PHYSIOLOGY OF MUSCULAR TISSUES

The muscle tissue is the driving force or power behind movement. The muscle tissue has properties that are intrinsic to it and each of these has to do with some movement. One of these properties is its contractility. Work is done each time a muscle contracts. For example food is moved along the digestive tract by a series of rhythmic waves of smooth muscle contraction. Contractions of skeletal muscles make the lower limbs to move at the ankle, knee and hip. Muscular contractions help to maintain body posture in sitting and standing positions.

Structure of Skeletal Muscles

Skeletal muscle tissue acquires its name because most of the muscles involved are attached to the skeleton and they make the skeleton to move. Skeletal muscle is composed of individual specialized cells called muscle fibres that are the “building blocks” of the muscular system just as neurons are the building blocks of the nervous system. The muscle cells are called fibres because they have long cylindrical shape and several nuclei.

Muscle fibers average 3.0cm in length with some measuring more than 30cm and some being as short as 0.1cm. Diameters range from 0.01cm to 0.001cm. Most skeletal muscles begin and end in tendons, and the muscle fibers are arranged in parallel between the tendinous ends. The fibrous connective tissue proteins within the tendons continue in an irregular arrangement around the muscle to form a sheath known as the epimysium.

Connective tissue from this outer sheath extends into the body of the muscle subdividing it into columns called fascicles (these are the strings in stringy meat). Each of these fascicles is surrounded by its own connective tissue sheath known perimysium. Further extensions of the connective tissue inwards that surround each muscle fibre separating it from other fibers are called endomysium.

Dissection of a fascicle under microscope reveals that it is in turn is composed of many muscle fibres, each muscle fibre is surrounded by a cell membrane or sarcolemma. These fibers are actually the muscle cells.

The skeletal muscle

The fibre contains several nuclei and a specialized type of cytoplasm called sarcoplasm. Within the sarcoplasm are many mitochondria and a number of individual threadlike fibres known as myofibrils.

The myofibrils are made of many thick and thin threads called myofilaments. Thick myofilaments are composed of a fairly large protein called myosin. The thin myofilaments are composed mainly of smaller protein, actin, and they also contain the proteins troponin and tropomyosin.

The contractile mechanism in skeletal muscles is dependent on these proteins. Despite their (unusual) shape, muscle cells all have the same organelles. The most distinct feature of the microscopic appearance of skeletal muscle fibres is their striated appearance. The striations are produced by alternating dark and light bands which appear to cross the width of the fibre. An overlapping of the thick myosin strands and the thin actin strands produces the dark a band; the thin actin strands alone act as the light I band.

Cutting across each I-band is a dark Z line and within the A band is a somewhat lighter H^–. Zone consisting of thick myosin strands only. Extending across the H – zone is a delicate M-line which connects adjacent thick filaments. The fundamental unit of muscle contraction is the sarcomere which is made of the muscle fibre that extends from one Z-line to the next Z-line.

Skeletal  muscles  are  also  called  striated  muscle,  because  of  this appearance of alternating light and dark strips. They are also described as voluntary muscle because we can contract them when we want to. However skeletal muscles are also capable of contracting without conscious control (involuntarily).

Muscles are usually in a partial contracted state which gives them tonus or more commonly “muscle tone”. Tonus is necessary to keep a muscle ready to react to the stimulus preceeding a complete contraction or to hold parts of the body such as the head erect and to aid in venous return to the heart.

Types of Muscle Contraction

Several types of muscle contraction have been identified including twitch, isotonic, isometric, treppe and tetanic contractions.

Twitch

This is a momentary spasmodic contraction of a muscle in response to a single stimulus (such as an electric current or a direct stimulation of a motor unit). It is the simplest type of recordable muscle contraction. Increasing the stimulus voltage increases the strength of a twitch up to a maximum. The strength of a muscle contraction can thus be graded or varied. If a second electrical shock is delivered immediately after the first it will produce a second twitch that may partiality add on the first. This is called summation of contractions.

Treppe

When a rested muscle receives repeated stimuli over a prolonged period, the first few contractions increase in strength (by summation). The recording on a myogram will look like an upward stair case. After several contractions a steady tension for contraction is reached and the contractions level. It stimuli and contractions continue, fatigue occurs. If controlled properly, however, as when athletes “warm up” treppe contractions increase blood flow to a muscle and prepare it for a maximum output of strength when it is needed. Treppe is believed to be due to an increase in calcium ions that bind to troponinc.

