"Compare and contrast physiological properties of
skeletal and cardiac muscle."

The properties of skeletal and cardiac muscle are defined by their function. Skeletal muscle has to function under neural stimulation and only on the demands of neural stimulation to produce a contraction of widely varying strength and duration. Cardiac muscle on the other hand has to produce a continual rhythmic contraction varying within certain strictly controlled limits and varied by neural stimuli.
One special adaptation of the cardiac muscle is the development of cells whose purpose is to generate the cardiac rhythm. This is principally in the sinoatrial (SA) and artrioventricular nodes. The cells here have a constantly changing membrane potential. A normal excitable cell (nerve or muscle) will have a resting potential that it returns to after every stimulus and until it is stimulated again. In the SA node there are three principle, ionic currents that act to produce regular depolarisation. The first of these is carried mainly by Na+ channels. These are a separate type from the fast channels that produce the upstroke of an AP. The sodium channels open when the membrane has repolarized to -50mV or below. The second type of channels are calcium channels that open at -55mV (they are inactivated whilst the cell is repolarizing) and are the producers of the action potential upstroke at the SA node. Opposing these two currents is the efflux of potassium from the cell. This efflux is continued well after the cell has repolarized but gradually decreases. The imbalance between outward if current and inward ik producing the gradual depolarisation of the cell before the action potential fires. The time between firing an action potential is controlled by release of acetylcholine from the end of the vagus nerve. There is no comparative system of this type in skeletal muscle
There are some important structural differences between the two muscle types. Skeletal muscle is made up of individual fibres each supplied by an axon. These fibres are long, individual cells (10s of centimetres) and are multinucleate, having been created in development by the fusing of many cells. Inside the cell membrane, referred to as the sarcolemma, there are numerous myofibrils. Each of which can be divided into individual filaments and it is the filaments that are the motile protein matrices. In an electron micrograph of muscle fibres distinct light and dark striations will be seen. The light zones constituting an I- band with a dark Z-line down the middle and the dark regions being termed A-bands having a slightly lighter M-line in the centre. These show the overlapping boundaries of the contractile proteins, which are all at regular intervals along separate filaments.
Cardiac muscle shows a similar pattern of striation in the electron micrograph. However, where some of the fine Z-lines appear in skeletal muscle there are distinctive intercalated disks. The intercalated disks show the boundaries between different cardiac muscle cells. Hence, it can be seen that cardiac muscle cells are significantly shorter than their skeletal equivalents. (Only about 100(m long compared to 10s of cm).
The intercalated disks of cardiac muscle are responsible for providing a strong cell-cell adhesion so that the pull of one cell on another will be adequately transmitted through the muscle. There are also considerable numbers of gap junctions between the cells of adjacent cardiac fibres and not in skeletal fibres. These allow the cells to function as a syncytium, or a single unit that allows rapid spread of excitation from one fibre to another.
An important difference between cardiac and skeletal muscle is in the protein composition of the outer cell membrane. In skeletal muscle the principally active membrane proteins in terms of action potential are sodium channels and potassium channels. Sodium channels are opened on depolarisation of the cell membrane and are quickly closed and inactivated. Potassium channels open with a slight delay and enable the cell to regain its resting potential ready for the next contraction. In cardiac muscle there is a third set of ion channels working with the action potential. These are voltage gated calcium channels and open slightly after the initial depolarisation. The influx of calcium through these channels causes a plateau in the action potential graph. This outward current of calcium almost compensates for the inward current of potassium and hence holds the cell membrane depolarised for longer and prevents the cardiac muscle cell from firing an action potential prematurely. It is also the influx of Ca2+ that triggers the release of calcium from the sarcoplasmic reticulum, rather than the action potential itself as in skeletal muscle.
The long delay before repolarisation of the membrane allows the cardiac muscle to have finished the main thrust of its contraction and to be well on the way to relaxing before the membrane is ready to fire another action potential. These enable the cardiac muscles to maintain a steady rhythm. In skeletal muscle the membrane is repolarised very quickly. This means that before the muscle has had a chance to even reach maximum contraction it is ready to be stimulated again, this second contraction will add to the first and produce a stronger contraction. Firing impulses of high frequency at the muscle can lead to action potentials building up and eventually reaching a maximum point. This is known as a tetanus and is a smoothing out of the muscle twitches to a maximum contractile force. Obviously if this was to happen in the heart then it would not be a good aid to the pumping of blood.
The method of contraction is the same for both skeletal and cardiac muscle and is though to work like this:
Actin filaments and myosin filaments are straight parallel proteins that interlink and slightly overlap. Myosin has a number of heads, (about 500 per filament) that are able to bind with sites on the actin proteins. Through hydrolysis of ATP they can then straighten and slide the two fibres past each other. This happens about 5 times a second for each head and with 500 heads working the contraction happens in a very short time period. The only problem with this would be that, as described, contraction could occur at any given moment. This is prevented by the placement of filaments of tropomyosin covering the binding sites of the actin molecules. The protein troponin is bound to the tropomyosin molecules at regular intervals. This protein has the receptor for calcium ions on it. If a calcium ion is bound to the receptor then this causes a small conformational change in the tropomyosin causing it to move laterally exposing the binding sites of the actin. The myosin filaments are then able to bind and slide the filaments past each other.
