Chapter 8 - exam 2 Flashcards
how is skeletal muscle attached to bone
by connective tissue = tendons
What is the origin mean of skeletal muscle
end of muscle attached to bone that doesnt move
What is the insertion mean of skeletal muscle
opposite end fixed to bone that moves during contraction
Explain the complete breakdown of structures in skeletal muscle down to the smallest unit
thin and thick filaments –> myofibrils –> muscle fiber (muscle cells) –> fasicle –> muscle bundle
What is the sarcolemma
casing outside muscle fiber that makes up a fasicle
What are the two subpopulations of mitochondria of skeletal muscle fibers
1) subsarcolemmal (SS) mitochondrion
2) intermyofibrillar (IMF) mitochondria
What are Subsarcolemmal (SS) mitochondria
- located directly beneath cell membrane (sarcolemma) - effect membrane potential and flow of ions to create potential
- produce cellular energy needed to maintain active transport of ions across the sarcolemma
What are Intermyofibrillar (IMF) mitochondria
- located near myofibrillar (contractile) proteins
- provide E needed to sustain muscle contraction
Satellite cells are a type of _______ and are important in what
type of myoblast and important in muscle growth/repair
- during muscle growth, satellite cells increase number of nuclei
satellite cells do what with nuclei
produce nuclei and transport them to muscle fiber
having more satellite cells allows for what synthesis
more satellite cells = more nuclei = greater protein synthesis
- important for muscle growth in response to strength training
on untrained muscle what happens with first training and afterwards with detraining and retraining
after first training satellite cells bring more nuclei onto muscle cell –> creating more protein synthesis and causing hypertrophy –> after detraining atrophy is the result and muscle shrinks —> with exercise get back to hypertrophy
What are the 3 functions of skeletal muscle
1) force production for locomotion and breathing
2) force production for postural support
3) heat production during cold stress
skeletal muscle produces what in response to contractions
produces myokines
What are the three functions of myokines
1) stimulate glucose uptake and fatty acid oxidation – b/c during exercise need more glucose in the cells and break down fatty acids
2) promote blood vessel growth in muscle
3) promote liver glucose production and triglyceride breakdown
- ned more glucose in muscles to perform force
What is IL-6
immune response
- both proinflammatory and anti-inflammatory
- produced during exercise and promotes anti-inflammatory effect
- increased glucose production in liver w/ exercise
does regular exercise promote anti-inflammatory, pro-inflammatory or no inflammatory environment
anti-inflammatory
- reduce chronic inflammation (vasodilate) and reduced risk heart disease, type 2 diabetes and certain cnacers
when is IL-6 hightest
during exercise and decreases after
What do flexors do
decrease joint angle
what do extensors do
increase joint angles
What is static movement
- muscle exerts force w/o changing length
- pulling against immovable object
-postural muscles
What are the two types of dynamic movements
1) Concentric
2) eccentric
What is Concentric dynamic movement
muscle shortens during force production
What is eccentric dynamic movement
- muscle produces force but length increases – resisting
- associated with muscle fiber injury and soreness “healthy” injury
- during workout focus on eccentric
What is the central nervous system
brain and spinal chord
what is the peripheral nervous system
cranial and spinal nerves
What is the direction of movement when starting with activating sensory receptors
active sensory receptors –> go to sensory division of PNS –> to CNS –> To the motor division of PNS for response
EITHER
- Somatic Nervous system – skeletal muscle
- Autonomic nervous system – smooth muscle, cardiac muscle, glands
The somatic motor neurons of the PNS are resonsible for what
carrying neural messages from spinal chord to skeletal muscles (tissue)
what is a motor unit
motor neuron and and all the fibers it innervates
what is the neuromuscular junction
gap between motor neuron and muscle fiber
what is the motor end plate
pocket formed around motor neuron by sarcolemma
-in sarcolemma form pocket for motor neuron fiber to fit into
myofibrils can be further subdivided into individual sarcomeres and what are the two major parts to this
arrangement of thin (actin, tropomyosin, troponin) and thick (myosin) filaments
Draw out one sarcomere and label the Z line, M lie, I band, A band, and H zone
draw and look at drawing
What happens that causes muscle shortening
due to movement of thin (actin) filament over the thick (myosin) filament
- form cross-bridges
Do z lines get closer or father away from each other during a contraction
get closer during contraction
What is required for muscle contraction
myosin ATPase breaks down ATP (already attached) as fiber contracts
What are the two sites on the heads of the myosin
- actin-binding site
- myosin ATPase site
what do you need ATPase to do that effects a contraction
break down ATP to release myosin head from actin filament
what is the source of ATP during muscle contraction
ATP-PC system
What are the 5 steps of the excitation-contraction coupling process in muscle contraction
1) action potential stimulates acetylcholine (Ach) release from alpha motor neuron at neuromuscular junction
2) Acetylcholine induces an action potential in the muscle fiber. Action potential spreads down sarcolemma and T-tubules
3)Action potential stimulates Ca2+ release from sarcoplasmic reticulum
