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bio 2401 chp 9

QuestionAnswer
motion results from alterating contraction (shortening) and relaxation of muscles; the skeletal system provides leverage and a supportive framework for this movement
the scientific study of muscles is known as myology
skeletal muscle tissue is primarily attached to bones. it is striated and voluntary
cardiac muscle tissue forms the wall of the heart. it is striated and involuntary, has intercleated discs
smooth (visceral) muscle tissue is located in hollow organs. it is nonstriated (smooth) and involuntary
neurotransmitter ach
key muscle functions- production of body_____ movement
key muscle functions- stabilizing body _____ positions
key muscle functions- regulating organ ______ volume
key muscle functioins- moving substances _____ within the body
key muscle functions- generating ___ heat
electrical excitability is the ability to respond to certain stimuli by producing electrical signals such as action potential (impulse)
contractility is the ability to shorten and thicken (contract) generating force to do work
in an isometric contraction, the muscle develops tension but does not shorten
in an isotonic contraction the tension remains constant while the muscle shortens
extensibility is the ability to be stretched without damaging the tissue
elasticity is the ability to return to original shape after contraction or extension
each skeletal muscle is a seperate organ composed of cells called fibers
fascia is a sheet or band of fibrous connective tissue that is deep to the skin and surrounds muscles ad other organs of the body
superficial fascia (or subcutaneous layer) separates muscle from skin and functions to provide a pathway for nerves and blood vessels, stores fat, insulates, and protects muscle from trauma
deep fascia lines the body wall and limbs and holds muscles with similar functions together, allows free movement of muscles, carries nerves, blood vessels, and lymph vessels, and fills spaces between muscles
extensions of deep fascia--epimysium covering the entire muscle;
extensions of deep fascia--perimysium covering fascicles
extensions of deep fascia--endomysium covering individual muscle fibers (cells)
tendons and aponeuroses are extensions of connective tissue beyond muscle cells that attach muscle to bone or other muscles.
tendon (synovial) sheaths enclose certain tendons and allow them to slide back and forth more easily
aponeurosis is a tendon that extends as a broad, flat layer EX epicranial aponeurosis
blood brings oxygen and nutrients for contraction
nerves (containing motor neruons) convey impulses for muscular contraction
during embryonic development, skeletal muscle fibers arise from myoblasts.
a few myoblasts persist in mature skeletal muscle as satellite cells
skeletal muscle consists of fibers (cells) covered by a cell membrane (sarcolemma)
"sarco" flesh
the fibers contain t tubules and sarcoplasm
t tubules are tiny invaginations of the sarcolemma that quickly spread the muscle action potential to all parts of the muscle fiber
sarcoplasm is the muscle cell cytoplams and contains a large amount of myoglobin for oxygen storage
each fiber contains myofibrils that consist of thin and thick filaments (myofilaments)
sarcoplasmic reticulum encircles each myofibril it is similar to smooth endoplasmic reticulum in on muscle cells and in the relaxed muscle stores calcium ions
muscular atrophy is a wasting away of muscles
muscular hypertrophy is an increase in the diameter of muscle fibers
myofibrils are composed of thick and thin filaments arranged in units called sarcomeres
"myo" muscle
calcium is stored in bone and muscle
sarcomeres are the basic functional units of a myofibril and show distinct dark (A band) and light (l band) areas
the darker middle portion, the A band, is the entire width of the thick filaments with some thin filaments overlapping the thick one
the lighter sides are the I bands that consist of thin filaments only
there are two z discs, one at each end of the sarcomere
a narrow H zone in the center of each A band contains thick but no thin filaments
exercise can result in torn sarcolemma, damaged myofibrils, and disrupted Z discs and results in soreness or pain the next day
contractile proteins generate force during contraction
myosin the main component of thick filaments, functions as a motor protein.
motor proteins push or pull their cargo to achieve movement by converting energy from ATP into mechanical energy of motion or force
actin the main component of thin filaments, connects to the myosin for the sliding together fo the filaments
myosin is thick
actin is thin
only striated have sarcomeres
muscle is protein
myosin is motor protein
regulatory proteins help swith the contractions on and off
the regulatory proteins tropomyosin and troponin are a part of the thin filament
in relaxed muscle, tropomyosin blocks the myosi-binding sites on actin preventing myosin from binding to actin
structural proteins keep the thick and thin filaments in the proper alignment, give the myofibril elasticity and extensibility, and link the myofirbrils to teh sarcolemma and extracellular matrix
titin (elastic filaments) help a sarcomere return to its resting length after a muscle has contracted or been stretched
dystrophin reinforces the sarcolemma and helps transmit the tesion generated by the sarcomeres to the tendons
during muscle contraction myosin cross bridges (heads) pull on thin filaments, causing them to slide inward toward the H zone
z discs come toward each other and the sarcomere shortens, but thick and thin filaments do not change in length.
