Muscle Physiology PDF

The Musculoskeletal system physiology The Musculoskeletal system Bones, muscles and joints, cartilage, tendons, ligaments and connective tissue make up the musculoskeletal system. This system gives your body its structure and support and lets you move around. The Skeletal System Bone t...

The Musculoskeletal system physiology The Musculoskeletal system Bones, muscles and joints, cartilage, tendons, ligaments and connective tissue make up the musculoskeletal system. This system gives your body its structure and support and lets you move around. The Skeletal System Bone tissue Bone tissue is continuously growing, remodeling, and repairing itself. Bone remodeling—the building of new bone tissue and breaking down of old bone tissue A bone is an organ made up of several different tissues : bone tissue, cartilage, dense connective tissue, epithelium, adipose tissue, and nervous tissue. The skeletal system functions 1. Support. The skeleton serves as the structural framework for the body 2. Protection. The skeleton protects important internal organs. 3. Assistance in movement. Most skeletal muscles attach to bones; when they contract, they pull on bones to produce movement. 4. Triglyceride storage. Yellow bone marrow consists mainly of adipose cells, which store triglycerides. The skeletal system functions 5. Mineral homeostasis (storage and release). Bone tissue stores minerals (calcium and phosphorus), 6. Blood cell production. Within certain bones, a connective tissue called red bone marrow produces red blood cells, white blood cells, and platelets, a process called hemopoiesis. Bone tissue Bone contains an abundant extracellular matrix that surrounds widely separated cells. The extracellular matrix is about 15% water, 30% collagen fibers, and 55% crystallized mineral salts. Bone’s hardness depends on the crystallized inorganic mineral salts, a bone’s flexibility depends on its collagen fibers which provide tensile strength.  Bone cells Four types of cells are present in bone tissue: 1-Osteoprogenitor cells: are unspecialized bone stem cells derived from mesenchyme. They are the only bone cells to undergo cell division; the resulting cells develop into osteoblasts. 2-Osteoblasts: are bone-building cells. They synthesize and secrete collagen fibers and other organic components needed to build the extracellular matrix of bone tissue, As osteoblasts surround themselves with extracellular matrix, they become trapped in their secretions and become osteocytes 3-Osteocytes: mature bone cells, are the main cells in bone tissue and maintain its daily metabolism, such as the exchange of nutrients and wastes with the blood. 4-Osteoclasts: are huge cells derived from the fusion of as many as 50 monocytes. secrete enzymes and acids that break down both the mineral salts and the collagen fibers of the extracellular matrix of bone (bone resorption). Fracture and Repair of Bone The process by which bone forms is called ossification Bone formation occurs in four principal situations: (1) The initial formation of bones in an embryo and fetus. (2)The growth of bones until their adult sizes are reached (Growth in Length and Thickness) (3) The remodeling of bone (replacement of old bone by new bone tissue throughout life). (4) The repair of fractures (breaks in bones) throughout life. Remodeling of Bone Bone remodeling is the ongoing replacement of old bone tissue by new bone tissue. bone resorption, the removal of minerals and collagen fibers from bone by osteoclasts, and bone deposition, the addition of minerals and collagen fibers to bone by osteoblasts. Factors Affecting Bone Growth and Bone Remodeling 1. Minerals. Large amounts of calcium and phosphorus are needed while bones are growing, as are smaller amounts of magnesium, fluoride, and manganese. 2. Vitamins. Vitamin A stimulates activity of osteoblasts. Vitamin C is needed for synthesis of collagen, the main bone protein. And vitamin D helps build bone by increasing the absorption of calcium from foods in the gastrointestinal tract into the blood. Vitamins K and B12 are also needed for synthesis of bone proteins. 