4) Ca2+ initiates tropomyosin displacement revealing myosin binding site
5) myosin forms cross-bridges w/ actin producing force
With an action potential what provides the cellular energy to actively transport Ca2+ across sarcolemma
the subsarcolemmal mitochondria
List the 7 stages of cross-bridge cycling
1) myosin binding sites on actin molecule are covered in resting fibers w/ ADP + Pi attached
2) Action potential releases calcium from sarcoplasmic reticulum
3) Calcium binds to troponin – cause tropomyosin to move revealing the myosin binding site
4) Cross-bridge forms when myosin heads bind to actin
5)myosin head pivots moving actin –> ADP and Pi dissociate from myosin head
6) myosin head releases actin when fresh ATP binds
7) myosin head binds next actin (flagged) –> ATP cleaved to ADP + Pi and cycle repeats
if a drug increases Ca2+ release from the SR but does NOT enhance muscle contraction. It is suspected that the drug accidentally bound to the thin filament. Blockage of which structure in the thin filament would prevent Ca2+ binding and skeletal muscle contraction
troponin
what are muscle cramps
-spasmodic involuntary muscle contractions
- often associated with prolonged, high intensity exercise
- electrolyte depletion and dehydration theory: H2O and Na2+ loss via sweat and hot environment
Explain the altered neuromuscular control theory
- abnormal spinal reflex activity due to fatigue
- result: increased excitatory activity of muscle spindles and reduced inhibitory effect of Golgi tendon organ
What happens with increased muscle spindle activity
muscle spindles detect stretch of muscle (doest want to stretch too much) –> sensory neurons conduct action potential to spinal chord –> sensory neurons synapse with alpha motor neuron –> situation of alpha motor neuron cause muscle to contract and resist stretch (CRAMP)
What happens with decreased Golgi tendon organ activity
golgi tendon organize detect tension applied to a tendon –> sensory neurons conduct action potentials to the spinal cord –> sensory neuron synapse with inhibitory interneurons that’s an abs with alpha motor neurons –> inhibition of the alpha motor neuron causes muscle relaxation leaving the tension applied to the tendon
Activation of Golgi tendon does what?
inhibits motor neurons in spinal chord, result in muscle relaxationW
What are Type I fibers
- slow-twitch fibers
-slow oxidative fibers
What are Type II fibers
- intermediate fibers
-fast-oxidative glycolytic fibers
what are type IIx fibers
(less resistant to fatigue)
- fast twitch fibers
-fast glycolytic fibers
What effects the oxidative capacity in muscle fiber types
number of capillaries (increase blood and O2 to tissues), mitochondria (need O2 to generate ATP - slow fatigue), and amount of myoglobin (increase O2 deliver to tissue)
Do each type of muscle fiber types have low/moderate/high number of mitochondria
- Type I: High
- Type IIa: High/moderate
- Type IIx: Low
Do each type of muscle fiber types have low/moderate/high resistance to fatigue
- Type I: High
- Type IIa: High/moderate
- Type IIx: Low
what are the predominant energy systems in the muscle fiber types
- Type I: Aerobic
- Type IIa: Combination
- Type IIx: Anaerobic
The type of myosin ATPase effects what in each muscle fiber type
speed of ATP degredation
What is the ATPase activity in each muscle fiber type
- Type I: Low
- Type IIa: High
- Type IIx: Highest
How does the abundance of contractile proteins (actin and myosin) effect the muscle fiber type
increased contractile fibers = increased force
– see more in type II than I
The speed of shortening (contracting) is greater in what type of fibers
in fast fibers
- SR release Ca++ at faster rate
- higher ATPase activity
What is the maximal force production per unit of cross-sectional area dependent on
- max force in each tissue:
- NOT more/less fibers
- same cross-sectional area produce different force
** High in Type II and moderate in Type I
Why do larger muscle fibers produce more force than smaller fibers
because they contain more actin and myosin than small fibers (Type I lowest and type IIx highest max force)
Is there a sex or age differences in fiber distribution
NO == distribution b/t fiber types not between men and women
Do both men and women have same force produces in type I or II fibers
YES – only larger cross sectional fiber generates more force
How is maximal power output effected by fiber types
fast fibers have higher power output than slower
Power = force x shortening velocity
How is muscle fiber efficiency differentiated in muscle fiber types
lower amount of ATP used to generate force
- high efficiency = Type I
- moderate = Type IIa
- low efficiency = Type IIx
what accounts for difference in muscle fiber types
genetics, training, hormone production
What are the different types of exercise that have more fast fibers vs slow fibers
power athlete = fast fiber
endurance = slow fibers
What are the three ways force is regulated in the muscle
1) types and number of motor units recruited
2) initial muscle length
3) nature of the neutral stimulation of motor units
What are the three types of motor units
- Type S (slow): smallest motor neuron and innervate type I muscle fibers == fine control (eyes, hands)
- Type FR (fast, fatigue resistant): innervate type IIa muscle fibers
- Type FF (fast, fatigable): largest of motor neurons, innervate type IIx muscle fibers
Explain the recruitment pattern during graded exercise
Type I recruited first – plateaus and continues sustaining force generation –> right after plateau in type I, Type IIa is recruited if need more force –> reach plateau and continue force generation –> after plateau of Type IIa, recurit IIx if need even more force
