Muscle Tissue
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| Functions of Skeletal Muscle | 1. Produce skeletal movement 2. Posture & body position 3. Support soft tissue 4. Guard entrances & exits 5. Maintain body temp 6. Store nutrient reserves |
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| Skeletal Muscle Composition: Whole Muscle to Smallest Unit | 1 MUSCLE(surrounded by epimysium) --> Bundles of FASCICLES (interconnected/surrounded by perimysium) --> Muscle FIBERS/Cells (interconnected/surrounded by endomysium) | Each Muscle FIBER surrounded by endomysium (holds myosatellite cells,axons,capillaries) contains sarcoplasm (holds nuclei, mitochondria, and MYOFIBRILS(-->thin&thick MYOFILAMENTS) surrounded by triads (T tubule+2 sarcoplasmic cisternae from SR) |
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| Endomysium | Surrounds individual muscle fibers/muscle cells. Contains capillaries and nerve fibers contacting muscle cells. Contains myosatellite cells (stem cells) that repair damage. |
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| Perimysium | Surrounds muscle fascicles (bundles of muscle fibers). Contains blood vessel and nerve supply to fascicles. |
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| Epimysium | Surrounds entire muscle (sarcoplasm, fascicles, mitochondria, triads, nuclei). Made up of collagen. Separates muscle from surrounding tissue. Connected to deep fascia. |
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| Tendon | At the end of a muscle where collagen fibers in the epimysium, perimysium, & endomysium come together to form a BUNDLE that attach skeletal muscle to bone |
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| Aponeurosis | At end of a muscle where collagen fibers in the epimysium, perimysium, & endomysium come together to form a BROAD SHEET that attaches skeletal muscle to bone |
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| Muscle Formation | Myoblasts (mesodermal muscle germ cells; each with a nucleus) fuse to form muscle fibers (the myoblasts that don’t fuse stick around and are called myosatellite cells) |
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| Characteristices of Muscle Cells | Multinucelate (hundreds of nuclei just internal to the plasma membrane), very long (up to 1ft). |
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| Muscle Repair | Myosatellite cells can enlarge and fuse with damaged muscle fibers |
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| Sarcolemma | Plasma membrane of muscle cells/fibers. Surrounds the sarcoplasm. Changes in transmembrane potential begins contractions. |
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| Sarcoplasm | Cytoplasm of muscle fiber, surrounded by the sarcolemma. |
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| T (Transverse)-Tubules | Narrow tubes. Same properties as sarcolemma. Extend into sarcoplasm at right angles to the cell surface. Action potentials travel down the tubules to initiate muscle contractions, allow entire muscle to contract simultaneously. 1/3 of a triad. |
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| Myofibrils | Lengthwise subdivisions within muscle fiber. Made up of protein filament bundles (myofilaments, thick and thin) which are responsible for muscle contraction. |
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| Triad | Formed by 1 T tubule and 2 terminal cisternae (formed by SR, concentrate Ca2+ via ion pumps and release it into sarcomeres to begin contraction. |
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| Sarcomere | The contractile units of muscle. Repeating functional units of myofilaments. Form visible patterns (striations) within myofibrils of alternating dark, thick filaments (A bands) and light, thin filaments (I bands) at Z line boundaries. | Shortens during contraction |
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| A Bands | Length of thick filaments (dark). Center=M line, thick around m line=H band, and to left and right of h band, made of thick AND thin=Zone of overlap | Always remains constant length. Pulls thin filaments during contraction. |
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| I Bands | Parts with ONLY thin, (light) filaments (no thick) of 2 adjacent sarcomeres. Split through center by Z line. | Shortens during contraction. Regions of exclusively thin filament moves into zone of overlap. |
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| M Line | Connection point of thick filaments in sarcomere, perpendicular to the midpoint of an A band. |
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| H Band | Region on either side of M line in sarcomere containing ONLY thick filaments. | Shortens during contraction. Regions with exclusively thick filament moves into zone of overlap. |
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| Zone of Overlap | Region of overlap between thick and thin filaments in sarcomeres | Gets longer during contraction. At expense of I bands and H bands |