Isotononic and Isometric Contractions

When a muscle contracts by becoming shorter and thicker, the contraction is called isotonic because the amount of force or tension remains constant as movement takes place. For example on pulling open a door, the arm muscle contracts and moves the arm which moves the door. In contrast, if the load on a muscle (opposing forces gravitational pull an object) is greater than the tension developed by a muscle, the muscle retains its original length, and the contraction is isometric.

That is, a typical contraction and shortening does not occur even though energy is used. For example holding a door open involves an isometric contraction since the arm muscle does not shorten but does become more tense without producing any movement. Another example – running produces noticeable isotonic contractions (active work) and standing produces isometric contractions. Most body movements involve both isotonic and isometric contractions.

Tetanic Contractions

If a muscle receives repeated stimuli at a rapid rate, it cannot relax completely between contractions. The tension achieved under such conditions is greater than the tension of a single twitch and is called summation of twitches. A more or less contraction of the muscle is called tetanic contractions or tetanus. When incomplete relaxations are evident between contractions the state is called incomplete tetanus. Complete tetanus occurs when the muscle is in a steady state of contraction with no relaxation at all between stimuli.

Nervous Control of Muscle Contractions

Muscle fibres usually contract in groups. Skeletal muscles are packed together into fascicles having an average of about 150 fibers. The fibers within each fascicle are controlled by a single motor neuron. One motor neuron may stimulate so many fibres, up to 1600 in the powerful leg muscles. The cell body of a somatic motor neuron is located in the ventral horn of the gray matter in the spinal cord and gives rise to a single axon that emerges in the ventral root of a spinal nerve.

Each axon can however produce a number of collateral branches to innervate a number of muscle fibres. This is why one motor neuron can stimulate many fibres (as much as 1600 in the leg muscles). Each motor neuron together with all the muscles fibres it innervates is known as a motor unit.

The Neuromuscular Junction

The site where a motor nerve ending contacts a muscle fibre is called a neuromuscular junction or myoneural junction. The axon terminals of motor neurons gain access to the muscle fibre through the endomysium. At the point of contact between the muscle fibre and the motor neuron, the muscle fibre membrane forms a motor end plate.

The motor end plate is the specialized portion of the sarcolemma of a muscle fibre, that surrounds the terminal end of the axon.

At the motor end plate, nerve endings are separated from the muscle fibre by a tiny gap called synaptic cleft. The chemical transmitter acetylcholine (ACH) is released from the synaptic vesicles of nerve endings. It bridges the synaptic cleft and flows into folds of the sarcolemma. Some ACH then become attached to the receptor sites in the sarcolemma, initiating an electro-chemical impulse across the sarcolemma of the muscle cell, so that sodium ions move into the sarcoplasm and potassium ions move out.

This results in depolarization across the membrane and beginning of a muscular contraction. This depolarizing potential is called end plate potential. The impulse is transmitted successively through the cell membrane to the sarcoplasmic reticulum where it triggers the release of calcium ions which stimulate the muscle to contract.

Acetylcholinesterase, and enzyme of the muscle fibre membranes, then breaks down acetylcholine into acetate and choline and the depolarization ceases, and the muscle fibre relaxes.

The All-Or-None Principle

Whenever a somatic motor neuron is activated by a sufficiently strong stimulus, all the muscle fibres it innervates (in a motor unit) are stimulated to contract fully. If the contraction is subthreshold however, the fibres will not contract at all. This tendency to contract fully or not at all is called the all-or-non principle. A stimulus of above threshold intensity however will not cause the intensity of the contraction to increase.

Although individual muscle fibres follow the all-or-none principle, whole muscles usually have graded contractions. Involves for these graded contractions. In order for these graded contractions to be smooth and sustained different motor units must be activated. The strength of a muscle contraction depends on how many fibres are stimulated; the frequency of stimulation and how many motor units are activated.

These processes of neuronal control of muscle contractions involve summation, i.e. varying numbers or frequencies of muscle contraction adding up to the force of contractions. Fine neural control over the strength of muscle contraction is optimal when there are many small motor units involved. For example in the extraocular muscles the innervating ratio (neuron to muscle fibre) of an average motor unit is one neuron per 23 fibres.

This makes for fine degree of control. The innervation ratio of large muscles like the gastrocnemius is an average of 1 neuron per thousand fibres. Such stimulation results in more powerful contractions at the expense of finer gradations in contraction strength. If a small job is to be done a few motor units will be involved at the same time.

Motor units do not all have the same threshold. If for example motor units with low threshold are stimulated a smaller number of motor units will contract. Higher intensities of stimulation lead to the activation of more motor units. This increase in the number of motor units activated is called recruitment of motor units.