3. Hormones. The hormones most important to bone growth are the A-insulin-like growth factors (IGFs), which are stimulate osteoblasts. B-Sex hormones (estrogens and testosterone) contribute to bone remodeling by slowing resorption of old bone and promoting bone deposition. C-Parathyroid hormone (PTH) secreted by the parathyroid glands. PTH hormone increases blood Ca2+ level. Fracture and Repair of Bone fracture is any break in a bone. Bone heals more rapidly than cartilage because its more blood supply. The repair of a bone fracture involves the following phases: 1-Reactive phase. This phase is an early inflammatory phase. Blood vessels crossing the fracture line are broken. As blood leaks from the torn ends of the vessels, a mass of blood clot forms around the site of the fracture (a fracture hematoma). Usually forms 6 to 8 hours after the injury. Because the circulation of blood stops at the site the fracture nearby bone cells die. Swelling and inflammation occur in response to dead bone cells. Fracture and Repair of Bone 2 Reparative phase: two stages Fibrocartilaginous callus formation followed by Bony callus formation. Fibrocartilaginous callus formation: Blood vessels grow into the fracture hematoma and phagocytes begin to clean up dead bone cells. Fibroblasts invade the fracture site and produce collagen fibers and chondroblasts produce fibrocartilage. These events lead to the development of a fibrocartilaginous (soft) callus, a mass of repair tissue consisting of collagen fibers and cartilage. Fracture and Repair of Bone 2 Reparative phase: Bony callus formation osteoprogenitor cells develop into osteoblasts, which begin to produce spongy bone trabeculae. The trabeculae join living and dead portions of the original bone fragments. In time, the fibrocartilage is converted to spongy bone, and the callus is then referred to as a bony (hard) callus. The bony callus lasts about 3 to 4 months. Fracture and Repair of Bone 3-Bone remodeling phase. The final phase of fracture repair is bone remodeling of the callus. Dead portions of the original fragments of broken bone are gradually resorbed by osteoclasts. Compact bone replaces spongy bone around the periphery of the fracture. Bone’s Role in Calcium Homeostasis Bone is the body’s major calcium reservoir. One way to maintain the level of calcium in the blood is to control the rates of calcium resorption from bone into blood and of calcium deposition from blood into bone. Nerve and muscle cells, Blood clotting and many enzymes require a requires Ca2+ to function properly. changes in Ca2+ concentration may prove fatal. The heart may stop (cardiac arrest) if Ca2+ level goes too high. Breathing may stop (respiratory arrest) if Ca2+ level falls too low. Bone’s Role in Calcium Homeostasis The role of bone in calcium homeostasis is to help “buffer” the blood Ca2+ level, releasing Ca2+ into blood plasma (using osteoclasts) when the level decreases, and absorbing Ca2+ (using osteoblasts) when the level rises. Ca2+ exchange is regulated by hormones, the most important of which is parathyroid hormone (PTH) secreted by the parathyroid glands. PTH hormone increases blood Ca2+ level. PTH increases the number and activity of osteoclasts, which increases bone resorption. The resulting release of Ca2+ from bone into blood. Bone’s Role in Calcium Homeostasis PTH acts on the kidneys to decrease loss of Ca2+ in the urine. PTH stimulates formation of calcitriol (the active form of vitamin D), a hormone that promotes absorption of calcium from foods. The thyroid gland secrete calcitonin (CT). Calcitonin inhibits activity of osteoclasts, speeds blood Ca2+ uptake by bone, and accelerates Ca2+ deposition into bones. The net result is that Calcitonin promotes bone formation and decreases blood Ca2+ level. Exercise and Bone Tissue Bone tissue can alter its strength in response to changes in mechanical stress. When placed under stress, bone tissue becomes stronger through increased deposition of mineral salts and production of collagen fibers by osteoblasts. Bones of athletes, which are repetitively and highly stressed, become notably thicker and stronger than those of astronauts or nonathletes. Aging and Bone Tissue From birth through adolescence, more bone tissue is produced than is lost during bone remodeling. In young adults, the rates of bone deposition and resorption are about the same. In old age, loss of bone through resorption occurs more rapidly than bone gain. the level of sex hormones decreases during middle age, (especially in women after menopause), a decrease in bone mass occurs because bone resorption by osteoclasts outpaces bone deposition by osteoblasts. There are two principal effects of aging on bone tissue: loss of bone mass and brittleness.  Aging and Bone Tissue Loss of bone mass results from demineralization: the loss of calcium and other minerals from bone. The loss usually begins after age 30 in females, accelerates greatly around age 45 as levels of estrogens decrease, and continues until as much as 30% of the calcium in bones is lost by age 70. In males, calcium loss typically does not begin until after age 60. Brittleness results from a decreased rate of protein synthesis. slow collagen fiber synthesis causes the bones to become very brittle and susceptible to fracture. Muscular Tissue physiology Types of Muscular Tissue The three types of muscular tissue—skeletal, cardiac, and smooth About 40 % of the body is skeletal muscle, and perhaps another 10 % is smooth and cardiac muscle. The different types of muscular tissue share some Properties and they differ from one another in their microscopic anatomy and location, and in how they are controlled by the nervous and endocrine systems. Muscular Tissue physiology Properties of Muscular Tissue 1. Electrical excitability, a property of both muscle and nerve cells. Is the ability to respond to certain stimuli by producing electrical signals called action potentials (impulses). 