Transcript Chapter 10
Chapter 10 Anatomy & Physiology Fifth Edition Seeley/Stephens/Tate (c) The McGraw-Hill Companies, Inc. The Muscular Characteristics and Function • Human muscles do a mechanical action by sliding many many tiny segments in muscles fibers or cell. When they become 2/3 of their original length, the muscle becomes 2/3. • A muscle fiber is a cell that is the full length of the muscle. • The three types of muscle tissue are: skeletal, cardiac and smooth muscles. See Table 10.1 for comparison. • Muscles have least four properties: – They excite responding to neuronal (electrical) or hormonal stimulation. – They contract. – Even after being stretched beyond the resting length, they can still contract- extensibility. – They are elastic and return to the original length after contraction. • Overall Functions: skeletal muscles includes the skeletal tissue, C.T., blood, and nerve tissues. • Together they: – Make the body move. – Maintain posture and body position. – Support soft tissues. – Control entrances and exits of the body. – Maintain body temperature. • The Anatomy – Muscles to Muscles Fibers – Figure 10.3 summarizes the organization of skeletal muscle. • Skeletal muscles: – Tendon attaches to periosteum of the bone – Epimysium wraps around: • Perimysium – C.T. fibers • Blood vessels and nerves • Muscle fascicle (fasciculus) · Endomysium – C.T. · Muscle fiber with motor neurons · Stem cells • Anatomy of Muscle Fibers • Muscle fibers are the largest of cells in the human body. • Skeletal muscle fibers are small in diameter (~100um or 0.1 mm), but the length could be as long as the full length of muscles (0.030 um). • Skeletal muscle fibers are multinucleated and rich in mitochondria. Thus, when need arrives, the cells can generate ATP, and synthesize enzymes and structural muscle proteins quickly. • The cell membrane of muscle fiber is the sarcolemma. • The cytoplasm of muscle fiber is the sarcoplasm. • T-tubules (transverse tubules), run across the muscle fiber and open on the surface of sarcolemma. Thus, the contents of T-tubules have direct connection to the extracellular fluid and can become highway to transport extracellular fluid to the inner region of muscle fibers. This is important since during the muscle contraction, entire myofibrils will be stimulated at the same time. – Transverse tubules and the sarcoplasm reticulum • Through the T-tubules, electrical and chemical signals can be brought deep into the muscle fibers where myofibrils are found. • Myofibrils are bundles of contracting proteins. • The myofibrils are surrounded with sarcoplasmic reticulum and their end, terminal cisternae, closely make contract with Ttubules, which wrap around the myofibrils. • At the resting stage of muscle, in these cisternae a high concentration of Ca++ is found, while its concentration in the sarcoplasm is kept low. • Myofibrils and Myofilaments are contractile proteins – Within each muscle fiber, there are hundreds to thousands of myofibrils of 1-2 um in diameter. – Thin, as they may be, in order to perform contraction, these myofibrils are as long as the total length of muscles fibers and attach sarcolemma at the both ends. – Each myofibrils consist of bundles of myofilaments, filamentous forms of thin actin and thick myosin filament. – Thin actin myofilaments are about 8 nm in diameter and 1000 nm in length. – Thick myosin myofilaments are about 12 nm in diameter and 1800 nm in length. – In addition to being surrounded with sarcoplasmic reticulum, myofibrils are also surrounded with mitochondria and glycogen granules, which will provide energy in the form of ATP. • Sarcomere Organization (Fig. 10.3, 10.4, 10.8) – Within myofibrils repeating units of sarcomeres are found. – Each sarcomere has Z-lines (disk) on both ends, where thin filaments attach. In fact, the thin filaments extends on both sides of the Z disk and create isotropic I band. – Thick filaments which are held together at the M line form A band and move into the thin filaments. – Thus, these Z disks, I bands and A bands create striations, perpendicular to the length of myofibril, spreading into the entire muscle fiber. This striations is possible due to the presence of T-tubules. – A sarcomere is the smallest basic unit in muscle and there are more than 10,000 sarcomeres for each fibril. – Note that if each sarcomere is 2.6 um, what is the length of muscle fiber? (2.6 cm) – If the sarcomere is shortened by 1/3. The entire muscle will contract by 1/3. • Thin and Thick Filaments – Thin and thick filaments are the basic components of muscular contraction. – Energy is supplied from mitochondria and quick contraction is initiated when Ca++ is supplied from cisternae. – Thin filaments consist of actins connected with a pair of tropomyosins into twisted form. Each actin has an myosin binding active site, but at the resting stage of muscle, the active site is covered with strategically placed tropomyosin. – Thick filaments are bundles of myosin molecules, which consist of an elongated tail section and a globular head. They are connected with a hinge. – The entire process of contraction, sliding of thin and thick filaments, start with a burst supply of Ca++ from the sarcoplasmic reticulum…Ca++, upon binding with troponins, expose the active sites of actin then bind with tropomyosins and the heads of myosin. Sliding Filaments. (fig 10.8) The Control of Muscle Fiber Contraction and Relaxation • How the neuromuscular junctions are made – Communication