Two different methods of summation are employed in gradations of muscle contraction. In multiple motor unit summation, gradations of contraction between minimal and maximal is achieved by varying the number of units contracting. In wave summation, it is achieved by having each motor unit contracting in quick succession that can be so close together that the new ones add to the force of the new ones add the older ones thereby increasing the overall strength of contractions.

Refractory Period

A skeletal muscle loses its irritability and cannot contract again for about 0.005 seconds. This period is called the refractory period. In cardiac muscles it lasts about 0.3 second. There is the absolute refractory period (from the threshold stimulus, till repolarization is one third complete) and the relative refractory period (from end of the absolute period to the start of a new depolarization).

The absolute refractory period is a period during which no stimulus, no matter how long or strong will cause a muscle fibre to be stimulated. In the relative refractory period, stronger-than-normal stimuli are needed to stimulate a muscle fibre.

Mechanism of Muscle Contraction

Sliding filament theory of muscle contraction. The arrangement of the myosin and actin molecules in the myofilaments is crucial to the mechanism of muscular contraction. An actin myofilament in the muscle is made up of actin, tropomyosin and troponin (troponin in itself is composed of 3 subunits, troponin I, T and C, sometimes referred to as the troponin complex).

The molecules of actin, tropomyosin and troponin are arranged in thin twisted strands. The thicker myosin myofilament is composed of myosin molecules that have oval heads and long tails. For muscular contraction to occur, the heads of the myosin molecules have to move towards the actin myofilaments and form crossbrdiges. Myosin cross-bridges only get activated when they are attached to actin myofilaments.

In the sliding filament theory, the myelin cross bridges act as hooks to pull the actin myofilaments along so that the actin and myosin myofilaments slide past each other, the sarcomere becomes pulled toward each other, the sarcomere becomes shorter. The same thing happens in other sarcomeres and other fibers causing the muscle to contract.

The process can be summarized in the following sequence:

Nerve impulses from brain and spinal cord are carried to muscle fibres by motor neurons.

Each motor neuron releases Ach which diffuses across the neuromuscular junction.

The wave of depolarization initiated by Ach spreads over the sarcolemma and T-tubules, which is in contact with the sarcoplasmic reticulum, from where calcium ions are released.

When calcium is present, they bind to troponin in the actin myofilament, causing the troponin complex to shift and expose active sites on the actin strands. The myosin cross bridges then attach to the actin myofilaments to form actomyosin.

At the same time myosin is activated by calcium to perform the role an enzyme. It splits ATP molecule into ADP and an inorganic phosphorus releasing energy.

The energy is stored in the head of the myosin and is used to move the heads of the myosin molecules toward the actin myofilaments. The myosin head form a cross bridge which attaches to the exposed active site on the actin myofilament to form actomyosin. The myosin heads tilt and change shape, pulling the actin myofilament along, so that the myosin and actin myofilament slide past each other.

As they slide, the cross bridges detach and from one site and attach to the next site. Skeletal muscle contractions occur so rapidly that each myosin cross bridge may attach and release the active sites on the actin myofilament as many as 100 times.

When the thin actin and thick myosin myofilaments slide past each other, the actin myofilaments from opposite ends of a sarcomere move toward each other and the muscle contracts. The widths of I-bands shorten, that of A-bands remain the same and the Z-lines move closer together.

Muscle Relaxation

For a muscle to relax, the following occurs:

Acetylcholine is broken down by acetylcholinesterase which is released from the muscle. This breakdown prevents further stimulation of the muscle by the nerve ending.

The calcium ions move from the myofilaments back to the sarcoplasmic reticulum to be stored when there is no more nervous stimulation.

Without calcium, troponin and tropomyosin prevent actin from combining with myosin by blocking the active sites on the actin myofilament. Thus the myosin cross bridges can no longer attach to actin myofilaments.

As the myosin and actin myofilament returns to their original positions in the sarcomere, the I-bands become larger and the Z-lines more farther apart. The sarcomeres return to their original (resting) length and the muscle fibre relaxes.

Regulation of Contraction

Cross bridges, are part of the myosin proteins that extend from the axis of the thick filaments to form “arms” that terminate in globular heads. These cross-bridges attach to actin, undergo power strokes and cause muscle contractions. To prevent contraction so that a muscle can relax, the attachment of myosin cross-bridges to actin must be prevented.

Two proteins associated with actin in the thin filaments regulate cross bridge attachment to actin. These are tropomyosin and troponin. These two works together to regulate the attachment of cross bridges to actin; and therefore serve as a switch for muscle contraction and relaxation. Tropomyosin physically blocks the cross bridges from binding to specific attachment sites in the actin. In order for myosin cross bridges to attach to actin, the tropomyosin must be moved. This requires the interaction of troponin with Ca⁺⁺.

