Muscle Exam 6 Flashcards
What is the difference between voluntary and involuntary muscle movement
Voluntary -> consciously controlled activity (somatic nervous system)
Involuntary -> subject to subconscious control (diaphragm)
What is smooth muscle tissue
-Non-striated muscle tissue
-Located in the walls of hollow organs and tubes (blood vessels, airways)
-Usually involuntary
-Regulated by autonomic nervous system
What is cardiac muscle tissue
Striated muscle tissue
-Found in only walls of heart
-Involuntary -> contraction & relaxation aren’t consciously controlled
Regulated by ANS
What is skeletal muscle tissue
Usually attached to bones
Under conscious control
Somatic Nervous System
Striated muscle
Functions of muscle tissue: production of movement, stabilization of body positions, and generating heat
Production of movement: walk/running and localized movement
Stabilization of body positions: posture
Generating heat: contracting muscle produces heat -> shivering to warm up
How does the muscle tissue store and move substances within the body
Storage via contractions of sphincters (smooth muscle)
Heart muscle pumping blood (striated muscle)
Moving substances in the digestive tract (smooth muscle)
Moving blood back to the heart (venous return)
Productions of Muscular tissue: excitability and contractility
Excitability:
Ability to respond to stimuli -> production of action potential
-Chemical stimuli -> NT release (skeletal and smooth muscle)
-Autorhythmic signals -> cardiac muscle
Contractility:
Ability to contract forcefully when stimulated
Productions of muscular tissue: extensibility and elasticity
Extensibility:
Ability to stretch without being damaged (smooth muscle and cardiac muscle)
Elasticity:
Ability to return to its original length and shape after contraction or extension
Skeletal Muscle
Organ made up of fascicles
Fascicles contain muscle fibers (cells) nerves, blood vessels, wrapped in epimysium
Muscle attaches to the bone by tendon
Muscle Fiber: T-tubule and sarcoplasmic reticulum
T-tubule:
Invagination of the plasma membrane -> muscle action potentials travel through the T tubules
Sarcoplasmic reticulum:
Storage of calcium
Ca2+ release -> muscle contraction
Encircle each myofibril
Muscle Fiber: Sarcoplasm and Myofibrils
Sarcoplasm:
Cytoplasm, glycogen, myoglobin, mitochondria
Myofibrils:
Are the contractile organelle in skeletal muscle
What is the sarcolemma
The plasma membrane of the muscle cell/muscle fiber
What is the epimysium, perimysium, and endomysium in connective tissue components of the muscle
Epimysium: surrounds the whole muscle
Perimysium: surround bundles of muscle cells
Endomysium: separates individual muscle cells
*all form the tendon
Organization of myofibril
Striated pattern results from arrangement of cytosolic proteins organized into two types of filaments (thick and thin)
Filaments arranged in cylindrical bundles called myofibrils
Thin (actin) Thick (myosin) filaments arranged in units called sacromeres
Myofibril Proteins: Contractile, regulatory, structural
Contractile: generate force during contraction -> myosin and actin
Regulatory: switch contraction processes on and off -> tropomyosin and troponin
Structural: align thick and thin filaments properly, provide elasticity and extensibility, link myofibrils to sarcolemma
Contractile Protein: Myosin
-Forms thick filaments
-Motor proteins in all muscle types
-Two heavy chains forming a tail
-Two globular heads extend out to the sides, forming cross-bridges (head is ATPase and has actin binding sites)
Contractile Protein: Actin
-Form thin filaments
-Monomeric proteins known as globular actin (G-actin)
-Active sites that bind the head to myosin molecule (regulatory proteins troponin and tropomyosin bind actin)
Tropomyosin and Troponin in Actin
Tropomyosin:
binds actin, covers myosin-binding sites on actin
Troponin:
bind tropomyosin
Three subunits, (TN-C ca2+ bind, TN-I actin bind, TN-T bind tropomyosin)
What does tropomyosin and troponin do with intracellular Ca2+
Increase intracellular Ca2+ -> troponin binds Ca2+ causing tropomyosin to uncover myosin binding sites allowing muscle contraction
Decrease intracellular Ca2+ -> Ca2+ dissociates from troponin
Structural Proteins: Nebulin, titin, myomesin
Nebulin: helps align actin
Titin: stabilizes position of myosin and thick filaments
Myomesin: binds titin connecting thick filaments in M line
Structural Proteins: alpha-actinin and dystrophin
Alpha-actinin: make Z disc, binds actin and titin
Dystrophin: links thin filaments to membrane proteins
Sliding filament model of muscle contraction
When sarcomeres shorten, thick and thin filaments slide past one another
Z lines move closer together
Contraction cycle steps 1 and 2
ATP hydrolysis:
-Myosin ATPase enzyme in myosin head hydrolyzes an ATP molecule
-Hydrolysis of ATP reorients and energizes myosin head
Formation of cross-bridges:
-Myosin head attaches to the myosin-binding site on actin
Contraction cycle steps 3 and 4
Power stroke:
-Rotation of myosin head pulls thin filament toward center of sarcomere