if you have a high force production how fast is the movement
usually slower
progressive recruitment of motor units begins with what
begin w/ smallest and progress to larger
how does initial muscle length effect force regulation
- “ideal” sarcomere length for force generation: to have max # of crossbridges formed over sarcomere
- increased cross-bridge formation
What is the optimal overlap to have with the myosin and actin in order to have the greatest tension produced
if there is myosin head overlap and actin is able to move over myosin it is best at the greatest distance without sacrificing cross bridges
- if completely relaxed or fully contracted there isnt as much force
How does the nature of the neural stimulation of motor units effect force regulation in muscle
effects the frequency of stimulation
- simple switch
-summation
-tetanus
normal body movements involve sustained contractions that are NOT _______
simple twitches
how many action potentials does a single twitch give
one action potential == with delay, contraction phase and relaxation phase
what are the three phases of a muscle twitch
- 5ms = stimulus –>latent period
-40ms = twitch and Ca2+ released causing contraction almost at peak remove Ach = more relaxation - 50ms = relaxation
explain the difference between simple twitch, summation, and tetanus
simple twitch: single twitches that increase in force and then decrease
summation: when simple switches summate into higher and higher force – if generate another twitch before relaxation = sum of twitch
tetanus: constant force maintained
increasing the frequency of the stimulus results in what
summation of the twitches and finally tetanus
Why is the force production additive in relation to Ca2+ availablility
after calcium is released from sarcoplasmic reticulum onto the sarcomeres == calcium used and released and using ATP, Ca2+ is pumped back into the sarcoplasmic reticulum
Explain DOMS
delayed onset muscle soreness
- appear 24-48 hours after strenuous exercise
- due to microscopic tear in muscle fiber or connective tissue
- eccentric exercise (downhill running) causes more damage than concentric exercise (cycling)
Explain why there is no physiological evidence that lactate production causes muscle soreness
= lactate removal is rapid (w/i 60 min) following exercise
= w/ continuous exercise produce same lactate - not always sore though
What are the three types of exercise induced muscle injury
1) sarcomere damage (hours to days) = tearing
2) immune cell infiltration (days) = response to initial damage: inflammatory response
3) satellite cell activation (days to weeks) = important in muscle cell hypertrophy – build muscles
explain the breakdown of what happens during DOMS
1) structural damage to muscle fibers
2) membrane damage
3) Ca2+ leaks out of the sarcoplasmic reticulum
4) Protease activation == result in breakdown of cellular proteins - cellular apoptosis
5) inflammatory response
6) edema and pain
How do muscle fibers repair themselves
use resident satellite cell populations == ***** myogenic precursor cells
What happens to force production with DOMS
force production decreases because there is increased sarcomere (force producing unit) damage = force loss – high chance of injury
- ability to send signal = inhibited
- impair ability for high intensity exercise
What two substances are found in muscle that hints towards muscle damage (only in muscle not blood)
- myoglobin
= creatine kinase (high at 48 hours and super high at 4 days): immediate E production===== delayed response = Doms and high muscle damage at 4 days
What are the three consequences of DOMS
E-C coupling failure, contractile protein loss, physical disruption
What is the repeated bout effect
bout of unfamiliar exercise results in DOMS
- another bout of same exercise results in minimal injury
initial bout of exercise –> muscle damage or injury –> adaptation –>
Neural Theory: change in Nervous System
Connective Tissue Theory: increased intramuscular connective tissue
Cellular Theory: cellular changes that strengthen and protect muscle fibers –> repeated bout of exercise
–> less muscle damage == more adaptation
- slowly begin specific exercise over 5-10 sessions to avoid DOMS and do eccentric submax exercise
What parts of the sarcomere change width during a concentric contraction
A band: does not change
H- zone: width decreases
I-band: width decreases
sarcomere: width decreases
thick filament: does not change
thin filament: does not change
myoglobin delivers O2 to where
to the mitochondria = increase oxidative fibers and decreases fatigure
What is the difference in BP and Hr with arm vs. leg exercises
at same O2 uptake arm work results in higher:
- BP b/c of vasoconstriction of large inactive muscle mass
- HR due to higher sympathetic stimulation
with intermittent exercise what effects HR and BP
- fitness level
-temperature and humitidity - duration and intensity of exercise : lower intensity = less drift
During prolonged exercise how is Q, SV, and HR effected
Q maintained, gradual decrease in SV because of a higher HR and dehydration, increase in HR b/c of heat – cardiovascular drift
Why does cardiac output stay the same when HR and SV are effected
b/c wth the equation no change in Q = increase in HR * decrease in sV
Explain the effects of cardiovascular drift
increase in HR and decrease in SV
- to prevent maintain hydration and decrease intensity in cooler environment
explain the transition from exercise to recovery and how HR, SV, and Q are effected
decrease HR, SV, and Q towards resting
Depends on: duration and intensity and training state
- in the EPOC all decrease over time