The Role of Ca⁺⁺ in Muscle Contraction

When the muscle is relaxed and tropomyosin blocks the attachment of cross bridges to actin, the concentration of Ca⁺⁺ in the sarcoplasm is very low. When a muscle is stimulation in made to rise rapidly. Some of the Ca ⁺⁺ attaches themselves to a subunit of troponin causing a conformated change that moves troponin and its attached tropomyosin out of the way so that cross bridges can attach to actin.

Once the attachment sites on the actin are exposed, it becomes possible for myosin cross-bridges to attach to actin, undergo power strokes and produce muscle contraction. The position of the troponin-tropomyosin complex is adjustable based on whether Ca⁺⁺ is attached to troponin or not and this controls muscle contraction. Muscle contraction is turned on when sufficient amounts of Ca⁺⁺ bind to troponin.

This occurs when the concentration of Ca⁺⁺ in the sarcoplasmic reticulum rises above 10⁶ molar. For muscles to relax Ca⁺⁺ levels have to drop below this level. Muscle relaxation is achieved by the active transport of Ca⁺⁺ out of the sarcoplasm into the sarcoplasmic reticulum. As long as action potentials continue to be produced – which is as long as nervous stimulation of the muscle is maintained, Ca⁺⁺ will remain attached to troponin and cross bridges will be able to undergo contraction cycles.

Neural Control of Skeletal Muscles

Motor neurons in the spinal cord (lower motor-neurons) as previously discussed have their cell bodies in the ventralhorns of spinal cord and axons within the nerves that stimulate muscle contraction. The activity of these neurons is influenced by (1) sensory feedback from muscles and tendons and (2) facilitatory and inhibitory effects from upper motor neurons in the brain which contribute axons to descending motor tracts.

The lower motor neurons are therefore said to be the final common pathway by which sensory stimuli and higher brain centres exert control over skeletal movements.

As previously discussed, axons of these lower motor neuron cell bodies leave the ventral side of the spinal cord to form the ventral roots of spinal nerves. The dorsal roots of spinal nerves contain sensory fibers whose cell bodies are in the dorsal root ganglia. Both sensory and motor fibers join in a common connective tissue sheath to form the spinal nerves each segment of the spinal cord.

In order for the nervous system to control skeletal movements properly, it must receive continuous sensory feedback information concerning the effects of its actions. This sensory information includes (1) the tension exerted by the muscle on its tendons provided by the Golgi tendon organs and (2) muscle length provided by the muscle spindle apparatus. The muscle spindle apparatus functions as length detector.

The information from these sensory receptors (Golgi tendon organs and muscle spindles) are used to inform the motor areas of the brain, of muscle length and tension and to control muscle length and tension in negative feedback fashion by means of local spinal reflexes.

Muscle spindles are distributed throughout the fleshy part of skeletal muscles and consist of collections of specialized muscle fibers known as intrafusal fibers which lie within spindle-shaped connective tissue capsules parallel to the “ordinary” extrafusual fibres.

Whenever the whole muscle is stretched, the intrafusal fibers within its muscle spindles are stretched, increasing the rate of firing in the afferent fibres whose sensory endings terminate on stretched spindle fibres. The afferent neuron directly synapses on the alpha motor neurons that innervate the extrafusal fibres of the same muscle resulting in contraction of that muscle. This stretch reflex serves as a local negative -feedback mechanism to resist any passive changes in muscle length so that optimal resting length is maintained (The classical example of the stretch reflex is the knee-jerk reflex which you can read up privately).

Golgi tendon organs are located in the tendons of the muscles where they respond to changes in the muscle’s externally applied tension rather than to changes in its length. The Golgi tendon organs consist of endings of connective tissue – fibres that make up the tendon. When the extrafusal muscle fibres contract, the resultant pull on the tendon tightens the connective tissue bundles, which in turn increase the tension exerted on the bone to which the tendon is attached. In the process the entwined Golgi organ afferent receptor endings are stretched causing the afferent fibers to fire. The frequency of firing is directly related to the tension developed.

The afferent information is sent to the brain. Other branches of the afferent neuron arising from the Golgi tendon organ inhibit through an interneuron in the same muscle. When the tension becomes great enough, the high level of inhibitory input from the activated. Golgi tendon organs counter-balance excitatory inputs. This inhibitory response halts further contraction and brings about sudden reflex relaxation, thus helping prevent damage to muscle or tendon from excessive tension – developing muscle contractions.