2. Elasticity: is the ability of muscular tissue to return to its original length and shape after contraction or extension. Muscular Tissue physiology 3. Contractility: is the ability of muscular tissue to contract forcefully when stimulated by an action potential. 4. Extensibility is the ability of muscular tissue to stretch, within limits, without being damaged. Normally, smooth muscle is subject to the greatest amount of stretching. Functions of Muscular Tissue 1. Producing body movements. Movements of the whole or parts body such as walking. 2. Stabilizing body positions. Skeletal muscle contractions stabilize joints and help maintain body positions. 3. Storing and moving substances within the body. Storage is accomplished contractions of ringlike bands of smooth muscle called sphincters. Cardiac muscle contractions of the heart pump blood Smooth muscle contractions move food through the gastrointestinal tract Skeletal muscle contractions promote the flow of lymph and aid the return of blood in veins to the heart. Functions of Muscular Tissue 4. Generating heat. As muscular tissue contracts, it produces heat by a process known as thermogenesis. Much of the heat generated by muscle is used to maintain normal body temperature. Involuntary contractions of skeletal muscles, known as shivering, can increase the rate of heat production.  Skeletal muscles Skeletal muscle anatomy Each of your skeletal muscles is a separate organ. Muscle organ consists of Fascicles Fascicles consists of muscle fibres grouped into bundles. Muscle fibers extends the entire length of the muscle and innervated by only one nerve ending, located near the middle of the fiber. muscle fibres =muscle cells Skeletal muscle Skeletal muscle fibers (cells) contains contractile organelles (myofibrils). Each muscle fiber contains several hundred to several thousand myofibrils fuse to form one skeletal muscle fiber. Myofibrils packed with contractile proteins Myosin (Thick and dark bands ) and Actin (thin and light bands) filaments. Myosin and Actin are arranged in overlapping arrangement called sarcomere. Sarcomeres responsible for the striations in muscles Muscle fiber Anatomy of muscle fiber Sarcoplasm: The spaces between the myofibrils ICF. Also present are tremendous numbers of mitochondria. Sarcoplasmic Reticulum: This reticulum has a special organization that is extremely important in controlling muscle contraction (Contain Ca+2 ions). Transverse (T) tubules: Thousands of tiny tunnels from the sarcolemma surface toward the center of each muscle fiber. Because T tubules are open to the outside of the fiber, they are filled with interstitial fluid. Filaments and the Sarcomere Within myofibrils are smaller protein structures called filaments or myofilaments Thin filaments are composed of the protein actin. Thick filaments are composed of the protein myosin. Both thin and thick filaments are directly involved in the contractile process. There are two thin filaments for every thick filament Thin and thick filaments are arranged in compartments called sarcomeres which are the basic functional units of a myofibril. sarcomeres Z discs: separate one sarcomere from the next. sarcomere extends from one Z disc to the next Z disc were actin binds. A band: The darker middle part of the sarcomere which extends the entire length of the thick filaments. Toward each end of the A band is a zone of overlap, where the thick and thin filaments lie side by side. The I band is a lighter, less dense area that contains the rest of the thin filaments but no thick filaments. A narrow H zone in the center of each A band contains thick but not thin filaments. Supporting proteins that hold the thick filaments together at the center of the H zone form the M line. Contraction of Skeletal Muscle Every Muscle fiber is controlled by a motor neuron (nerve cell), that originate from large motoneurons in the anterior horns of the spinal cord. Each nerve fiber normally branches and stimulates from three to several hundred skeletal muscle fibers. Each nerve ending makes a junction with muscle fiber near its midpoint, called the neuromuscular junction. Nerve impulses causes initiating of action potential in muscle fiber via the neuromuscular junction. The action potential initiated in the muscle fiber by the nerve signal travels in both directions