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| Z Lines | Boundaries between adjacent sarcomeres (gives muscle the striated appearance). Surrounded on either side by thin filament of 2 different sarcomeres. | Move closer together during contraction. |
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| Titin | Elastic protein that attaches THICK filaments to Z lines (thin filament sarcomere boundaries) in sarcomere | More coiled, shortened during contraction |
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| Thin Filaments Composed of: | Actin (main), Nebulin, Tropomyosin, Troponin |
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| Actin | (THIN) F Actin (filament) is composed of two rows of 300-400 connected molecules of G Actin (globular) actin molecules. Each G Actin molecule contains an active site that can bind to myosin |
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| Nebulin | (THIN) Runs through middle of F Actin strand, holds it together. Length determines length of f-actin strand. |
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| Tropomyosin | (THIN) Double stranded protein that covers seven active sites on G Actin molecules. Each is bound to one troponin molecule which only moves (exposing active site for myosin heads) if Ca ions attach to troponin. |
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| Troponin | [Thin filament fiber] Contains 3 subunits (C,T,I). When Ca ions bind to its C sub-unit receptor, it changes shape and moves tropomyosin strand off of active sites |
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| Troponin C | Has a receptor that can bind two calcium ions (calcium levels only increase to initiate contraction) |
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| Troponin T | Binds to tropomyosin strands, locking them together as a troponin-tropomyosin complex. |
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| Troponin I | Binds to one G actin molecule, holding the troponin-tropomyosin complex in position (in relaxed state/without Ca ions attached to C sub unit) |
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| Thick Filaments Composed of: | Myosin and Titin |
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| Myosin | (THICK) Contains about 300 myosin molecules. Each has a free head that interacts with actin (forms a cross bridge) and has a tail that is pointed toward M line, bound to other myosin molecules in the thick filament. |
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| Titin | (THICK) Elastic protein that can recoil. It organizes myosin, prevents overstretching, and helps return sarcomere to resting length |
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| During Contraction | 1. Thin filaments slide toward center of each sarcomere alongside thick filaments 2. H zones and I bands get smaller 3. Zones of overlap get larger 4. Z lines move closer together 5. Width of A band remains constant |
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| Myosin Head-ATP | 1.Cocked myosin head bound to ADP&P forms crossbridge w/actin, P released, makes bond stronger...2.Energy stored in the myosin head is used to move it, pulling the actin, releasing the ADP. [energy needed to cock myosin head,like holding a catapult down] | 3. Myosin-actin bond broken when ATP attaches to myosin head.... 4. Myosin head acts as ATPase, hydrolyzes (breaks down) the ATP, and absorbing released energy which cocks it back to move to step 1 (Continues as long as there are Ca ions and ATP) |
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| Neuromuscular Junction (NMJ) | The site where a motor neutron stimulates a muscular fiber. Is a chemical synapse consisting of the points of contact between the axon terminals of a motor neuron and the motor end plate of a skeletal muscle fiber. |
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| Synaptic Terminal | Nerve axon branches and ends here. Contains vesicles filled with acetylcholine (ACh) |
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| Synaptic Cleft | Narrow space between synaptic terminal & sarcolemma. Contains enzyme acetylcholinesterase (AChE) which breaks down ACh |
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| Motor End Plate | Sarcolemmal surface containing ACh receptors that cause influx of Na ions. |
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| Steps that occur during neural stimulation of a muscle fiber | 1. Action potential arrives at the synaptic terminal 2. Voltage gated Ca channels open and calcium ions diffuse into the terminal. 3. Ca entry causes synaptic vesicles to release ACh by exocytosis. | 4.ACh diffuses across a synaptic cleft and binds to ACh receptors which contain ligand gated cation channels. 5. Ligand gated cation channels open. 6. Na ions enter muscle fiber, K ions exit fiber. Causes membrane potential to become less negative. | 7. Once threshold value is reached, action potential propogates along sarcolemma. 8. Ceases when ACh is removed from synaptic cleft by either ACh diffusion away from synapse or if ACh is broken down by ACh-esterase. Some ACh breakdown product is recycled.