Upper Motor Neuron Control

Upper motor neurons are those in the brain that influence the control of skeletal motor neurons by lower motor neurons. Neurons in the precentral gyrus of the cerebral cortex contribute axons that cross to the opposite side of the pyramids of the medulla oblongata; these pyramidal tracts include the lateral and ventral corticospinal tracts.

The extra-pyramidal tracts are from neurons in other areas of the brain and the major one is the reticulospinal tracts from the reticular formation of the medulla and pons. Brain areas that influence the activity of the extra-pyramidal tracts are believed to produce the inhibition of lower motor neurons. The cerebellum like the cerebrum receives sensory information from muscle spindles and Golgi tendon organs.

It also receives fibres from areas of the cortex devoted to vision, hearing and equilibrium. The cerebellum affects motor activity only indirectly through its output to the vestibular nuclei, red nuclei and basal nuclei. These structures influence lower motor neurons through the vestibulospinal, rubrospinal and reticulospinal tracts. All output from the cerebellum is in-hibitory. The inhibitory effects aid motor coordination by eliminating inappropriate neural activity. Damage to the cerebellum causes inability to coordinate movements with spatial judgement.

The basal nuclei act directly via the rubrospinal tract and indirectly through synapses in the reticular formation and thalamus to exert profound effects on the lower motor neurons. In particular, through their synapses in the reticular formation the basal nuclei exert inhibitory influence on the activity of the lower motor neurons. Damage to the basal nuclei results in increased muscle tones.

Energy Requirements of Skeletal Muscles

Skeletal muscles at rest obtain most of their energy from aerobic respiration of fatty acids. During exercise, muscle glycogen and blood glucose are also used up as energy sources. Energy obtained by cell respiration is used to make ATP, which serves as the immediate source of energy for (1) the movement of the cross bridges for muscle contraction, and (2) the pumping (active transport) of Ca⁺⁺ into the sarcoplasmic reticulum for muscle relaxation.

Metabolism of Skeletal Muscles

Skeletal muscles respire anaerobically for the first 45 – 90 seconds of moderate to heavy exercise, because the cardiopulmonary system requires this amount of time to increase the oxygen supply to the exercising muscles. If the exercise is moderate and the person is physically healthy, aerotic respiration contributes the major portion of the skeletal muscle energy requirements after the first two minutes of exercise.

The maximum rate of oxygen consumption (by aerobic respiration) called the maximal oxygen uptake is determined by a person’s age, size and sex. It is 15% – 20% higher for males than females and highest at age 20 for both sexes. Genetic factors can affect it. Training can also increase it by about 20% maximum.

When a person stops exercising, the rate of oxygen uptake does not go back to pre-exercise levels at once. It returns rather slowly with the person breathing heavily for some time. The extra oxygen at this time used to repay the oxygen debt incurred during exercise.

The oxygen debt includes oxygen withdrawn from savings deposit (haemoglobin in blood and myoglobin in muscles); the extra oxygen required for metabolism by tissues warmed up during exercise; and the oxygen needed for the metabolism of the lactic acid produced during anaerobic respiration.

During sustained muscle activity, ATP may be used faster than it can be produced through cell respiration. At these times the rapid renewal of ATP is extremely important. This is accomplished by combining ADP with phosphate derived from another high-energy phosphate compound called phosphocreatine or creatine phosphate.

The concentration of this compound in muscle cells is more than thrice that of ATP. Therefore it becomes a ready reserve of high energy phosphate that can be donated directly to ADP. During rest, the depleted reserve of phosphocreatine can be restored by reverse reaction the phosphorylation of creatine with phosphate derived from ATP.

Fast Twitch, Slow Twitch Fibres

Skeletal muscles fibres can be divided on the basis of their contraction speed (time required to reach maximum tension) into slow-twitch or type 1 fibers and fast-twitch or type II fibers. This classification is usually a function of the type of myosin ATPase enzyme type. The contraction speed ranges from about 7.3 milliseconds (for very fast twitch fibers like the extraocular muscles that move the eyes) to up to 300msec for large leg muscles. Other muscles are in a range between these two types.

Slow-twitch or type I fibers like the soleus muscle of the leg are able to sustain a contraction for a long period of time without fatigue. The resistance to fatigue is as a result of other characteristics of slow-twitch fibres. Slow twitch fibers are endowed with a high oxidative capacity for aerobic respiration. They have a rich capillary supply, numerous mitochondria and aerobic respiratory enzymes and high concentration of myoglobin pigment. (Myoglobin is a red pigment in muscles, similar to haemoglobin in red blood cells). Myoglobin improves the delivery of oxygen to slow-twitch fibers. Slow twitch fibers are also called red muscle because of their high myoglobin content. They have low myosin ATPase content.