toward the muscle fiber ends. The neuromuscular junction (NMJ). A synapse is a region where communication occurs between two neurons, or between a neuron and a target cell (muscle fiber). At most synapses a small gap, called the synaptic cleft , separates the two cells (cells do not physically touch). The action potential cannot “jump the gap” from one cell to another Instead, the first cell communicates with the second by releasing a chemical messenger called a neurotransmitter. At the NMJ, the end of the neuron, called the axon terminal, divides into a cluster of synaptic bulbs. within each synaptic end bulb are several sacs called synaptic vesicles. Inside each synaptic vesicle are thousands of molecules of acetylcholine (Ach) the neurotransmitter released at the NMJ. The neuromuscular junction (NMJ). A nerve impulse (nerve action potential) elicits a muscle action potential in the following way: 1- Release of acetylcholine. The nerve impulse at the synaptic end bulbs stimulates Ca2+ voltage-gated channels to open. Calcium ions are more concentrated in the extracellular fluid, Ca2+ flows inward through the open channels. The entering Ca2+ stimulates the synaptic vesicles to undergo exocytosis liberating ACh into the synaptic cleft. The neuromuscular junction (NMJ). 2- Activation of ACh receptors. Binding of two molecules of ACh to receptor on the sarcolemma opens an ion channel, cations most importantly Na+, can flow across the membrane. 3- Production of muscle action potential. The inflow of Na+ (down its Concentration gradient) makes the inside of the muscle fiber more positively charged. This change in the membrane potential triggers a muscle action potential. The neuromuscular junction (NMJ). 4- Termination of ACh activity. The effect of ACh binding lasts only briefly because ACh is rapidly broken down by an enzyme called acetylcholinesterase. Acetylcholinesterase breaks down ACh into acetyl and choline, products that cannot activate the ACh receptor. EXCITATION-CONTRCTION Each nerve impulse normally elicits one muscle action potential. The muscle action potential then propagates along the sarcolemma into the system of T tubules. This causes the sarcoplasmic reticulum to release its stored Ca2+ into the sarcoplasm, and the muscle fiber subsequently contracts. EXCITATION-CONTRCTION Action potential must move along fiber membrane and must penetrate deeply into the muscle fiber to myofibrils to generate muscle contraction. Action potential pass through transverse tubules (T tubules) that penetrate all the way through the muscle fiber. T tubule action potentials cause release Ca++ from sarcoplasmic reticulum inside the muscle fiber sarcoplasm myofibrils takes up Ca++ to make muscle contraction. EXCITATION-CONTRCTION At the end of contraction, Ca++ pump located in the walls of the sarcoplasmic reticulum pumps Ca++ away from the myofibrils back into the sarcoplasmic tubules Contraction and Relaxation of Skeletal Muscle Fibers The model describing skeletal muscle contraction process is known as the sliding filament mechanism. The Sliding Filament Mechanism: Muscle contraction occurs because myosin heads attach to and “walk” along the thin filaments at both ends of a sarcomere, progressively pulling the thin filaments toward the M line. As a result, the thin filaments slide inward and meet at the center of a sarcomere. Shortening of the sarcomeres causes shortening of the whole muscle fiber, which in turn leads to shortening of the entire muscle Sliding filament mechanism; Relaxed state, the ends of the actin filaments extending from two successive Z discs. Contracted state, these actin filaments have been pulled inward among the myosin filaments, overlap one another. Also Z discs have been pulled to each others. The Sliding Filament Mechanism: Mechanism of Contraction Myosin cross bridges pull on thin filaments Thin filaments slide inward Z Discs come toward each other Sarcomeres shorten. The muscle fiber shortens. The muscle shortens Notice :Thick & thin filaments do not change in length The Proteins of Muscle Myofibrils are built of 3 kinds of protein 1-Contractile proteins: myosin and actin. 2-Regulatory proteins: which turn contraction on & off troponin and tropomyosin. 3-Structural proteins: which provide proper alignment, elasticity and extensibility titin, myomesin (form the M line), nebulin and dystrophin. The Proteins of Muscle - Myosin  The Proteins of Muscle - Actin Thin filaments are made of actin, troponin, & tropomyosin The myosin-binding site on each actin molecule is covered by tropomyosin in relaxed muscle Tropomyosin: Binds to actin and blocks the myosin binding sites on actin. Troponin: The tropomyosin strands in turn are held in place by troponin molecules When calcium ions (Ca2+) bind to troponin, troponin undergoes a conformational change (change in shape); this change moves tropomyosin away The Contraction Cycle At the onset of contraction, the sarcoplasmic reticulum releases calcium ions (Ca2+) into the sarcoplasm. Calcium ions bind to troponin. Troponin then moves tropomyosin away from the myosin- binding sites on actin. Once the binding sites are “free,” the contraction cycle —the repeating sequence of events that causes the filaments to slide—begins.  