. The intrinsic contractility of the heart (its inotropic state) determines its efficiency as a pump. The increased contractility of the heart that results from stimulation of the sympathetic nerves is called a positive inotropic effect, while a decrease in contractility is a negative inotropic effect.
The positive inotropic effect of the sympathetic nerves occurs without any change in the length of the cardiac muscle fibers (Fig. 7.15). There is no similar effect in skeletal muscle. The increase in contractility is caused by an increase in calcium influx following activation of /3-adrenergic receptors and the subsequent generation of cyclic AMP. The cyclic AMP activates protein kinase A which phosphorylates the calcium channels of the plasma membrane. The phosphorylated channels remain open for longer following depolarization and this, in turn, leads to an increased calcium influx which results in an increase in the force of contraction.
7.6 Smooth muscle
Smooth muscle is the muscle of the internal organs such as the gut, blood vessels, bladder, and uterus. It is a distinct variety of muscle with a unique range of physiological properties and consists of sheets containing many small, spindle-shaped cells linked together at specific junctions (Figs 7.1 and 7.16). Individual cells are 2—5 yU/in in diameter and about 50-200 μ-m in length. Each cell has a single nucleus. In some tissues—such as the alveoli of the mammary gland and in some small blood vessels—the smooth muscle cells are arranged in a single layer known as myoepithelium. Myoepithelial cells have similar physiological properties to other smooth muscle cells.
No cross-striations are visible under the microscope (hence its name) but, like skeletal and cardiac muscle, smooth muscle cells contain actin and myosin. In addition, they contain cytoskeletal intermediate filaments which assist in transmission of the force generated during contraction to the neighboring smooth muscle cells and connective tissue. While there are no Z lines in smooth muscle, they have a functional counterpart in dense bodies that are distributed throughout the cytoplasm and which serve as attachments for both the thin and intermediate filaments. The thin and thick filaments of smooth muscle fibers are arranged as myofibrils which cross the fibers obliquely in a lattice-like arrangement. The filaments of contractile proteins are attached to the plasma membrane at the junctional complexes between neighboring cells, as shown in Fig. 7.16. A comparison of some
Fig. 7.16 The organization of the contractile elements of smooth muscle fibers, (a) Note the points of close contact for mechanical coupling and the gap junction for electrical signaling between cells, (b) A simple model of the contraction of smooth muscle. As the obliquely running contractile elements contract, the muscle shortens.
of the properties of smooth, cardiac, and skeletal muscle is given in Table 7.1.
Smooth muscle is innervated by fibers of the autonomic nervous system which have varicosities along their length (Chapter 6). In some tissues each varicosity is closely associated with an individual muscle cell (e.g. the piloerector muscles of the hairs) while, in others, the axon varicosities remain in small bundles within the bulk of the muscle and are not closely associated with individual fibers (e.g. the smooth muscle of the gut). The varicosities release their neurotransmitter into the space surrounding the muscle fibers rather than onto a clearly defined synaptic region as is the case at the neuromuscular junction of skeletal muscle.
In many tissues, particularly those of the viscera, the individual smooth muscle cells are grouped loosely into clusters that extend in three dimensions and the cells are connected by gap junctions, so that the whole muscle behaves as a functional syncytium. In this type of muscle, activity originating in one part spreads throughout the rest of the muscle. This is known as single-unit smooth muscle. It is characterized by spontaneous myogenic contractures that originate in specific pacemaker areas (see Fig. 7.17). As the individual fibers are connected by gap junctions, the activity spreads to the whole muscle. The smooth muscle of the gut, uterus, and bladder are good examples ol single-unit smooth muscle. The activity of many single-unit muscles is strongly influenced by hormones circulating in the bloodstream as well as by the activity of autonomic nerves.
Table 7.1 A comparison of the properties of skeletal, cardiac, and smooth muscle
|Gutter=18> 1 Introduction||Gutter=17> 22. 1 Introduction|
|Gutter=17> 1 Introduction||Gutter=17> 23. 1 Introduction|
|Gutter=16> 1 Introduction||Gutter=17> 15. 1 Introduction|
|Gutter=18> 1 Introduction||Gutter=17> 17. 1 Introduction|
|Gutter=17> 19. 1 Introduction||Gutter=17> 16. 1 Introduction|