the sliding of filaments and shortening of sarcomeres causes the shrotening of the whole muscle fiber and ultimately the entire muscle this is called the sliding filament mechanism
at the beginning of contraction, the sarcoplasmic reticulum releases calcium ions which bind ot troponin and cause the tropnin- tropomysium complex to uncover the myosin-binding site on actin. when the binding sites are "free" the contraction cycle begin
the contraction cycle is a repeating sequence of events that causes the filaments to slide. it consists of ATP hydrolysis, attachment of myosin to actin to form cross bridges, the power stroke, and detachment of myosin from actin.
an increase in calcium ion concentration in the cytosol starts muscle contraction; a decrease stops it
the muscle action potential releases calcium ions form the sarcoplasmic reticulum that combine with troponin causing it to pull on tropomyosin to change its orientation, thus exposing myosin-binding sites on actin and allowing the actin and myosin to bind together
z discs are like fingers sliding together
ATP is split in ATP hydrolysis
calcium ions causes contraction to take place
for active transport ATP is needed
the use of calcium ions to remove the contraction ihibitor and the joining of actin and myosin constitute the excitation-contraction coupling, the steps that connect excitation muscle action potential propagation through the T tubules to contraction of the muscle fiber
calcum ion active transport pumps return calcium ions to the sarcoplasmic reticulum
rigor mortis a state of muscular rigidity following death, results from a lack of ATP to split myosin-actin cross bridges
muscle action potentials arise at the neuromuscular junction (NMJ) the synapse between a somatic motor neuron and a skeletal muscle fiber
a synapse is a region of communication between two neurons or a neuron and a target cell
target cell = muscle cell
synapses separate cells from direct physical contact
neurotransmitters bridge that gap
the neurotransmitter at a NMJ is acetylcholine (ACH)
a nerve action potential elicits a muscle action potential through the release of acetycholine activation of ACh receptors, production of a muscle action potential, and termination of ACh activity
several plant productions and drugs selectively block events at the NMJ
curare block acetylocholine binding sites
black widow venom stimulates acetylcholine release
during excitation, action potentials in the nerve fiber give rise to action potentials in the muscle fiber
action potentials in the synaptic knob trigger the release of ACh from synaptic vesicles. ACh is released into the synaptic cleft and is detected by the ligand-gated ion channels in the motor end plate
binding of ACh opens the sodium gated ion channels on the motor end plate
sodium ions rush into the muscle cell, which quickly reverses polarity depolarization (more positive inside)
potassium ions rush out, and memrbane polarity is reestablished (repolarization)
during repolarization, a muscle fiber is said to be in a refactory period because the cell cannot be stimulated again until repolarization is complete
this rapid change in polarity at the motor end plate triggers the opening of voltage gated sodium and potassium ion channels adjacent to the motor end plate, and action potentials spread away from the plate in all directions
once initiated the action potential is unstoppable. it ultimately results in contraction of muscle fiber
during excitation-contraction coupling, action potentials in the muscle fiber lead to activation of the myofilaments (actin and myosin)
the wave of action potential travels down the t tubules and continues to the sarcoplasmic reticulum
after the action potential reaches the sarcoplasmic reticulum it releases a flood of calcium ions into the cytosol
calcium ions bind the troponin of the thin myofilaments, causing the troponin-tropomyosin complex to shift aside, exposing the myosin binding sites on the actin filaments
exocitosis requires ATP
the myosin heads can now bind to the myosin binding sites on actin and initiate contraction
during the contraction phase, sliding of the thin myofilaments past the thick ones causes the muscle fiber to shorten
the sliding filament theory suggests that thin filaments slide over thick ones causing sarcomeres to shorten
the head of each myosin molecule contains myosin ATPase that releases energy from ATP, in preparation for action, the myosin binds and hydrolyzes an ATP molecules, and is now in the "cocked" position
when the myosin binding sites on the actin filaent are exposed, the myosin head contacts the active site, releases energy, and performs a power stroke
at the end of a power stroke, myosin binds to a new ATP, releases the actin, and returns to its original position in a recovery stroke. many myosin heads pull on the actin at once, so the actin does not slip back into its original position
the cycle of power stroke and recovery is repeated many times during muscle contraction
when nervous stimulation ceases, the muscle relaxes
acetycholinesterase (AChE) breaks down ACh so the muscle stops generating its action potentials