between the neurons and muscle fibers is done through a neuro-muscular junction. – Each skeletal muscle fiber is controlled by a motor neuron. – Recall neuro-physiological terms: synaptic knob, acetylcholine, acetycholinesterase, synaptic cleft, motor endplate, etc… • The function of neuromuscular junction (Excitation-contraction coupling) – Also recall how acetylcholine is released at the cleft in response to the action potential. – In case of neuro-muscular junction, postsynaptic excitation will end up spreading the action potential throughout the surface of sarcolemma. – The excitation will travel through the T-tubes to cisternae, which forces release of Ca++ from the sarcoplasmic reticulum. – The release of such large quantities of Ca++ react with troponin which will move tropomyosin to uncover the active sites of actin. • Relaxation – Relaxation of muscle fiber requires the removal Ca++. – By removing Ca++, tropomyosin will no longer initiate binding of myosin and actin. – Ca++ will be moved back into sarcoplasmic reticulum with the consumption of ATP. Inhibition of neuro-muscular Synapses • Against acetycholinesterase – organophosphates (insecticides, nerve gas) inhibits the acetycholinesterase, Ach accumulates in synaptic cleft and causes continued post synaptic membrane depolarization. • Against acetylcholine receptors: curare,( S.Am cotton mouth), keeps the Na+ pumps closed which results no contraction of muscle (flaccid paralysis). • Against Na+ gated channel – tetratodoxin , blocks Na+ channel and results in no depolarization (flaccid paralysis) A mode of muscle of contraction • Electrical stimulation (direct electrical stimulation or through a nerve) • Depolarization followed by spreading of action potentials up to –80 to –90 mV over the muscle (via T. tubules) fibers lasting 1 to 5 milliseconds, about 3 times as long as in large myelinated nerves. • The rate of spread is 3 – 5 meters per second. About 1/18 the velocity of conduction in the large myelinated nerve fibers. • Latency period for another couple of milliseconds. Spread of action potentials and release of calcium. • All-or-none contraction and relaxation pf muscle fibers lasting up to several scores of milliseconds consisting of contraction and relaxation phases. During contraction a series of cycles starting with the injection of Ca++ to bind troponin, leading to the reorientation of tropomyosin which facilitates the binding of actin to myosin. The energy from ATP now bends the myosin head, while a phosphate is released. The bending is translated into a sliding motion to contract the muscle fiber. The relaxation phase is the time when ATP breaks up the bridges and Ca++ returns to sarcoplasmic reticulum. • Review Table 10.2 • The amount of tension created by the contracting muscle is related to the number of actin/myosin cross bridges formed. Length-tension diagram, fig 10.19. Twitching muscle fibers • The rate of contraction of muscle varies according to which organ the muscle is found. • The duration of stimulation, contraction and relaxation cycle of muscle fiber for blinking is faster (7.5msec) than that of calf muscle fiber (100msec). • After complete relaxation of muscle fiber, they are capable of repeating another all-or-none process of contraction. • When the muscle fibers are stimulated before complete relaxation, a larger tension will be created. Termed summation. • The fibers will relax in a similar manner. • If the process is repeated, say 10 stimuli per second, the wavy tension will be formed until it reaches an incomplete tetanus. • If the stimulation is given before relaxation occurs, about 100 stimuli per second, the wavy form will disappear and the fibers will reach complete tetanus. • During complete tetanus, next stimulus appears before uncoupling of the bridges and return of Ca++ to sarcoplasmic reticulum. • Complete tetanus is normal behavior of muscle contraction. • The number of excited muscle fibers determines the forces of contraction. – As the muscle fiber undergo complete tetanus, they will exert a certain tension. – The amount of tension created depends on the number of muscle fibers involved and how closely they will contract in synchrony. – In life, muscle fiber are stimulated with neurons and each muscle fiber receives at least one neuron. – Each neuron may, however, stimulates a large number of muscle fibers. – The muscle fibers controlled by a single motor neuron is called a motor unit. – The number of muscle fibers controlled by one motor neuron appears to be related to the precise movement required of the muscles. • Apparently, a smaller number of muscle fibers, which perform more precise movement, appears to be controlled with a single neuron. • To generate a maximum tension slowly, the number of motor units activated will increase slowly- recruitment. • For sustained tetanic contraction of muscle, the motor units may be alternatively activated so that energy can be alternatively supplied to the muscles under each motor unit. • If you happen to see the muscle of a dead person, you will notice something is different from that of an alive person. We call this muscle tone. • The difference come from the fact that for a person who live is alive, even at the resting state of muscle, some motor units are always in activated state. • Stimulation of muscles, ii.e. exercising muscles, will build muscles – hypertrophy. • But, under complete absence of stimulation, muscle will become atrophy. Dying muscle fiber and need for