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| Excitation-Contraction Coupling...Main Steps | Link between generation of action potential in sarcolemma and start of muscle contraction. Occurs at triads. Action potential travels down t-tubules and triggers Ca++ release from terminal cisternae of the sarcoplasmic reticulum. [Ca ions are responsible] | 1. Action potential travels across entire sarcolemma and is rapidly conducted into the interior of the fiber through t tubules. | 2. T tubules linked with SR (specifically terminal cisternae) by proteins that control Ca release (change shape when potential travels down t tubule, allowing flood of Ca into the sarcoplasm which triggers a contraction throughout the entire fiber
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| Origin | The end of the muscle that is usually fixed |
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| Insertion | The end of the muscle that moves (The fixed end moves the free end) |
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| Rigor Mortis | Fixed muscular contraction after death. Caused when ion pumps stop functioning, No ATP = cross bridges can’t be disconnected, calcium builds up in sarcoplasm. There is a sustained contraction that can last 15-25 hours. |
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| Single Muscle Fiber Tension | Exerted from contraction/shortening of muscle fibers. Amount of tension depends on the number of cross-bridges pulling(directly proportional). | Varies depending on: 1. the fiber’s resting length at time of stimulation (determines degree of overlap betw. thick&thin filaments) 2. The freq. of stimulation (affects the internal conc. of Ca ions, thus amt bound to troponins that expose active sites) |
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| Increased Length/Overstretching of Muscle Fibers | Zone of overlap is too small, thus cross-bridge interaction is reduced or absent. Not enough pulling to |
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| Decreased Resting Length of Muscle Fibers | Stimulated sarcomere cannot shorten very much (producing tension) before the thin filaments extend across the M line and collide w/ or overlap thin filaments on the other side. |
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| Twitch | A single stimulus-contraction-relaxation sequence in a muscle fiber. | Divided into 3 steps: Latent period, contraction phase, and relaxation phase. |
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| Sustained Contraction | Repeated stimulation of a muscle fiber. Can be in style of treppe, wave summation, incomplete tetanus, or complete tenanus. |
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| Treppe | [“Stairs”] When a second stimulus arrives immediately AFTER the relaxation phase has ended, the next contraction will develop SLIGHTLY HIGHER tension (due to increased Ca++ in sarcoplasm-not enough time to be pumped back into SR) Stimulus freq<50 per sec |
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| Wave Summation | When a second stimulus arrives BEFORE the relaxation phase has ended, the second contraction will have HIGHER tension. Stimulus freq>50 per sec |
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| Incomplete Tetanus | When there is increased stimulation frequency, muscle is never allowed to relax completely, so 4x the tension will be produced compared to wave summation. Almost reaches peak tension. |
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| Complete Tetanus | When higher frequency stimulation completely eliminates the relaxation phase, it causes continuous contraction. SR doesnt have time to reclaim the Ca ions, so the high Ca ion concentration prolongs the contraction. Rarely used this way in the body. |
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| Whole Muscle Tension | Depends on the tension produced by the stimulated muscle fibers and the total number of muscle fibers stimulated |
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| Motor Unit | All the muscle fibers (usually around 100) controlled by a single motor neuron |
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| Recruitment | Increasing the number of active motor units to increase the muscular tension produced (Max tension produced when all motor units in the muscle are in a short-lived state of complete tetanus) |
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| During sustained contraction, motor units are activated on a _______ basis | Rotating (asynchronous motor unit summation). Each motor unit can recover somewhat before it is stimulated again. |
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| Isotonic Contraction | ["equal tension"] When tension rises and skeletal muscle's length changes. Can be either concentric or eccentric. [lifting a baby] |
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| Concentric Isotonic Contraction | Muscle tension exceeds the resistance, muscle SHORTENS (picking up something heavy) |
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| Eccentric Isotonic Contraction | Muscle tension does not exceed the resistance, muscle ELONGATES (putting something heavy down slowly) |
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| Isometric Contraction | ["equal measure"] The muscle as a whole does not change length (but individual fibers shorten as connective tissue stretches) and the tension produced never exceeds the load. [holding a baby] |
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| Sarcoplasmic Reticulum (SR) | Membranous strcture surrounding each myofibril (myofilament bundle). Incr rate of action potential to myofibril. Similar structure to smooth ER. Forms chambers (terminal cisternae) attached to T tubules, situated at the zones of overlap for instant effect |
