Chapter 10 Muscular - Summary of notes which follows the course outline. PDF

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Summary of notes which follows the course outline. ...

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Chapter 10: Muscular Tissue

10.1 Overview of Muscular Tissue Types of Muscular Tissue 1. Skeletal Muscle Tissue    

Move the bones of the skeleton. Striated: Alternating light and dark protein bands. Voluntary: Activity is controlled consciously by neurons which are part of the somatic (voluntary) division of the nervous system. Most are also controlled subconsciously such as diaphragm (breathing) and muscles for posture.

2. Cardiac Muscle Tissue    

Forms the heart walls. Striated: Also striated. Involuntary: Controlled unconsciously like heart contraction. Autorhytmicity: natural peacemaker that initiates each contraction. Hormones and neurotransmitters control the speed.

3. Smooth Muscle Tissue    

Located in hollow internal structures such as blood vessels, airways, organs in abdominopelvic cavity, skin attached to hair follicles. Nonstriated: lacks striations and appears smooth. Involuntary: smoot muscles in gastrointestinal tract propel food and has autoarythmicity. Both Cardiac and Smooth Muscles are controlled by neurons of the autonomic (involuntary) division of the nervous system, which are controlled by hormones of the endocrine glands.

Functions of Muscular Tissue 1. Producing Body Movements 

Movements of whole body rely on integrated functions of skeletal muscles, bones, and joints.

2. Stabilizing Body Positions  

Skeletal muscle contractions stabilize joints and maintain posture. Postural muscles contract continuously i.e. holding neck, posture, etc.

3. Storing and moving substances within the body  

Accomplished by sustained contractions of sphincters (ring-like smooth muscles) to prevent outflow of contents in a hollow organ. Contractions help keep urine in bladder, move blood, move food and bile.

4. Generating Heat 1

 

Contraction of muscles produce heat (thermogenesis). Shivering is the involuntary movement of skeletal muscles to produce heat.

Properties of Muscular Tissue 1. Electrical Excitability  

Ability to respond to action potentials by producing electrical signals (action potential – impulses). Muscle Action Potentials. Two stimuli: o Autorhythmic electrical signals from muscle tissues o Chemical stimuli from neurotransmitters and hormones

2. Contractility  

Ability to contract forcefully when stimulated by action potentials. Contraction generates tension (force of contraction), but does not shorten.

3. Extensibility   

Ability to stretch within limits without being damaged. Connective tissue limits the range. Smooth muscles experience the most extensibility i.e. stomach filling with food, cardiac muscle filling with blood.

4. Elasticity 

Ability of muscular tissue to return to original length after contraction or extension.

10.2 Skeletal Muscle Tissue 

Skeletal muscle contains cells called Muscle Fibers, which are elongated. Muscle cells/fibers are the same term.

Connective Tissue Components 

Surrounds and protects muscular tissue.

1. Subcutaneous Layer (Hypodermis)    

Separates muscles from skin Composed of areolar connective tissue and adipose tissue. Provides pathways for nerves, blood vessels, lymphatic vessels to enter/exit muscles. Adipose tissue stores fat, insulation to reduce heat loss, protects muscle from physical trauma.

2. Fascia  

Dense sheet or broad band of irregular connective tissue. Lines the body walls, limbs, and supports/surrounds muscles and other organs of body.

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 

Holds muscles of similar functions together; allows free movement of muscles; carries nerves, blood vessels, and lymphatic vessels; fills spaces between muscles. Three layers: i. Epimysium  Outer layer encircling entire muscle.  Dense irregular connective tissue. ii. Perimysium  Surrounds groups of 10 to 100 muscles, into bundles called Fascicles. The fiber of “grain” of the meat.  Dense irregular connective tissue. iii. Endomysium  Penetrates interior of fascicles and separates individual muscle fibers.  Reticular fibers.

3. Tendon  

Epimysium, perimysium, or endomysium (connective tissue elements) extending beyond muscle fibers. Attaches muscles to periosteum of bone.

4. Aponeurosis 

Extension of connective tissue elements that form broad, flat sheets.

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Nerve and Blood Supply   

Well supplied with nerves and blood vessels. An artery and one or two veins accompany nerves in the skeletal muscles. Capillaries (microscopic blood vessels) are plentiful in muscle tissues. Bring in oxygen and nutrients and take out heat and waste.

Somatic Motor Neurons   

Neurons which stimulate skeletal muscle contraction. Contains threadlike axon extending from brain/spinal cord to a group of skeletal muscles. Many branches in muscles.