Fast -twitch or type II fibers are thicker have fewer capillaries and mitochondria than the slow-twitch fibres, and not as much myoglobin. The are also called white fibers. Fast-twitch fibers are adapted to respire anaerobically by a large store of glycogen and a high concentration of glycolytic enzymes. These also fatigue easily and have high myosin ATPase. In humans there can also be intermediate forms of fibres. These are rather fast twitch but have a high oxidative capacity.

The fibre type seems to be determined by the motor neuron. The conduction rate of motor neurons that innervate fast-twitch fibers is faster (80 – 90 meter per second) than the conduction rate to slow-twitch fibers.

Muscle Fatigue

This is the inability to maintain a particular muscle tension when the contraction is sustained or to reproduce a particular tension during rhythmic contractions over time. The first one is concerned with fatigue during a sustained maximal contraction, when all the motor units are used and the rate of neuronal firing is maximal for example when lifting an extremely heavy weight.

This appears to be due to an accumulation of extracellular K⁺ (call to mind that K⁺ leaves axons and muscle fibres during repolarization phase of action potential). This increases the membrane potential temporarily hindering production of action potential. Fatigue under these circumstances lasts only a short time. After a minutes rest or less, maximal tension can be achieved.

The second type occurs during rhythmic contraction, over time. It can occur during moderate exercise, over a period of time. As the slow-twitch fibres deplete their reserve glycogen and fast-twitch fibers get recruited to obtain energy through anaerobic respiration, converting glucose to lactic acid, there is an accumulation of intracellular H⁺. This reduces the pH. The fall in muscle ph in turn promotes muscle fatigue by mechanisms that are not completely understood.

 Adaptation to Exercise

All muscle fibre types adapt to endurance training by an increase in mitochondria activity and thus in aerobic respiratory enzymes. The maximal oxygen uptake can be increased by as much as 20% during endurance training. The maximal oxygen uptake obtained during very strenuous exercise, average 50ml of O2 per kilogram body weight per minute in males between the ages of 20 – 25 years. (Females average 25% lover). Trained endurance athletes (such as swimmers and long distance runners) can have maximal oxygen uptake as high as 86ml O2 per kilogram per minute.

During exercises which are performed at low levels of effort, such that the oxygen consumption rate is below 50% of its maximum, the energy for muscle contraction is obtained almost entirely from aerobic cell respiration. Anaerobic respiration with its production of lactic acid contributes to the energy requirement as the exercise level rises. Highly trained endurance athletes, however can continue to respire aerobically, with little lactic acid production at up to 80% of their maximal oxygen uptake. Such athletes thus produce less lactic acid at given level of exercise than the average person, and therefore are less subject to fatigue than the average person.

Endurance training does not increase the size of muscles. Muscle enlargement is produced only be frequent periods of high-intensity exercise in which muscles work against a high resistance, as in weight lifting. As a result of resistance training, type II muscle fibers become thicker, and the muscle therefore grows by hypertrophy (an increase in cell size, rather than number of cells).

This happens first because, the myofibrils within a muscle fibre thicken, due to the synthesis of actin and myosin proteins and the addition of new sarcomeres. After a myofibril attains a certain thickness it may split into two myofibrils, each of which may then become thicker due to the addition of sarcomeres. Muscle hypertrophy is associated with an increase in the size and then the number of myofibrils within the muscle fibers.

Heat Production

One of the useful by-products of muscle contraction is the production of heat. In the body heat production is necessary to help maintain a stable body temperature. Even a resting muscle gives off some heat. Initially heat is generated during muscle contraction and relaxation largely from the breakdown of phosphates. Thus initial heat is released quickly, in less than a second.

Recovery heat however is produced only after the muscle has completely relaxed after a contraction. It may take up to 5 minutes to produce. This heat comes as a result of the resynthesis of ATP and creatine phosphate and includes the aerobic breakdown of pyruvic acid into water and carbon dioxide and also aerobic conversion of lactic acid to water and carbon dioxide.

Smooth Muscle

Smooth and cardiac muscles are involuntary effectors regulated by autonomic motor neurons. Smooth muscles or visceral muscles are arranged in circular layers around the walls of blood vessels and bronchioles (small air passages in the lungs). There are circular and longitudinal smooth muscle layers in the tubular digestive tract, the ureters, the ductus deferens and the uterine tubes.