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| Neurotransmitter | A chemical released by a neuron to change the permeability or other properites of another plasma membrane. In skeletal muscle contraction, ACh alters sarcolemma (muscle fiber membrane) permeability, triggering muscle contraction. |
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| Length-Tension Relationship | # of pivoting cross-bridges depends on amt of overlap between thick and thin fibers. Range of optimum overlap produces greatest amt of tension. Normal resting length is 75%-130% of optimal length. |
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| Latent Period | 1. Before contraction, begins at stimulation. Action potential sweeps across sarcolemma and SR releases Ca ions. No tension produced yet. lasts ~2msec. |
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| Contraction Phase | 2. Tension rises to a peak. As tension rises, Ca ions are binding to troponin, moving tropomysin to expose actin active sites, and cross-bridges are forming. Lasts ~15msec |
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| Relaxation Phase | 3. Ca levels are falling, active sites covered by tropomyosin, cross-bridges detach. Tension falls to resting levels. Lasts ~25msec. |
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| ATP | The active energy molecule. A lot is used during sustained muscle contraction. Stored by muscles to start contraction. Must be manufactured by fibers as needed. |
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| Creatine Phosphate (CP) | A small molecule that muscle cells assemble from fragments of amino acids. Is the storage molecule for excess ATP energy in resting muscle. Energy recharges the ADP that is a product of ATP hydrolysis by myosin heads during contraction. | Resting skeletal muscle contains ~ 6x as much of this as ATP, but these energy reserves are exhausted by muscle fibers in about 15 seconds, then the muscle fiber must rely on other mechanisms to generate ATP from ADP. |
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| Creatine Phosphokinase (CPK or CK) | Enzyme that facilitates the reaction of CP recharging ADP to ATP (and make creatine). |
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| Aerobic Metabolism | Mitochondria absorb oxygen, ADP, phosphate ions, and organic substrates (such as pyruvic acid). Provides 95% of the ATP demands of a resting cell. Resting skeletal muscles rely almost exclusively on this form of metabolism of fatty acids to generate ATP. |
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| Glycolysis (Anaerobic Metabolism) | Breakdown of glucose (from glycogen reserves in sarcoplasm) to pyruvic acid in cell cytoplasm. Does not require O2. Provides net gain of 2 ATP and generates 2 pyruvic acid molecules from each glucose. Lactic acid is a byproduct, which causes cramping. |
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| Glycolysis with low energy demands, high oxygen availability | Only important to provide substrates for aerobic metabolism. Generates much less ATP than aerobic metabolism. |
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| Glycolysis with high energy demands, low oxygen availability | Enzymes split glycogen molecules, releasing glucose, which is used to generate more ATP. Important source of energy. |
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| Resting Muscle ATP Source | Fatty acids catabolized (aerobic respiration). The ATP produced is used to build energy reserves of ATP, CP, and glycogen. |
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| Moderately Active Muscle ATP Source | Glucose (anaerobic respiration) and fatty acids (aerobic respiration) are catabolized. The ATP produced is used to power contraction. |
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| Highly Active Muscle ATP Source | Most ATP produced through glycolysis, lactic acid is a byproduct from conversion of built up pyruvic acid (causes cramping). Mitochondrial activity (aerobic respiration) only provides ~1/3 of the ATP consumed. |
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| Muscle Fatigue | When muscles can no longer perform a required activity. |
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| Causes of Muscle Fatigue | -Depletion of metabolic reserves...-Damage to sarcolemma and SR...-Low pH (lactic acid)...-Muscle exhaustion and pain | Normal muscle function requires substantial intracellular energy reserves, a normal circulatory supply, normal blood oxygen levels, and normal blood pH. |
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| Recovery Period | Time required for muscles to return to normal after exertion. Oxygen becomes available. Mitochondrial activity resumes. |
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| The Cori Cycle | The removal and recycling of lactic acid by the liver. Liver converts lactic acid->pyruvic acid. Glucose is released to recharge muscle glycogen reserves. |
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| Oxygen Debt | After exercise or other exertion. The body needs more oxygen than usual to normalize metabolic activities, results in heavy breathing. |
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| Heat Production and Loss | Active muscles produce heat. Up to 70% of muscle energy can be lost as heat, raising body temperature. |
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| Power and Endurance | Power=Max amt of tension produced...Endurance=amount of time an activity can be sustained. Both depend on types of muscle fibers and physical conditioning. |
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| Types of skeletal muscle fibers | Fast, Intermediate, and Slow |