The calcium ions quickly become detached. With the action of the sarcoplasmic reticulum "mopping up" the released calcium ions by means of a Ca2+-Mg2+ ATPase the binding sites are quickly covered by tropomyosin in readiness for the next action potential to arrive.
Both skeletal and cardiac muscle have a system of invaginations of the sarcomere that is known as the T-tubule system. In skeletal muscles these are folds of membrane at the junction between the A and I bands. In cardiac muscles they lie at the Z-lines. These T-tubules are continuations of the extracellular space and enable the rapid transmission of the action potential to all the fibrils in the cell. In skeletal muscle the arrival of this action potential at the T-tubules, which are closely associated with the sarcoplasmic reticulum, causes release of calcium ions onto the fibrils. It is this calcium that enables the tropomyosin to move laterally and open the binding sites on the actin so that the myosin and actin filaments can slide past one another. In cardiac muscle however arrival of an action potential in the T-tubule system activates dihydropyridine channels in the T-system membrane. These channels open to allow passage of Ca2+ and it is the influx of Ca2+ into the cell that triggers release of large quantities of calcium ions from the sarcoplasmic reticulum. Hence, the filaments are able to contract.
As can be seen, there is a huge demand for ATP to produce this action and muscle metabolism revolves around the synthesis of ATP from various sources. In the short term, in skeletal muscle this comes from the hydrolysis of phosphorylcreatine. More important energy supplies come from the citric acid cycle of oxidation of carbohydrates and lipids, the system known as aerobic glycolysis. This requires the use of O2 from the blood. In times of extreme exercise, although the arteries supplying the muscle are able to dilate and hence supply more blood and hence O2 to the muscle, it cannot gain enough to supply its energy needs. Therefore skeletal muscle has a separate anaerobic mechanism to generate ATP by the oxidation of pyruvate to lactate avoiding the need for oxygen. This pathway is less energy efficient and will eventually come to a halt as the build up of lactate in the cell will alter pH enough to inhibit the enzymes involved.
Because of its continual motion cardiac muscle contains a significantly larger number of mitochondria (the oxidative energy producers in the cell) than skeletal muscle cells. It also contains myoglobin thought to act as an oxygen store. However, cardiac muscle is less able to use the alternative anaerobic pathway than skeletal muscle. It times of severe hypoxia it is estimated that up to 10% of cardiac energy requirements are supplied anaerobically. Skeletal muscle is able to provide up to 85% of its energy needs from this pathway. This is because the use of anaerobic respiration leads to an oxygen debt that must be recovered. Skeletal muscle is able to relax and quickly and efficiently use oxygen absorbed that is surplus to the immediate requirements of the cell to metabolise away the build up of any excess lactate. This simply is not possible in the heart, which must keep pumping at a significant rate of efficiency. That being said there is significant leeway for the resting heart to increase its output when oxygen needs to be transported around the body more quickly, as in exercise.
A feature of cardiac muscle that enables it to increase its output as necessary is the position of normality on its length-tension curve. It has been found that there is an optimum length for striated muscle to be held at before contraction in order to develop the maximum force available to it. When muscle is held in too short a position the actin/tropomyosin filaments tend to overlap each other. This means that the developed muscle tension is not as great as it could be because the number of cross-links each filament is able to form with actin is reduced. Stretched too tightly and the tension developed in a muscle will also decrease. In skeletal muscle this tends to be as the myosin filaments pull away from the tropomyosin/actin bundles. The smaller force developed is by reduction of the number of actin/myosin cross links available to participate in contraction. In cardiac muscle this is more to do with disruption of the fibres themselves.
The important point to note here is that for skeletal muscle the resting length, dependent on the position of the bones and other attachments, is around or just short of this maximum value. In cardiac muscle the position of the length-tension relationship lies on the upstroke of this curve. This gives the heart much more freedom to expand and increase blood pressure as demands on it increase. Starling defined this in his "law of the heart" when he stated that "energy of contraction is proportional to the initial length of the cardiac muscle fibre". For the heart, the length of the muscle fibres is proportional to the volume of blood taken in during diastole. This holds true under normal physiological conditions where the heart is not stretched so far it is near to destruction.
Cardiac muscle has developed to cope with maintaining a steady beat and being able to keep contracting for, well, a lifetime. To do this the muscle is able to increase its inactivated periods as and when needed. Myocardium is able to expand to the needs of the body as necessary and to manage nearly all of this through aerobic metabolic processes. Skeletal muscle on the other hand has developed to provide power in much shorter bursts. It has anaerobic mechanisms that allow the muscle for short periods to produce more power in times of emergency or hard exercise than the provided oxygen would otherwise allow. Aerobic mechanisms exist to use food more efficiently when severe demands are not being placed on the muscle and so are used more regularly. Skeletal muscle is produced at just the right length to produce as close to maximum power output as it can. Cardiac muscle leaves its options open and is able to respond to increasing demands of power output placed on it.

©Nick Manville 1998