The Contraction Cycle 1-ATP hydrolysis. a myosin head includes an ATP-binding site that functions as an ATPase—an enzyme that hydrolyzes ATP into ADP and energy. The energy generated from this hydrolysis reaction is stored in the myosin. the myosin head is perpendicular (at a 90° angle) relative to the thick and thin filaments and has the proper orientation to bind to an actin molecule. 2-Attachment of myosin to actin. The energized myosin head attaches to the myosin-binding site on actin and releases the previously hydrolyzed phosphate group. When a myosin head attaches to actin during the contraction cycle, the myosin head is referred to as a cross-bridge.  3-Power stroke. After a cross-bridge forms, the myosin head pivots, changing its position from a 90° angle to a 45° angle relative to the thick and thin filaments. the myosin head changes to its new position, it pulls the thin filament past the thick filament toward the center of the sarcomere. 4-Detachment of myosin from actin. At the end of the power stroke, the cross-bridge remains firmly attached to actin until it binds another molecule of ATP. As ATP binds to the ATP binding site on the myosin head, the myosin head detaches from actin. Muscle Metabolism Muscle uses ATP at a great rate when active (the ATP present inside muscle fibers is enough to power contraction for only a few seconds) Sarcoplasmic ATP only lasts for few seconds 3 sources of ATP production within muscle 1-Creatine phosphate 2-Anaerobic cellular respiration 3-Aerobic cellular respiration Creatine phosphate The use of creatine phosphate for ATP production is unique to muscle fibers While muscle fibers are relaxed, they produce more ATP than they need for resting metabolism. Most of the excess ATP is used to synthesize creatine phosphate. The enzyme creatine kinase (CK) catalyzes the transfer one phosphate groups from ATP to creatine, forming creatine phosphate and ADP. Creatine phosphate Creatine phosphate is three to six times more plentiful than ATP in the sarcoplasm of a relaxed muscle fiber. When contraction begins and the ADP level starts to rise, CK catalyzes the transfer of a phosphate group from creatine phosphate back to ADP generating new ATP molecules. Since the formation of ATP from creatine phosphate occurs very rapidly, creatine phosphate is the first source of energy when muscle contraction begins. Together, stores of creatine phosphate and ATP provide enough energy for muscles to contract maximally for about 15 seconds. Creatine phosphate Anaerobic respiration(Anaerobic Glycolysis) When muscle activity continues the supply of creatine phosphate in the muscle fiber is depleted, glucose is catabolized to generate ATP. Glucose passes easily from the blood into contracting muscle fibers via facilitated diffusion, and it is also produced by the breakdown of glycogen within muscle fibers. Anaerobic Glycolysis Series of reactions known as glycolysis breaks down each glucose molecule into two molecules of pyruvic acid and produces a net gain of two molecules of ATP. During heavy exercise, however, not enough oxygen is available to skeletal muscle fibers. Under these anaerobic conditions, the pyruvic acid generated from glycolysis is converted to lactic acid. Anaerobic Glycolysis Aerobic Respiration (Aerobic Glycolysis) If sufficient oxygen is present, the pyruvic acid formed by glycolysis enters the mitochondria, where it undergoes aerobic respiration, a series of oxygen- requiring reactions (the Krebs and the electron transport chain) that produce ATP, carbon dioxide, water, and heat aerobic respiration is slower than anaerobic glycolysis, it yields much more ATP. Aerobic Respiration (Aerobic Glycolysis) Oxygen sources Muscular tissue has two sources of oxygen: (1) oxygen that diffuses into muscle fibers from the blood (2) oxygen released by myoglobin within muscle fibers. Both myoglobin (found only in muscle cells) and hemoglobin (found only in red blood cells) are oxygen binding proteins. They bind oxygen when it is plentiful and release oxygen when it is needed. Oxygen Consumption after Exercise After muscle contraction has stopped, heavy breathing continues for a while. This extra oxygen is used to “pay back” or restore metabolic conditions to the resting level in three ways: (1) To convert lactic acid back into glycogen stores in the liver. (2) To resynthesize