The alternate contraction of circular and longitudinal smooth muscle layers in the intestine produces peristaltic waves, which propel the contents of these tubes in one direction. The action of smooth muscles is thus rhythmic. Smooth muscles fibres are long; spindle shaped and contain only one centrally located nucleus.

Smooth muscles do not contain sarcomeres (which produce striations in skeletal and cardiac muscle), they do contain a great deal of actin and some myosin, which produces a ratio of thin-to-thick filaments of about 16.1 (in striated muscles, the ratio is 2.1). Unlike striated muscles, in which the thick filaments are short and stacked between Z discs in sarwmees myosin filaments in smooth muscle cells are quite long.

The long length of myosin filaments and the fact that they are not organized into sarcomeres has advantages in smooth muscle function: (1) Smooth muscles can contract even when stretched very much. For example in the urinary bladder, the smooth muscle cells can stretch up to 22 times their resting length, and in the pregnant uterus can stretch up to eight times their original length. In contrast skeletal muscles lose their ability to contract when the sarcomeres are stretched to the point where actin and myosin no longer overlap.

Smooth  muscle  contraction  is  triggered  by  a  sharp  rise  in  Ca⁺⁺concentration in the sarcoplasm just like in striated muscle, but the sarcoplasic reticulum is not as developed as that of skeletal muscles. Therefore sustained contraction of smooth muscles is maintained by extracellular Ca⁺⁺ which diffuse into cell through the cell membrane. Also unlike in striated muscles where Ca⁺⁺ combines with troponin, smooth muscles do not have troponin but another protein with similar structure, calmodulin, is present in smooth muscle cytoplasm to combine with Ca⁺⁺.

Diagram of a smooth muscle

The concentration of Ca ⁺⁺ determines how many myosin cross bridges that will attach to actin and thus determines the strength of contraction. The concentration of calcium is in turn regulated by the degree of depolarization. Unlike in striated muscles which produce all-or-none action potentials, smooth muscle cells can produce graded depolarizations without producing action potentials; in many smooth muscles it is only these graded potentials that are conducted from cell to cell.

The triggering mechanism however are not impulses from voluntary nerves, but rather inputs that either act on the sarcoplasmic reticulum or on specific calcium channels in the sarcolemma to increase its movement into the cell. These triggering inputs include: stretching of the smooth muscle myofibrils (2) Spontaneous electrical activity (pace maker potential) within the sarcolemma, (3) Specific neurotransmitters released by autonomic neurons, (4) Hormones and hormone modulators like prostaglandins and (5) Local changes in the extracellular fluid around the smooth muscle (such as pH, O2 and CO2 levels).

The contractions of smooth muscles are slow and sustained. The slowness of contractions is thought to be due to a limited and slower amount of ATPase activity in splitting ATP. The slowness may be due to a Alatch@ mechanism whereby the cross bridge remains in the attached position for a long time, thus reducing the cycling rate and the rate of ATP consumption. Smooth muscles also use a wide variety of substrates for ATP production such as carbohydrates and fats. Smooth muscles use ATP as an immediate source of energy for contraction but they do not have such energy reserves as creatine phosphate found in skeletal muscle.

Smooth muscle fibres are usually functionally classified as single unit or multiunit types.

Single-Unit Smooth Muscles Most smooth muscle are the single unit types. This means that smooth muscles have numerous gap junctions (electrical synapses) between adjacent cells that weld them together electrically, so that they behave as a single (large) unit. When a muscle cell is stimulated, it contracts and spreads the stimulation to the adjacent cells. This method produces a steady wave of contractions, such as those that push food through the intestines. The smooth muscle fibre that receives the stimulus from a motor neuron initially and passes it to adjacent fibres is known as the pacemaker cell.

Two types of contractions take place in single-unit smooth muscles: tonic and rhythmic. Tonic contractions cause the muscle to remain in a constant state of partial contraction or tonus.

This is necessary for organs like the stomach and intestine, to help move food along, and for sphincters too. Tonus prevents stretchable organs like the stomach and bladder not to stretch out of shape permanently but to maintain tension in their walls.

Rhythmic Contractions are a pattern of repeated contractions produced by the presence of self exciting muscle fibres from which spontaneous impulses travel. These rhythmic contractions in the digestive system for example produce mixing movements and propulsive movements or peristalsis.

Multi Unit Smooth Muscles These are so named because each individual fibre can be stimulated by separate motor nerve endings. There are no connections between the fibres and each multi-unit fibre can function independently. Multi-unit smooth muscle is found in the iris and ciliary muscles of the eye where rapid muscular adjustments are needed for the eye to focus properly. Also the erector muscles in the skin that cause Agoose bumps@ are of the multi-unit type and the smooth muscle of the ductus deferens.