Microscopic Anatomy of a Skeletal Muscle Fiber Sarcolemma, Transverse Tubules, and Sarcoplasm 1. Sarcolemma  Plasma membrane of muscle cells; underneath, multiple nuclei of skeletal muscles are found. 2. Transverse (T) Tubules  Tiny invaginations of sarcolemma, tunnel from surface to center of each muscle fiber.  Filled with interstitial fluid.  Muscle action potential travels through sarcolemma and T tubules; spreads quickly through muscle fibers. 3. Sarcoplasm  Cytoplasm of muscle fibers.  Contains substantial amount of glycogen for ATP synthesis.  Contains red-colored protein, Myoglobin. o Found only in muscles; binds oxygen molecules from interstitial fluid. o Releases oxygen when needed for ATP production. Myofibrils and Sarcoplasmic Reticulum 1. Myofibrils  White treads, which are contractile organelles of skeletal muscles.  2 µm in diameter, extending the entire length of muscle fibers. 2. Sarcoplasmic Reticulum (SR)  Encircles each myofibril and similar to smooth endoplasmic reticulum.  Terminal Cisterns are dilated end sacs of sarcoplasmic reticulum. o Touches T tubules; Transverse tubules and two terminal cisterns form a triad.  Stores calcium ions (relaxed state).  Release of calcium ions from terminal cisterns trigger muscle contraction.

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Muscular Hypertrophy, Fibrosis, and Atrophy 1. Muscular Hypertrophy  Growth after birth occurs by enlargement of muscle cells.  Due to increased production of myofibrils, mitochondria, sarcoplasmic reticulum, and other organelles.  Results from forceful, repetitive muscular activity.  Testosterone promotes enlargement of muscle fibers. 2. Fibrosis  When not enough muscle fibers are formed to compensate for skeletal muscle damage/degeneration, muscular tissue undergoes fibrosis.  Replacement of muscle fibers with fibrous scar tissue. 3. Muscular Atrophy  Decrease in size of muscle fibers due to a loss in myofibrils.  Occurs when muscles are not used, such as in bedridden patients.

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Filaments and the Sarcomere 1. Filaments (myofilaments)  Smaller protein structures in myofibrils.  Thin Filaments o 8 nm in diameter and 1 – 2 µm long. o Composed of the protein actin.  Thick Filaments o 16 nm in diameter and 1 – 2 µm long.  Both are directly involved in contractile process.  Ratio: Two thin filaments for every thick filament. 2. Sarcomeres  Filaments arranged in compartments; basic unit of myofibrils. i. Z discs o Separate one sarcomere from the next. o Plate-shaped regions of dense protein material. o Sarcomeres extend from one z disc to another. ii. A Band o Darker middle part of sarcomere and extends the entire length of thick filament. o Each end of A Band is a zone overlap, where thick and thin filament lie side by side. iii. I Band (thin) o Lighter, less dense o Contains thin filaments, no thick. Z disc passes through the center of I band. 6

iv. v.

H Zone (thick) o Center of A band, with thick filaments. M Line o Support the proteins holding thick filaments in the H zone. o In the middle of sarcomere, thus M.

Muscle Proteins 

Myofibrils are made from 3 kinds of proteins: o (1) Contractile protein – generates contraction force. o (2) Regulatory protein – switches contraction on and off. o (3) Structural protein – keeps thick/thin filaments in alignment, gives myofibrils elasticity and extensibility, link myofibrils to sarcolemma and extra cellular matrix.

Contractile Proteins

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

Myosin and actin are the main contractile proteins.

1. Myosin is the main component of thick filaments, functions as motor proteins in all 3 types of muscle tissue. Shaped like two golf clubs twisted together. o o o

Motor Proteins Achieve movement by conversion of ATP to mechanical energy. Myosin Tails point towards M line (center of sarcomere). Tails of neighbouring myosin are parallel to each other forming shaft of thick filament. Myosin Heads project outward from tail in a spiraling fashion, which extends towards one of six thin filaments that surround thick filament.

2. Actin main components of thin filaments, which is twisted into a helix. o

Each actin molecule contains myosin-binding site, where a myosin head can attach.

Regulatory Proteins 1. Tropomyosin 

In relaxed muscles, tropomyosin blocks the myosin binding sites of actin.

2. Troponin  

Holds tropomyosin strands. Binds Ca2+

Structural Proteins 1. Titin     

Third most abundant protein in skeletal muscles (after actin and myosin). Huge mass (~50x larger than average protein), extends from Z disc to M line. Connects Z disc to M line, stabilizing position of thick filament. Elastic molecule; extensible and elastic. Titin helps return sarcomere in original position after being stretched. Prevents over extension, and maintains central location of A bands.

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10.3 Contraction and Relaxation of Skeletal Muscle Fibers Sliding Filament Mechanism     

Skeletal muscle shortens during contraction due to thick and thin filaments sliding past one another. Myosin heads walk along thin filaments at both end of sarcomere, pulling thin filaments towards the M line. As thin filaments slide towards the middle, I band and H zone become narrow and eventually disappear. Width of A band and individual thick and thin filaments remain unchanged. Z-discs come close together, shortening the whole muscle.

