Neuromuscular Nervous System Flashcards
What are the three types of muscles?
- skeletal
- cardiac
- smooth
Skeletal muscle:
- voluntary
- there are over 600
- moves the skeleton
Cardiac muscle:
- involuntary
- only in the heart
Smooth muscle:
- involuntary
- in the walls of blood vessels and internal organs
Skeletal muscle functions:
- movement
- posture
- stabilize joints
- heat
Muscle structure:
- tendon
- periosteum (outer most layer of the bone)
Muscle structure:
- epimysium
- perimysium
- endomysium
Epimysium
- surrounds entire muscle
- fascia of fibrous connective tissue
Perimysium
- surrounds individual bundles of muscle fibers
- bundles call fascicles
Endomysium:
- surrounds each muscle fiber
- fine layer of connective tissue
Muscle fiber structure:
- sarcolemma
- myofibril
- sarcoplasm
- transverse tubules (t-tubules)
- sarcoplasmic reticulum
- sarcomeres
sarcolemma:
- thin elastic membrane surrounding the muscle fiber
- includes z-line, m-line, h-zone, a-band, I-band
Myofibril
- contain contractile proteins
- actin and myosin
Sarcoplasm
- serves as cytoplasm of muscle cell
- has unique features: glycogen storage, mitochondria
- what feeds/provides energy for muscle movement
Transverse tubules (t-tubules)
- extends inward from the sarcolemma
- carry action potential deep into muscle fiber
- balloon wraps around finger analogy
Sarcoplasmic reticulum
- Ca2+ storage
- at rest this is where calcium should be sitting
sarcomeres
- functional unit of the muscle cell
- basic contractile element of skeletal muscle
- end-to-end for full myofibril length
- to make most efficient: stack sarcomeres parallel so they transmit signal across entire fiber
- red “E” parts and everything in between
- thick and thin filaments
Look at z-disc to determine:
how many sarcomeres are present
What is the z-disc?
dark band which is end border of one sarcomere
A-band:
- dark area in mid region
- overlap between thick and thin filaments
I-bands
- lighter areas
- only contains thin filament
H-zone
- middle of A-band
- hard to see on micro view
- only contain myosin heads
M-line
- middle of sarcomere
- no distinctive marking
Actin (thin filaments)
- projects between myosin filaments
- contains active sites that bind to myosin
- composed of three proteins
- anchored at z-disc
What three proteins compose actin (thin filaments)?
- actin: contains myosin-binding site
- tropomyosin: covers active site at rest
- troponin (anchored to actin): moves tropomyosin
Myosin (thick filament)
- about 2/3 of muscle protein is myosin
- two intertwined filaments
- globular heads
- titin as stabilizer
globular heads:
- “myosin head”
- protrude 360 degrees from thick filament axis
- will interact with actin filaments for contraction
- heads will flutter which drives shortening of sarcomere
- two heads present
Titin
- stabilizer for myosin
- anchors thick filament to z-disc
- muscle injury will disrupt titins which causes thick filaments to fall over
- more likely damaging in muscle injury
Motor unit
a single alpha motor neuron and all the muscle fibers it innervates
Synapse (Neuromuscular cleft)
gap between the neuron and sarcolemma
neuromuscular junction
- consists of synapse between alpha motor neuron and muscle fiber
- serves as the site of communication between neuron and muscle
motor end plate
- pocket formed around motor neuron by sarcolemma
- other side that would receive the signal and start new propagation of muscle signal
Muscle actions
- static
- dynamic
static muscle action:
- muscles generate force without movement taking place
- measurement of effort at a single joint angle at a time
- muscle length remains the same (isometric)
dynamic muscle action:
- apply force to move an object/body segment
- measurement of effort through a range of joint angles
- muscle length changes during movement
Muscle shortening:
Muscle lengthening:
concentric
eccentric
after someone has had an injury what muscle action do you start with?
static because you won’t irritate the muscle by changing its length
Muscle concentric action
- a muscle performs work by shortening
- this action pulls on tendons attached to the bone and movement occurs
When we say “i want to lift my arm up” what happens?
we pull sarcomeres in on each other, shorten sarcomeres up gives us length change of overall muscle
Sliding filament theory:
- relaxed state
- contracted state
relaxed state of sliding filament theory
- no actin interaction occurs at binding site
- myofilaments overlap a little
- go through periods of relaxed state where calcium is basically locked up and no contraction is happening (micro level: brighter mid section)
contracted state of sliding filament theory
- when activated, myosin binds with actin
- myosin head pulls actin toward sarcomere center (power stroke)
- filaments slide past each other
- sarcomeres, myofibrils, muscle fiber all shorten
- pulling fibers over each other (power stroke)
H-zone from relaxed to contracted
- shortens
- area that contains only myosin heads reduced
I-band from relaxed to contracted
- smaller
- area that contains only actin (thin filaments)
A-band relaxed to contracted
- stays constant
- just length of thick filament
- never changes
M-line relaxed to contracted
- no change
- middle of sarcomere
describe the central governor theory and its importance during fatigue
- central control center regulates exercise performance
- reduces motor output to exercising muscle
- protects against catastrophic disruptions of homeostasis
- basically tells muscle to stop working so hard
define cardiac output, what two factors contribute to cardiac output?