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| Fast Fibers | --Large diameter--produce higher tension/power (b/c are larger, so higher # of myofibrils)--low resistance to fatigue (use more ATP)--White b/c less myoglobin (low O2 reserve), mitochondria, capillaries--more glycolytic enzymes--Anaerobic ATP production-- | ex: in arms |
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| Slow Fibers | --Smaller diameter--produce lower tension/power--high resistance to fatigue--Red b/c Lots of myoglobin (large O2 reserves), mitochondria (ATP production), capillaries (blood supply)--low amt of glycolytic enzymes--Aerobic ATP production-- | ex: in legs |
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| Hypertrophy vs. Atrophy | Hypertrophy=from heavy training. Increase muscle fiber diameter, number of myofibrils, mitochondria & glycogen reserves...Atrophy=from lack of muscle activity. Reduce muscle size, tone, and power. |
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| Structural Characteristics of Cardiac Muscle Tissue/Cardiocytes | Striated. Branched cardiocytes. 1. Small 2. single nucleus 3. Have short, wide T tubules 4. Have SR with NO terminal cisternae 5. No triads (have T tubules, but no terminal cisternae) 5. Aerobic(high in myoglobin, mitochondria) 7.Have intercalated discs |
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| Cardiocyte Nuclei | Typically single, centrally placed. |
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| Cardiocyte T Tubules | Short and broad, no cisternae around them to form triads. Encircle the sarcomeres at the Z lines rather than zones of overlap. |
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| Cardiocyte SR | Lacks terminal cisternae. Contact the plasma membrane as well as the T tubules. |
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| Intercalated Discs | Sites where each cardiocyte is extensively intertwined and bound together by gap junctions and desmosomes to several other cardiocytes. Stabilize structure. Creates direct chemical, electrical, & myofibril connections. Syncs all cells as one giant cell |
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| Functional Characteristics of Cardiac Muscle Tissue | 1. Automaticity (contracts without neural stimulation) with pacemaker cells that determine timing of contractions. 2. Innervation by nervous system can alter pace and adjust tension. | 3. Contractions last ~10x longer than skeletal & have longer refractory period (time between stimuli) and do not readily fatigue. 4. Membranes prevent wave summation and tetanic contractions. Cannot receive additional stimuli until fully relaxed. |
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| Smooth Muscle Tissue | Forms sheets, bundles, or sheaths around other tissues in almost every organ. Found in blood vessels, respiratory passageways, walls of the digestive, reproductive, and urinary tract. | Cells surrounded by CT, but the collagen fibers never unite to form tendons or aponeuroses. |
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| Structural Characteristics of Smooth Muscle Tissue | 1. Long, slender, and spindle shaped. 2. Single, centrally located nucleus. 3. No T tubules and SR forms loose network throughout sarcoplasm. Also lack myofibrils and sarcomeres. Non striated. | 4. Thick filaments scattered throughout sarcoplasm, more myosin heads per thick filament. Myosin organized differently. 5. Thin filaments attached to dense bodies. |
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| Dense Bodies | Structures distributed throughout smooth muscle sarcoplasm in a ntwk of intermediate desmin filaments. Anchor thin filaments such that when sliding occurs between thin and thick filaments, the cell shortens. Transmit contractile signals between cells. |
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| Functional Characteristics of Smooth Muscle Tissue | Differ from other muscle tissue in: 1. Excitation-contraction coupling, 2. length-tension relationships, 3. Control of contractions, and 4. smooth muscle tone. |
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| Smooth Muscle Excitation-Contraction Coupling | Free Ca ions in cytoplasm trigger contraction. Ca ions bind with calmodulin (Ca-binding protein) in the sarcoplasm, activate myosin light-chain kinase (not troponin). Enzyme breaks down ATP, enables myosin head-actin attachment and initiates contraction |
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| Smooth Muscle Length-Tension Relationships | Thick and thin filaments scattered. Resting length unrelated to tension development. Functions over a wide range of lengths (plasticity). Contractions can be just as powerful as skeletal muscles. Can also undergo sustained contractions |
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| Multiunit Smooth Muscle Control of Contractions | smooth muscle cells DIRECTLY connected to motor neuron(s). Occur more slowly than other muscle cells. Located on iris, along portions of male reproductive tract, and arrector pili muscles of the skin (connected to hairs). |
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| Visceral Smooth Muscle Control of Contractions | Smooth muscle cells arranged in sheets or layers of gap-junction-connected cells. NO contact with motor neurons. Rhythmic cycles of activity controlled by pacesetter cells. In walls of digestive tract, gallbladder, urinary bladder & more internal organs. |
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| Smooth Muscle Tone | Normal background level of activity. Graded contraction depends on level of Ca ions and # of cross bridges formed |
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