calcium is carried back to the sarcoplasmic reticulum by active transport and a protein called calsequestrin
rigor mortis is a state of muscular rigidity that begins 3-4 hours after death and lasts about 24 hours after death
CA+2 ions leak out of the SR and allow myosin heads to bind to actin. since ATP synthesis has ceased, myosin cross bridges cannot detach from actin until proteolytic enzymes begin to digest the decomposing cell
active muscle cells require large quantities of ATP there are there sources of ATP production in muscle cells
creatine phosphate and ATP can power maximal muscle contration for about 15 seconds and is used for maximal short bursts of energy
creatine phosphate is unique to muscle fibers
there is a vontroversey regarding the effectiveness of creatine supplementation
the partial catabolism of glucose to generate ATP occurs in anaerobic cellular respiration. this system can provide enough energy for about 30-40 seconds of maximal muscle acitivty
muscular activity lasting more than 30 seconds depends increasingly on aerobic cellular respiration (reactions requiring oxygen) this system of ATP production involves the complete oxidation of glucose cia cellular respiration (biological oxidation)
muscle tissue has two sources of oxygen: diffusion from blood ad release of myoglobin inside muscle fibers
the aerobic system will provide enough ATP for prolonged activity so long as sufficient oxygen and nutrients are available
a state of physiologial inability to contract even though the muscle still may be receiving stimuli is the inability of a muscle to maintain its strength of contraction or tension is called muscle fatigue.
ionic imbalances and an increase in lactic acid in the muscle are probablt the main causes of fatigue
3 sources of ATP creatine phosphate, anaerobic pathway, aerobic respiration
elevated oxygen use after exersie is called oxygen deficit, for a msucle to return to is resting state its oxygen reserves must be repleished; the accumulated lactic acid must be reconverted to pyruvic acid; glycogen stores must be replaced, and; ATP and creatine phosphate reserves must be resynthesized
when considering the contraction of a whole muscle, the tension it can generate depends on number of muscle fibers that are contracting in unison
a motor neuron and the muscle fibers it stimulates form a motor unit
a single motor unit may innervate as few as 10 or as many as 2,500 muscle fibers, with an averae of 150 fibers being innervated by each motor neuron
a twitch contraction is a brief contraction of all the muscle fibers in a motor unit in response to a single action potential
a record of a muscle contraction is called a myogram and includes three periods; latent, contraction, and relaxation
the refactory period is the time when a muscle has temporarily lost excitability with skeletal muscles having a short refactory period and cardiac muscle having a long refactory period
wave summation is the increased strength of a contraction resulting from the application of a second stimulus before the muscle has completely relaxed after a previous stimulus.
a sustained muscle contraction that permits partial relaxation between stimuli is called incomplete (unfused) tetanus
a sustained muscle contraction that lacks even partial relaxation between stimuli is called complete (fused) tetanus
the process of increasing the number of active motor units is called recruitment (multiple motor unit summation)
MMUS prevents fatigue and helps provide smooth muscular contraction rather than a series of jerky movements
aerobic tranining builds endurance
anaerobic training builds muscle strength
a sustained partial contraction of portions of a relaxed skeletal muscle results in a firmness known as muscle tone.
at any given moment, a few muscle fibers within a muscle are contracted while most are relaxed. this small amount of contraction is essential for maintaining posture
muscle tone involuntary contraction of a small number of motor units (alternately active and inactive in a constantly shifting pattern)
muscle tone keeps muscles firm even though relaxed
muscle tone does not produce movement
muscle tone is essential for maintaining posture (head upright)
muscle tone is important in maintaining blood pressure because of tone of smooth muscles in walls of blood vessels
isotonic contractions occur when a constant load is moved through the rang of motions possible at a joint and include concentric contractions and eccentric contractions;
in a isometric contracion the muscle does not shorten but tension increases
isotonic contractions = a load is moved
concentric contraction = a muscle shortens to produce force and movement
eccentric contractions= a muscle lengthens while maintaining force and movement
isometric contraction= no movement occurs
same length isometric
same tension isotonic
tension is generated without muscle shortening such as while maintaining posture and supporting objects in a fixed position
not all skeletal muscle fibers are identical in structure or function
endurance fibers= slow oxidative
color varies according to the content of myoglobin, an oxygne-storing reddish pigment.