creatine phosphate and ATP in muscle fibers. (3) To replace the oxygen removed from myoglobin. Types of Skeletal Muscle Fibers Based on structure and function, speed of ATP hydrolysis, skeletal muscle fibers are classified as 1- Slow oxidative (SO) fibers. Red in color (lots of mitochondria, myoglobin & blood vessels) prolonged, sustained contractions for maintaining posture and for aerobic, endurance-type activities such as running a marathon. Generate ATP mainly by aerobic respiration Very resistant to fatigue and are capable of prolonged, sustained contractions for many hours. Types of Skeletal Muscle Fibers 2- Oxidative-glycolytic (FOG) fibers. Red in color (lots of mitochondria, myoglobin & blood vessels) The largest fibers with a moderate to high resistance to fatigue. Generate ATP by aerobic and anaerobic glycolysis. Split ATP at very fast rate; used for walking and sprinting. Types of Skeletal Muscle Fibers 3-Fast glycolytic (FG) fibers. White in color (few mitochondria & BV, low myoglobin) Contain large amounts of glycogen and generate ATP mainly by glycolysis very fast. Anaerobic movements for short duration; used for weight-lifting. Types of Skeletal Muscle Fibers The content of muscle fibers in each muscle varies depending on the action of the muscle, the person’s training regimen, and genetic factors. The continually active postural muscles of the neck, back, and legs have a high proportion of SO fibers. Muscles of the shoulders and arms, in contrast, are not constantly active but are used briefly now and then to produce large amounts of tension, such as in lifting and throwing. These muscles have a high proportion of FG fibers. Leg muscles, which not only support the body but are also used for walking and running, have large numbers of both SO and FOG fibers. Exercise and Skeletal Muscle Tissue The total number of skeletal muscle fibers usually does not increase with exercise, the characteristics of those can change. Endurance-type (aerobic) exercises, such as running or swimming, cause a gradual transformation of some FG fibers into FOG fibers. The transformed muscle fibers show slight increases in diameter, number of mitochondria, blood supply, and strength. Endurance exercises also result in cardiovascular and respiratory changes that cause skeletal muscles to receive better supplies of oxygen and nutrients but do not increase muscle mass. Exercise and Skeletal Muscle Tissue Exercises that require great strength for short periods produce an increase in the size and strength of FG fibers. The increase in size is due to increased synthesis of thick and thin filaments. The overall result is muscle enlargement (hypertrophy), as evidenced by the bulging muscles of body builders. Motor Units Even though each skeletal muscle fiber has only a single neuromuscular junction, the axon of a somatic motor neuron branches out and forms neuromuscular junctions with many different muscle fibers. A motor unit consists of a somatic motor neuron plus all of the skeletal muscle fibers it stimulates A single somatic motor neuron makes contact with an average of 150 skeletal muscle fibers, and all of the muscle fibers in one motor unit contract in unison. Typically, the muscle fibers of a motor unit are dispersed throughout a muscle rather than clustered together. Isotonic and Isometric Contractions Muscle contractions may be either isotonic or isometric. In an isotonic contraction the tension (force of contraction) developed in the muscle remains almost constant while the muscle changes its length. Isotonic contractions are used for body movements and for moving objects. The two types of isotonic contractions are concentric and eccentric. In a concentric isotonic contraction, the muscle shortens and pulls on another structure, such as a tendon, to produce movement and to reduce the angle at a joint. (Picking up a book from a table)  When the length of a muscle increases during a contraction, the contraction is an eccentric isotonic contraction.( you lower the book to place it back on the table). In an isometric contraction: the muscle does not change its length. An example would be holding a book steady using an outstretched arm. Smooth Muscle physiology Excitation and Contraction of Smooth Muscle Smooth Muscle is composed of smaller fibers than skeletal muscles Some principles of contraction are similar in both smooth muscle as to skeletal muscle; like attractive forces between myosin and actin, but the internal physical arrangement of smooth muscle fibers is different.  Smooth muscle tissue is usually activated involuntarily. Two types of smooth muscle tissue: 1-Visceral (single-unit) smooth muscle tissue (more common ). 2- Multi-unit smooth muscle tissue. 