Flashcards in Exam 4 - chapter 9 Deck (28)
3 basic types of muscle tissues
skeletal, cardiac, smooth
4 functions of muscle tissue
-movement of bones or fluids (e.g., blood)
-maintaining posture and body position
-heat generation (esp. skeletal muscle)
gross structure of a skeletal muscle
epimysium - surrounds entire muscle (blends with fascia)
perimysium - surrounds fascicles (groups of muscle fibers)
endomysium - between individual muscle fibers
microscopic anatomy of a skeletal muscle fiber
-long cylindrical cell
-multiple peripheral nuclei
-sarcolemma - plasma membrane
-densely packed, rodlike elements
-80% of cell volume
-contain sarcomeres (contractile units)
-exhibit striations - perfectly aligned repeating series of dark A bands and light I bands
sarcoplasmic reticulum (SR)
-network of smooth endoplasmic reticulum surrounding each myofibril
-pairs of terminal cisternae form perpendicular cross channels
-functions in regulation of intracellular calcium levels (stores & releases calcium)
-continuations of sarcolemma
-lumen continuous with extracellular space
-increase muscle fiber's surface area
-penetrate cell's interior at each A band & I band junction
-associate with paired terminal cisterns to form triads that encircle each sarcomere
which band does not change in width during muscle contraction
i bands shorten, z discs closer, h zones disappear
'A' BANDS LENGTH STAYS THE SAME
relate i bands, a bands, h zone, and z lines to the arrangement of thick and thin myofilaments in sarcomeres
I bands are light,
A bands are dark,
h zones: lighter region in midsection of dark A band where filaments do not overlap
Z lines are coin-shaped sheets of proteins on midline of light I band that anchors thin filaments and connects myofibrils to one another
explain how muscle fibers are stimulated to contract by describing events that occur at the neuromuscular junction
1. action potential arrives at axon terminal of motor neuron
2. voltage-gated calcium ion channels open and calcium ion enters axon terminal moving down the gradient.
3. calcium ion causes ACh (neurotransmitter) to be released.
4. ACh difusses across the synaptic cleft and binds to receptors on cell membrane.
5. ACh binding opens ion channels in the receptors that allow sodium in and potassium out.
6. ACh effects are terminated by acetylcholinesterase and diffuse away from junction.
sliding filament model of contraction
during contraction, the thin filaments slide past the thick ones so that the actin and myosin filaments overlap to a greater degree.
when nervous system stimulates muscle fibers, the myosin heads on the thick filaments latch onto myosin-binding sites on actin in the thin filaments, and the sliding begins.
these cross bridge attachments form and break several times during a contraction, acting like tiny ratchets to generate tension and propel the thin filaments toward center of sarcomere.
as this occurs, muscle cell shortens
i bands shorten, z discs get closer together, h zones disappear
'A' BANDS LENGTH STAYS THE SAME
events of excitation-contraction coupling that lead to cross bridge activity
1. action potential propogates along the sarcolemma and down t-tubles.
2. calcium ions released
3. calcium binds to troponin and removes the blocking action of tropomysin
4. contraction begins.
motor neuron and all muscle fibers it supplies (4-several hundred)
smaller motor units = fine control. (eyes, fingers)
larger motor units = weight-bearing, larger muscles (hip muscles)
motor unit's response to single action potential of its motor neuron. simplest observable in lab, recorded as myogram
events in a muscle twitch
latent period - events of excitation-contraction coupling, no muscle tension
period of contraction: cross bridge formation; tension increases
period of relaxation: calcium ion reentry into SR; tension declines to zero
no shortening, muscle tension increases but does not exceed load (holding something in place)
muscle shortens because muscle tension exceeds load (in concentric). (when you pick up a book)
in eccentric, muscles lengthen (calf muscle when walking up a hill)
3 ways that ATP is regenerated during skeletal muscle contraction
muscles store only 4-6 seconds of ATP, and must be hydrolyzed to ADP and inorganic phosphate in muscle fibers to regenerate ATP within a fraction of a second. It does so in the following ways:
direct phosphorylation energy source and how it is used
creatine phosphate + ADP forms creatine and ATP almost instantly
catalyzed by the enzyme creatine kinase.
creatine phosphate is a high-energy molecule stored in muscles, and is tapped to regenrate ATP while metabolic pathways adjust to the sudden high demand for ATP.
ATP + CP provide for max muscle power for 15 seconds
CP reserves are replenished during periods of rest or inactivity.
anaerobic pathway energy source and how it is used
break down glucose from blood or glycogen stored in the muscle.
glucose is broken down to two pyruvic acid molecules, releasing enough energy to form small amounts of atp - 2 ATP per glucose.
when you exercise vigorously, bulging muscles constrict blood flow and oxygen delivery, and glycolysis is converted into lactic acid.
most of it is diffused into blood stream, and liver, kidney and heart use it as energy, or liver can reconvert it to pyruvic acid or glucose and release it back into the bloodstream for muscle use, or convert it to glycogen for storage.
30-40 seconds of energy is provided
occurs in mitochondria, requires oxygen, and involves this sequence:
glucose + oxygen breaks down and becomes CO2, H2O, and ATP.
CO2 is diffused and released out of the body by lungs.
after 30 minutes of activity, fatty acids are the major sources of fuel. requires continuous delivery of oxygen and nutrient fuels to keep going.
oxygen debt & how it arises
excess postexercise oxygen consumption
for a muscle to return to its resting state, all of the following must occur:
1. its oxygen reserves in myoglobin must be replenished
2. the accumulated lactic acid must be reconverted to pyruvic acid
3. glycogen stores must be replaced
4. atp and CP reserves must be resynthesized.
it is the difference between the amount of oxygen needed for totally aerobic muscle activity and the amount actually used.
starts to stiffen 3-4 hours after death, muscles peak stiffen with weak rigidity at 12 hours after death
dying cells take in calcium, which promotes formation of myosin cross bridges. atp cynthesis ceases, but atp continues to be consumed, and cross bridge detachment is impossible.
3 types of muscle fiber types
slow oxidative - endurance type activites (marathon, maintaining posture)
fast oxidative - sprinting, walking
fast glycolytic - short-term intense, powerful movements like hitting a baseball
axon terminal: nerve ending attached to muscle fiber,
synaptic vesicle: contains ACh (neurotransmitter),
cholinesterase: acetylcholinesterase - terminates ACh into its building blocks (acetic acid & choline) - removes ACh to prevent elongated muscle fiber contraction,
synaptic cleft: axon terminal and muscle fiber are close, but do not touch - space = synaptic cleft,
motor-end-plate: aka neuromuscular junction,
neurotransmitter: ACh - triggers the opening of Na+ K+ gates, allowing sodium in and potassium out,
receptor molecule: receptors on sarcolemma, which have gates
optimal sarcomere operating length
aerobic exercise's effects on skeletal muscles and other body systems
number of capillaries surrounding muscle fibers increases
number of mitochondria within the muscle fiber increases
fibers synthesize more myoglobin
RESULT: more efficient muscle metabolism; greater endurance, strength, and resistance to fatigue; and converts fast glycolytic fibers into fast oxidative fibers.