The innervation of smooth muscles differs from the way skeletal muscles are innervated. Instead of having only one junction with a somatic fibre, with receptors for the neurotransmitter located in the neuromuscular junction, the entire surface of smooth muscle cells contains neurotransmitter receptor proteins.

Cardiac Muscle

Cardiac muscle tissue is found only in the heart. It contains the same type of myofibrils and protein components as skeletal muscle and the contractile process as for the skeletal muscles.

Structure

The cardiac muscle fibre refers to a chain of cells joined end to end by cell junctions, (electrical synapses) and not a single fibre as in skeletal and smooth muscles. The cells are short, branched and interconnected. Cardiac muscles are striated, and they contain actin and myosin filaments, arranged in form of sarcomeres. The fibres are crossed by dark bands that occur in place of, but are wider than the Z lines in skeletal muscle.

These bands are called intercalated discs. The discs separate the cells within a muscle fibre, strengthen the junction between cells and help an impulse to pass quickly from one cell to the next.

                  Diagram of a cardiac muscle

Functioning

The cardiac muscle depends on nerve impulses only to some extent, being able to contract rthymically on its own at about half its normal rate. Cardiac action potentials normally originate in a specialized group of cells called the pacemaker. When an electrical impulse originates at any point in the myocardium, it can spread to all the cells through the gap junctions, because the cells are Aconnected@ to each other by intercalated discs into a continuous network.

A myocardium functions as a single functional unit, thus unlike skeletal muscles that produce graded contractions depending on the number of fibres stimulated, the cardiac muscle contracts to its full extent each time because all of its cells contribute to the contraction.

The cardiac muscle contains two distinct myocardial – the atria and the ventricles. Instead of contracting (beating) independently, the cells are all coordinated so that their rate and rhythm are appropriate for the job of pumping blood 24 hours a day.

Cardiac muscle differs from skeletal muscle in some ways:

The sarcoplasmic reticulum is less extensive in cardiac muscle.

The calcium-ion sensitivity of intact cardiac muscle is much greater than that of skeletal muscle. A significant amount of calcium enters the cardiac muscle cell during contraction; therefore the cell can actually contract for longer periods than a skeletal muscle cell. Cardiac muscle is also affected more by calcium imbalances than any other excitable tissue.

Cardiac muscle has in-built safety feature against developing a tetanic contraction. This is avoided because of the extended period of depolarization (refractory period) in cardiac muscle which is up to 200 milliseconconds as against 1 B 2 ms in skeletal muscles. Because of this a second contraction cannot be produced until the muscle has relaxed, which is not fast enough to cause tetanic contractions. Contractions of the heart last between 200 and 250 milliseconds.

Comparison of Skeletal, Cardiac and Smooth Muscle

Skeletal muscle

Skeletal Muscles are those which attach to bones and have the main function of contracting to facilitate movement of our skeletons. They are also sometimes known as striated muscles due to their appearance. The cause of this ‘stripy’ appearance is the bands of Actin and Myosin which form the Sarcomere found within the Myofibrils.

Skeletal muscles are also sometimes called voluntary muscles, because we have direct control over them through nervous impulses from our brains sending messages to the muscle. Contractions can vary to produce powerful, fast movements or small precision actions. Skeletal muscles also have the ability to stretch or contract and still return to their original shape.

Skeletal muscle fibre type

Not all fibres within Skeletal muscles are the same. Different fibretypes contract at different speeds, are suited to different types of activity and vary in colour depending on their Myoglobin (an oxygen carrying protein) content.

Smooth muscle

Smooth muscle is also sometimes known as Involuntary muscle due to our inability to control its movements, or Unstriated as it does not have the stripy appearance of Skeletal muscle. Smooth muscle is found in the walls of hollow organs such as the Stomach, Oesophagus, Bronchi and in the walls of blood vessels. This muscle type is stimulated by involuntary neurogenic impulses and has slow, rhythmical contractions used in controlling internal organs, for example, moving food along the Oesophagus or contricting blood vessels during Vasoconstriction.

Cardiac muscle (heart muscle)

This type of muscle is found solely in the walls of the heart. It has similarities with skeletal muscles in that it is striated and with smooth muscles in that its contractions are not under conscious control. However this type of muscle is highly specialised. It is under the control of the autonomic nervous system, however, even without a nervous imput contractions can occur due to cells called pacemaker cells. Cardiac muscle is highly resistant to fatigue due to the presence of a large number of mitochondria, myoglobin and a good blood supply allowing continuous aerobic metabolism.