1-Visceral (single-unit) smooth It is a mass of thousands of smooth muscle fibers that contract together as a single unit. The fibers usually are arranged in sheets or bundles. cell membranes are adherent to one another at multiple points (by gap junctions) so that force generated in one muscle fiber can be transmitted to the next. When a neurotransmitter, hormone, or autorhythmic signal stimulates one fiber, the muscle action potential is transmitted to neighboring fibers, which then contract in unison, as a single unit. Multi-Unit Smooth Muscle. Separated smooth muscle fibers. Each fiber is innervated by a single nerve ending, examples of multi-unit smooth muscle are the ciliary muscle of the eye. Consists of individual fibers, each with its own motor neuron terminals. Stimulation of one visceral muscle fiber causes contraction of many adjacent fibers, but stimulation of one multi-unit fiber causes contraction of that fiber only. Main differences between skeletal muscles and smooth muscles Main differences between skeletal muscles and smooth muscles Smooth muscle contains both actin and myosin filaments. Contractile process is activated by Ca, and ATP. There are differences between smooth/ skeletal muscles, in: 1-Contraction in a smooth muscle fiber starts more slowly and lasts much longer than skeletal muscle fiber contraction. Main differences between skeletal muscles and smooth muscles Sarcoplasmic reticulum is found in small amounts in smooth muscle. Calcium ions flow into smooth muscle sarcoplasm from both the interstitial fluid and sarcoplasmic reticulum. There are no transverse tubules in smooth muscle fibers (there are caveolae instead), it takes longer for Ca2+ to reach the filaments in the center of the fiber and trigger the contractile process. Main differences between skeletal muscles and smooth muscles 2-Smooth muscle can both shorten and stretch to a greater extent than the other muscle types. 3- lower Amount of ATP required for contraction. 4-Vesicles of skeletal muscle junctions, contain acetylcholine, While here the autonomic nerve fiber endings contain acetylcholine in some fibers and norepinephrine in another, (both are excitatory or inhibitory depends on receptors ). Main differences between skeletal muscles and smooth muscles 5- Do not contain troponin like in skeletal muscles, instead contain regulatory protein called calmodulin binds to Ca2+ in the sarcoplasm and activates an enzyme called myosin light chain kinase. This enzyme uses ATP to add a phosphate group to a portion of the myosin head. Once the phosphate group is attached, the myosin head can bind to actin, and contraction can occur. Because myosin light chain kinase works rather slowly, it contributes to the slowness of smooth muscle contraction. Main differences between skeletal muscles and smooth muscles have not striated arrangement of actin /myosin as is found in skeletal muscle. Instead, large numbers of actin filaments attached to dense bodies. These bodies are attached to the cell membrane or dispersed inside the cell. large numbers of actin filaments radiating from two dense bodies; the ends of these filaments overlap a myosin filament located midway between the dense bodies.  Action Potentials with Plateaus The smooth muscle cell membrane has far more voltage-gated Ca-channels and few voltage-gated Na channels Therefore, Na participates little in the generation of the AP in smooth muscle. Instead, flow of Ca++ to the interior is mainly responsible for the AP. Also, Ca-channels open more slowly than Na-channels, and remain open much longer >>> prolonged plateau. Also, Inflow of these Ca act directly on the smooth muscle contractile mechanism to cause contraction. Stress-Relaxation of Smooth Muscle. An important characteristic of smooth muscle, especially in visceral hollow organs; allow a hollow organ to maintain about the same amount of pressure inside its lumen despite long-term, large changes in volume. For example, a sudden increase in fluid volume in the urinary bladder >>> stretching the smooth muscle in the bladder wall >>> increase in pressure in the bladder. SO by stress – relaxation of smooth muscles after 15 sec to 1 min, the pressure returns back to the original level. Cardiac Muscle physiology Cardiac Muscle physiology Cardiac muscle fibers have the same arrangement of actin and myosin and the same bands, zones, and Z discs as skeletal muscle fibers. However, intercalated discs are unique to cardiac muscle fibers. These microscopic structures are irregular transverse thickenings of the sarcolemma that connect the ends of cardiac muscle fibers to one another. The discs contain desmosomes, which hold the fibers together, and gap junctions, which allow muscle action potentials to spread from one cardiac muscle fiber to another. Cardiac Muscle physiology In response to a single action potential, cardiac muscle tissue remains