red muscle fibers have high myoglobin content while the myoglobin content of white muscle fibers is low
myoglobin makes muscles darker--more oxygen
fiber diameter varies, as do the cell's allocations of mitochondria, blood capillaries, and sarcoplasmic reticulum
contraction velocity and resistance to fatigue also differ between fibers
on the basis of structure and function, skeletal muscle fibers are classified as slow oxidative, fast oxidative, and fast glycolytic fibers
most skeletal muscles contain a mixture of all three fiber types, their proportions varying with the usual action of the muscle. all fibers of any one motor unit, however, are the same
altough the number of different skeletal muscle fibers does not change, various types of exercise can alter the characteristic of those present
the use of anabolic steroids by athletes to increase muscle size, strength, and endurance has been shown to have very serious side effects, some of which are life threatening
slow oxidative is red
fast oxidative is pink
fast glycolytic is white
cardiac muscle tissue is found only in the heart wall
cardiac muscle fibers are arranged similarly to skeletal muscle fibers
cardiac muscle fibers connect to adjacent fibers by intercalated discs, which contain desmosomes and gap junctions
cardiac muscle contractions last longer than the skeletal muscle twitch due to the prolonged delivery of calcium ions from the sarcoplasmic reticulum and the extracellular fluid
cardiac muscle fibers contract when stimulated by their own autorhythmic fibers
this continuous, rhythmic activity is a major physiological difference between cardiac and skeletal muscle fibers
smooth muscle tissue is nonstriated and involuntary and is classified into two types
visceral (single unit) smooth muscle is found in the walls of hollow viscera and small blood vessels; the fibers are arranged in a network
multiunit smooth muscle is found in large blood vessels, large airways, arrector pili muscles, and the iris of the eye. the fibers operate singly rather than as a unit
the duration of contraction and relaxation of smooth muscle is longer than in skeletal muscle
in smooth muscle, the regulator protein that binds calcium ions in the cytosol is calmodulin (in place of the role of troponin in striated muscle);
calmodulin activates the enzyme myosin light chain kinase, which facilitates myosin-actin binding and allows contraction to occur at a relativly slow rate
the prolonged presence of calcium ions in the cytosol of smooth muscle fibers provides for smooth muscle tone, a state of continued partial contraction
fibrosis scar tissue formation
smooth muscle fibers can stretch considerably without developing tension; this phenomenon is termed the stress relaxation response
smooth muscle lacks striatioins and have little Sarcoplasmic Reticulum for calcium storage
skeletal muscle fibers cannot divide after 1st year
growth is enlargement of existing cells hypertorphy
repair--satellite cells and bone marrow produce some new cells
repair--fibrosis occurs most often
cardiac muscle fibers cannot divide or regenerate
all healing is done by fibrosis
smooth muscle fibers -- regeneration is possible
cells can grow in size (hypertrophy)
some cells (uterus) can divide (hyperplasia)
new fibers can form from stem cells in blood vessel walls
beginning at about 30 years of age, there is a progressive loss of skeletal muscle, which is replaced by fat
there is also a decrease in maximal strength and a slowing of muscle reflexes
neuromuscular disease involves problems wiht somatic motor neurons, neuromuscular junctions, or muscle fibers
myopathy signifies a disease or disorder of the skeletal muscle tissue itself
myasthenia gravis progressive autoimmune disorder that blocks the ACh receptors at the neuromuscular junction
with myasthenia gravis the more receptors that are damaged the weaker the muscle
myasthenia gravis is more common in in women 20 to 40
myasthenia gravis begins with double vision and swallowing difficulties and progresses to paralysis of respiratory muscles
myasthenia gravis treatments include inhibitors of acetylcholinesterase and steroids to reduce antibodies against ACh receptors
muscular dystrophies is inherited, muscle-destroying desease
muscular dystrophies--when muscle contracts sarcolemma tears
muscular dystrophies is mutated gene is on X chromosomes so disorder is in Males almost exclusively
muscular dystrophies appears by age 5 in males and by 12 may be unable to walk
muscular dystrophies is degeneration of individual muscle fibers produces atrophy of the skeletal muscle
muscular dystrophies is the most common form ducheone muscular dystrophy
intense exercise can cause muscle damage
electron micrographs reveal torn sarcolemmas, damaged myofibrils and disrupted Z discs
increased blood levels of myoglobin and creatine phosphate found inside the muscle cell
delayed onset muscle soreness (DOMS) 12 to 48 hours after strenuous exercise, stiffness, tenderness and swelling due to microscopic cell damage
atrophy wasting away of muscles, caused by disuse (disuse atrophy) or severing of the nerve supply (denervation) atrophy
hypertrophy increase in the diameter of muscle fibers, results from very forceful, repetitive muscular activity and an increase in myofibrils, SR & mitochondria
Created by: morgan8
 

 



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