Contraction Cycle 1. ATP Hydrolysis o Hydrolysis of ATP into ADP + phosphate group reorients and energizes myosin head. o ADP + Phosphate group is still attached to the myosin head. 2. Attachment of myosin to actin to form cross-bridges 9

Energized myosin attaches to myosin-binding site on actin, and the phosphate is released. o When a myosin attaches to an actin, it is called cross-bridges. 3. Power Stroke o During power stroke, cross-bridge holding the ADP opens and releases the ADP. o Rotation of cross-bridge towards the center of sarcomere creates force, which slides the thin filaments towards the M line. 4. Detachment of myosin from actin o As another ATP binds to the ATP-binding site on the myosin head, myosin detaches from actin. o

Excitation-Contraction Coupling 1. Ca2+ Release Channels o Muscle action potentials causes Calcium Release Channels in the sarcoplasmic reticulum (SR) membrane to open. o Ca2+ is released into sarcoplasm and around thick/thin filaments. o Released calcium with troponin causing a shape change. o Shape change causes tropomyosin to move away from myosin-binding site on actin. o This allows myosin to attach and form a cross-bridge, starting the cycle. o This event can be referred to as excitation-contraction coupling. 2. Ca2+ Active Transport Pumps o SR contains membranes which uses ATP to move Ca2+ from sarcoplasm into SR. o Ca2+ flow into the sarcoplasm faster than they come out. o After last action potential through T tubules, the Ca2+ channels close. 10

o o o

Calcium in sarcoplasm decreases; In SR, calcium-binding proteins (calsequestrin) bind to Ca2+, enabling more to be stored. Ca2+ is 10,000 times higher in the SR than in cytosol of a relaxed muscle fiber. Drop in Ca2+ in the cytosol, causes tropomyosin to attach to actin, thus relaxing muscle.

Length-Tension Relationship 

  

Length-Tension Relationship indicates how forcefulness of muscle contraction depends on the length of sarcomere within a muscle before contraction begins. o Sarcomere length of 2.0 – 2.4 µm develops maximum tension. o Maximum tension occurs when overlap of thin and thick filament extends from edge of H zone to one end of the thick filament. As the zone of overlap shortens, fewer myosin heads can make contact with thin filaments, thus a decreased tension. If a sarcomere is stretched, no overlap, no myosin can bind to thin filaments thus no contraction. If a sarcomere is compressed, thick filaments crumple, decreasing the tension that can be developed.

Neuromuscular Junction 11

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Muscle action potential arise in the Neuromuscular Junction (NMJ), the synapse between somatic neuron and skeletal muscle fiber.

1. Somatic Neurons   

Neurons that stimulate skeletal muscles to contract. Has threadlike axon extending from brain/spinal cord to a group of skeletal muscle fibers. Muscle fiber contracts in response to action potentials propagating along sarcolemma and T tubules.

2. Synapse 

Region where communication occurs between two neurons, neuron and a target cell, in this case somatic motor neuron and muscle fiber.

3. Synaptic Clef  

Small gap in the synapses, separating two cells. Action potentials jump the gap from one cell to another, by the release of chemical messengers called neurotransmitters.

4. Axon Terminal  

The end of a motor neuron. This divides into clusters of synaptic end bulbs which is the neural part of the NMJ.

5. Synaptic Vesicles 

Each synaptic bulb contains hundreds of synaptic vesicles containing acetylcholine (ACh).

6. Acetylcholine (ACh) 

Stored in synaptic vesicles, which releases neurotransmitters into the NMJ.

7. Motor End Plate  

Region of sarcolemma opposite to synaptic end bulbs. It is the muscle fiber part of the NMJ, which contains acetylcholine receptors.

8. Acetylcholine Receptors  

Transmembrane proteins to which acetylcholine (ACh) specifically binds. Abundant in the Junctional Folds, which are deep grooves in the motor plate which provides large surface area for ACh.

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Muscle Action Potential 1. Release of Acetylcholine o Nerve impulse at synaptic end bulbs stimulates opening of channels. o Ca2+ concentration higher in the extracellular fluid, thus flows in the channels. o Ca2+ causes exocytosis of synaptic vesicles releasing ACh into the synaptic cleft. o ACh diffuses between motor neuron and motor end plate. 2. Activation of ACh Receptors o Attachment of two ACh molecules in the motor end plate opens ion channels in ACh receptors. o Small cations, such as Na+, flow across the membrane. 3. Production of Muscle Action Potential o Inflow of Na+ (down electrochemical gradient), causes the inside of muscle fiber to be more +. o Change in membrane potential triggers muscle potential. o Muscle potential propagates along sarcolemma into T tubules. o Sarcoplasmic Reticulum releases stored Ca2+ causing muscle fibers to contract. 4. Termination of ACh Activity o Effect of ACh is rapid as it is quickly broken down by acetylcholinesterase (AChE). o AChE is found in the collagen fibers in extracellular matrix of synaptic cleft. o ACh is broken down into acetyl and choline.

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10.4 Muscle Metabolism Production of ATP in Muscle Fibers Three ways to produce ATP: 1. From creatine phosphate 2. Anaerobic glycolysis 3. Aerobic respiration

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