-Myosin head releases ADP and Pi, head remains attached to actin
Detachment of myosin from actin:
-As the next ATP binds to the myosin head, the myosin head detaches from actin
-The contraction cycle repeats as long as ATP is available and the Ca2+ level is sufficiently high
Excitaition-Contraction Coupling
Action Potential spreads down into T tubule -> open volt gated Ca2+ channels in sarcolemma and T tubule
Increase Ca2+ activates Ryanodine Receptors in sarcoplasmic reticulum in cells -> increase Ca2+
Ca2+ binds to troponin in thin filaments and moves tropomyosin away, so actin and myosin bind allowing power stroke
Neuromuscular Junction
-Skeletal muscle never contracts unless stimulated by a nerve
-Neuromuscular junction chemical synapse formed between motor neuron and a muscle fiber
-Somatic motor neurons
—Nerve cells, whose cell bodies are in the brainstem and spine innervate skeletal muscle
—Nerve fiber branches out to a number of muscle fibers
Tiggering Muscle Contraction
Activate somatic neuron -> depolarize and increase Ca2+, release ACh from neuron
ACh activates nicotinic receptors (Na+ channels) on muscle cells -> depolarization of end plate
Depolarization of end plate activates Ca2+ channels increasing intracellular Ca2+ channels
Ca2+ used for muscle contraction
Sources of Calcium
Propagation of muscle action potential activates voltage-gated Ca2+ channels
Increase intracellular Ca2+ activates release of more Ca2+ from sacroplasmic reticulum
Increase in intracellular Ca2+ triggers muscle contraction
Troponin/Tropomyosin
Myosin binding site on actin gets exposed
Myosin binds to actin -> muscle contraction
Sarcolemma and Calcium
Sarcolemma contains voltage-gated Ca2+ channels or L-type Ca2+ channels
-Activated by depolarization
-Responsible for entry of extracellular Ca2+ into cytosol of muscle cells
Sarcoplasmic Reticulum and Calcium
SR contains ryanodine receptors (RyR)
-RyR activated by Ca2+
-Release of Ca2+ from SR into sarcoplsm increase Ca2+ levels
Ca2+ -ATPase
-Transport Ca2+ from the sarcoplasm into SR -> needs energy
-Helps decrease levels of intracellular Ca2+
Termination of ACh activity
-ACh broken down by acetylcholinesterase
-AChE is attached to membrane of muscle cells at synpasis
-AChE metabolizes ACH into acetate and choline
-Metabolism of ACh ends production of muscle action potential and muscle contraction
Obtain ATP by creatine phosphate
-Creatine synthesized primarily in liver and kidney
-Relaxed muscle fibers produce more ATP than needed for resting metabolism -> Excess ATP used to synthesize creatine phosphate by creatine kinase
-When muscle contraction begins the regeneration of new ATP occurs
—ADP phosphorylated by creatine kinase using phosphate group from creatine phosphate to form ATP -> provides enough energy for contraction (15 seconds)
Obtain ATP by anaerobic cellular respiration
Produce ATP in absence of O2
Yields little ATP and lactic acid, a major factor in muscle fatigue
(Glycogen -> Glucose from blood -> 2 pyruvic acid -> 2 lactic acid into blood)
30-40 sec max activity, produce 2 ATP
Obtain ATP by Aerobic Respiration
Glucose yields 36 molecules of ATP
Two sources of O2 -> Oxygen from hemoglobin in blood, Oxygen released by myoglobin in muscle cells
What happens when intracellular Ca2+ is removed by SR
Decreases intracellular Ca2+ concentration
Tropomyosin covers myosin-binding site on actin
Contraction ends, relaxing cardiac muscle
Smooth muscle types: Multi-unit and Visceral (single unit)
Multi-unit:
Unorganized cells that contract as individual cells
Visceral:
form sheets of muscle, connected by gap junctions, contract as a group, rhythmic contraction
Smooth muscle characteristics
Sarcoplasm contains both thick and thin filament
-No sarcomeres
-Contain myosin and actin (no troponin)
-Caveolae in plasma membrane (small pouch-like invaginations, contain extracellular Ca2+)
-Small amount of sarcoplasmic reticulum for storage of Ca2+
Thin filaments attach to structures called dense body (like Z discs)
5 Steps of Smooth Muscle Contraction
1: Intraceulluar Ca2+ enters cells from SR
2: Ca2+ binds to calmodulin
3: Ca2+ calmodulin activates myosin light chain kinase (MLCK)
4: MLCK phosphorylates light chains in myosin heads and increases myosin ATPase activity
5: Active myosin cross-bridges slide along actin and create muscle tension
4 Steps in relaxation in smooth muscle
1: Free Ca2+ in cytosol decreases when Ca2+ is pumped out of cell or back into SR
2: Ca2+ unbinds from calmodulin
3: Myosin phosphatase removes phosphate from myosin decreasing myosin ATPase activity
4: Less myosin ATPase results in decreased muscle tension
Blood Vessel Smooth Muscle Relaxation
-Nitric oxide is synthesized in endothelial cells
-Produces the effect in smooth muscle
-Diffuses from endothelial cells to the muscle
-Protein kinase G phosphorylates and activates ALC-phosphatase -> dephosphorylation of myosin
Where is the effect produced and used up in blood vessel smooth muscle relaxation
Produced in endothelial cell
Not used until it is in Smooth Muscle cells