therapy. • Isotonic a isometric contraction • Isotonic contraction: contraction with the same weight, ii.e. rowing a boat or weight lifting. • Isometric contraction: increasing tension under the same length. i.e. press • Concentric and eccentric contractions • The fast and slow muscle fibers – Fast muscle fibers contract in 10 msec or less after stimulation. Muscle fibers large in diameter have many myofibrils. Mostly glycolysis as energy source (anaerobic). They contain less mitochondria with glycogen reserves. Fatigues quickly. – Slow fibers are thinner and slow to contract. Use aerobic metabolism and rich in mitochondria. So called dark meat, since they have myoglobin as oxygen reservoir. Relaxation – Going back to the original length • First the sliding cross bridges must be uncoupled and this process requires ATP. • Ca++ must be removed back into the sarcoplasmic reticulum before the start of next contraction. • But, uncoupling by itself does not initiate elongation of contracted muscles to the original length. • There are at least two ways to bring back the length of the muscles to the original length. – Elastic forces of intracellular organelles and extracellular fibers, tissues, tissue, etc..- relatively slow. – Contraction of the opposing muscles –could be fast. The energetics of muscular activity • ATP performs three important functions during muscle contraction: – The energy released by ATP to ADP and P is used by myosin to cock its head group in position. – ATP must bind to break up the bridge between myosin and actin. – The energy from ATP is necessary for Ca++ pump to reclaim Ca++ back into the sarcoplasmic reticulum. – Large quantity of ATP consumption of an active muscle fiber may reach as large as 600 trillion molecules per second (1n moles) without counting the Ca++ those used for the Ca++ pump. • Quick energy source (ATP) and the reserves (creatine phosphate) – Through steady consumption of ATP continues at resting muscles, the muscles are capable of generating more than this rate of consumption and the excess energy will be transferred to creatine phosphate (CP) for storage and the formation of glycogen. – There are 6 times as much CP than ATP. When active muscles consume ATP, CP will be converted to ATP. But, after 3minutes CP and ATP will be exhausted. – Oxygen Debt – the amount of oxygen needed to restore the resting metabolism after exercise. • Tired muscle fibers – Physiologic contracture and rigor mortis • Insufficient supply of ATP ends up as fatigued muscle fibers – physiologic contracture. • For relatively slow exercise, aerobic metabolism can provide sufficient ATP. • But for rapid exercise, glycolysis provides ATP. Thus if the burst of activity is prolonged, there may be lactic acid formation. • If ATP is completely exhausted, Ca++ may not be accumulated back into sarcoplasmic reticulum. • Rigor mortis occurs after death and is similar to physiologic contracture and is the stiffing of the muscles. • The recovery • The recovery is essentially a wash off of lactic acid. • Physical conditioning • Addition of proteins, but not muscle fibers. – Anaerobic endurance – requires anaerobic metabolism, glycolysis, in fast muscles. Short distance runner, body builder, etc…Hypertrophy muscles. – Aerobic endurance – powered by mitochondria activities for respiration. Use large quantities of ATP in sustained low levels of activities, such as long distance running, etc….. Slow burning process, reason a marathon runner stores up with carbohydrates. Smooth Muscles Structure: • smaller than skeletal muscles, 15-2– um in length and 5-10 in diameter. • Contains a single nucleus and is spindle shaped. • Less amounts of actin and myosin. • Myofilaments contain actin and myosin, but are not ordered and contain no sacromere. • They have non-contractile intermediate filaments. • These filaments attach to dense bodies are scattered throughout the cell and also attach to plasma membrane. • Much less sarcoplasmic reticulum and no T-Tubules. • Instead the areas called caveloae of unknown function are on the membrane. • • • • • • • • Contraction Contraction of smooth muscle cells require Ca++. Slowly picked up Ca++ binds with calmodulin. Activated calmodulin activate myosin kinase, which transfers a phosphate of ATP to the head section of myosin. Phosphate bound myosin binds actin and slow sliding begins. When myosin phosphatase removes the phosphate from the myosin, the bridge is broken very slowly. The whole process could be slow, especially the reaction of phosphatase. The result is slow sustained contraction with relatively low consumption of energy. • Two types of smooth muscles • Visceral (unitary) or multiunit muscle • Visceral muscle is common and appears in sheet form. Found in the digestive, reproductive, and urinary tracts. • Action potential is transmitted from one cell to another leading to wavy contraction of the entire muscle sheet. • Autorhythmic, but some respond to stimulation. • Multiunit smooth muscle also occurs in sheets as the walls of blood vessels, or in bundles of arrector pili and the iris of the eye, etc….. • Electric response of smooth muscle • Relatively low (55 – 60 mV) resting potential. • Responding to slow rhythmic depolarization, the membrane potential fluctuates. • The fluctuating membranes potential propagates and action potentials may be superimposed. • No all-or-none response. • Some smooth muscle cells become the leader in generating electrical potential and contraction. The End.