contracted 10 to 15 times longer than skeletal muscle tissue The long contraction is due to prolonged delivery of Ca2+ into the sarcoplasm. In cardiac muscle fibers, Ca2+ enters the sarcoplasm both from the sarcoplasmic reticulum (as in skeletal muscle fibers) and from the interstitial fluid that bathes the fibers. Because the channels that allow inflow of Ca2+ from interstitial fluid stay open for a relatively long time, a cardiac muscle contraction lasts much longer than a skeletal muscle contraction. Cardiac Muscle physiology cardiac muscle tissue contracts when stimulated by its own autorhythmic muscle fibers. Under normal resting conditions, cardiac muscle tissue contracts and relaxes about 75 times a minute. (Heart rate) The mitochondria in cardiac muscle fibers are larger and more numerous than in skeletal muscle fibers. This structural feature correctly suggests that cardiac muscle depends largely on aerobic respiration to generate ATP, and thus requires a constant supply of oxygen. Like skeletal muscle, cardiac muscle fibers can undergo hypertrophy in response to an increased workload. This is called a physiological enlarged heart and it is why many athletes have enlarged hearts.  Heart cells Cardiac muscle cells are autorhythmic cells (10%) and contractile cells (90%). Because autorhythmic cells are self-excitable. They repeatedly generate spontaneous action potentials (pacemaker potential) that then trigger heart contractions. Cardiac Muscle as a Syncytium The heart is composed of two syncytiums: 1- Atrial syncytium: two atria. 2- Ventricular syncytium: two ventricles. The atria are separated from the ventricles by fibrous tissue. A.P are not conducted from the atrial syncytium into the ventricular syncytium directly through this fibrous tissue. only by way of a specialized conductive system called the A-V bundle. Action Potentials in Cardiac Muscle The resting membrane potential of a normal cardiac muscle fiber is −85 to −95 mV The action potential recorded from a single cardiac muscle fiber is unusually long and can be divided into five distinct phases: Phase 0: Rapid depolarization. Phase 1: Initial rapid repolarization. Phase 2: Plateau. Phase 3: Repolarization. Phase 4: Resting potential. Phase 0: Rapid depolarization In mammalian heart, depolarization lasts about 2 ms. In this phase, amplitude of potential reaches up to +20 to +30 mV The initial rapid depolarization are due to the rapid opening of voltage-gated Na+ channels and rapid influx of Na+ ions similar to that occurring in the nerve and the skeletal muscle. At −30 to −40 mV membrane potential the calcium channels also open up and influx of Ca2+ ions also contributes in this phase. Phase 1: Initial rapid repolarization Rapid depolarization is followed by a very short-lived slight rapid repolarization The membrane potential reaches from +30 mV to −10 mV during this phase. The initial rapid repolarization is due to closure of Na+ channels and opening of K+ channels. Phase 2: Plateau During plateau phase the cardiac muscle fiber remains in the depolarized state. The membrane potential falls very slowly only to −40 mV during this phase. This plateau in action potential explains the 5–15 times longer contraction time of the cardiac muscle as compared to skeletal muscle. Phase 2: Plateau Very slow repolarization during the plateau phase is due to: 1-Slow influx of Ca2+ ions resulting from opening of sarcoplasmic Ca2+ channels. 2-Closure of a distinct set of K+ channels. Phase 3: Repolarization During this phase, complete repolarization occurs and the membrane potential falls to the approximate resting value. The slow repolarization results from the Ca2+ channels closing and opening of K+ channels: Phase 4: Resting potential. In this phase of resting membrane potential (also called as polarised state), the potential is maintained at −90 mV The resting membrane potential is maintained by a resting K+ levels. The resting ionic composition is restored by Na+−K+ ATPase pump. Action Potentials in Cardiac Muscle Refractory Period of Cardiac Muscle. Refractory period refers to the period following action potential during which the cardiac muscle does not respond to a stimulus. Since the heart has to function as a pump, it must relax, get filled up with blood and then contract to pump out the blood. Cardiac muscle has a long refractory period. It is of two types: Refractory Period of Cardiac Muscle. 1. Absolute refractory period (ARP). During this period, the cardiac muscle does not show any response at all. It extends from phase 0 to half of phase 3 of action potential, 2. Relative refractory period. During this period, the muscle shows response if the strength of stimulus is increased to maximum. It extends from second half of the phase 3 to phase 4 of the action potential.  Thank you