- the amount of blood pumped by the heart each minute
- stroke volume and HR
The process why which a nerve stimulus initiated in the brain causes a muscle contraction:
brain > nerve > muscle > contraction
Muscle contraction: excitation-contraction coupling
- action potential (AP): reaches muscle fiber
- Calcium release: Ca2+ is released
- Troponin activated: Ca2+ binds to troponin
- cross-bridge: myosin head attaches to actin, cross bridges formed
- power stroke: myosin head pulls actin inward, using “power stroke”
- reset: myosin detaches from actin, resets
step 1: AP arrives at axon terminal
- ACh is released and the muscle membrane is depolarized
- calcium pushes vesicles to outer edge
- once bound, AP forms on sarcolemma or muscle membrane
- AP goes both ways so it gets the whole muscle
step 2: calcium released
- Ca2+ released from SR
- AP comes down and in t-tubule there is another specialized receptor which is voltage gated
- calcium leaves the sarcoplasmic reticulum and floods muscle cell
- calcium will continue to flood out
- when calcium exits, it binds with tropomyosin
step 3: calcium activates troponin
- at rest, tropomyosin covers myosin-binding site, blocking actin-myosin attraction
- Ca2+ binds to troponin, configuration changes
- physically moves tropomyosin; exposing binding sites
- myosin head can now form cross bridge with actin
step 4: cross-bridge
- myosin heads bind to actin, forming a cross bridge
step 5: myosin moves actin
- myosin head moves actin toward the M-line called the power stroke
- action requires ATP
- moves from energized to non-energized position
- ATP was already bound, which is why it was energized
step 6: reset
- myosin head detaches from myosin-actin binding sites
- myosin head moves back to the initial position
- requires ATP
- reset to keep process moving
- New ATP comes into play, attaches to myosin head which signals “release” from actin site (causes de-coupling of cross bridge)
Muscle relaxation: Ca2+ uptake
- as long as neural impulses arrive and Ca2+ concentration remain high, force generation continues
- when the impulse stops, calcium levels drop and force decreases as Ca2+ is pumped back into SR
- once Ca2+ drop below a critical level, thin filament inhibition again resumes
- last step in muscle relaxation
energy for muscle contraction
- muscular action requires energy (chemical (ATP) > mechanical (contractions))
- myosin contains the binding site for ATP
- enzyme located on myosin head (ATPase) splits ATP into adenosine diphosphate (ADP), inorganic phosphate (Pi) - “hydrolyzes” ATP - and energy
- energy released during this process is used to drive muscle contraction
- ATP > ADP + Pi + energy
source of ATP
- phosphocreatine (PC)
- glycolysis
- oxidative phosphorylation
Muscle fiber types
- three muscle fiber types exist in human skeletal muscle and differ in their function properties
contractile properties of muscle fiber types
- maximal specific force production (labeled specific force production)
- speed of contraction (Vmax)
- maximal power output = force x shortening velocity
- fatigue resistance
- muscle fiber efficency
Nonathletes fiber type and performance
- approx 50% slow and 50% fast fibers
- of fast-twitch fibers: 25% IIa and 25% IIx
- older adults typically lose their fast fibers
Power athletes fiber type and performance
- higher percentage of fast fibers
- e.g. elite sprinters (70-75% type II)
endurance athletes fiber type and performance
- higher percentage of slow fibers
- e.g. distance runners (70-80% type I)
Ratio of fiber type and performance is largely driven by:
genetics
fiber type is not the only variable that determines the success of an athlete:
- cardiovascular function
- motivation
- training habits
- muscle size
size principle:
smallest alpha motor neuron recruited first: smaller cell volume means the same stimulus has a greater impact on its resting potential
types of motor units:
- type I (slow) (smallest)
- type IIa (fast, fatigue resistant) (intermediate size)
- tyoe IIx (fastest, fatigable) (largest)
recruitment pattern during incremental exericse
type I > type IIa > type IIx
speed of myosin ATPase varies
- type I - slow myosin ATPase = slow contraction cycling
- type II - fast myosin ATPase = fast contraction cycling
sarcoplasmic reticulum fiber type characteristics
- type II more highly developed SR
- calcium more quickly available; pumped faster (fast fibers)
Motor units fiber type characteristics
- type I - small cell body <300 fibers
- type II - larger cell body >300 fibers
How are muscle fibers typed?
- muscle biopsy
- immunohistochemical staining
- gel electrophoresis
muscle biopsy
- small piece of muscle removed
- may not be representative of entire body
immunohistochemical staining
- selective antibody binds to unique myosin isoforms
- fiber types differentiated by differences in color
gel electrophoresis
- identify myosin isoforms by separating myosin isoforms on gel
What affects the force and speed of muscle contraction?
- types and number of motor units recruited (activated)
- increase motor units = increase force
- increase type II fibers = increase force and velocity
- length-tension relationship (sarcomere length)
- frequency of stimulus
- force-velocity relationship
muscle twitch
- contraction as the result of a single depolarization (caused by a stimulus)
- latent period (action potential arrived but contraction has not started)
- contraction
- relaxation
speed of contraction is faster in type II fibers
- SR releases Ca2+ at a faster rate
- faster myosin ATPase activity
Summation
- multiple stimuli occur quickly enough that the muscle cannot fully relax between stimuli and the force from one twitch is added to the force from the previous twitch
tetanus
- summation where stimuli occur fast to prevent any relaxation between stimuli (causes smooth contraction)
Force-velocity relationship
- high force lifts can only happen slowly
- low force lifts can be fast
high force lifts can only happen slowly
- need of more actin and myosin cross-bridge connection at any one point in time to maintain and generate force
low force lifts can be fast
- fewer cross-bridge connections are needed at one point in time to maintain force
- more myosin heads can let go at any one point in time while maintaining the required force
- allows for faster cross bridging cycle to occur
satellite cells
- play a key role in muscle growth and repair
- a single nuclei can only maintain (produce proteins for) a finite volume
- satellite cells merge with the much fiber and become new nuclei for that fiber
muscle fatigue
- fatigue is defined as a decline in muscle power output
- cause of muscle fatigue dependent upon exercise intensity and duration
- central fatigue
high-intensity short-duration exericse
accumulation of lactate, H+, ADP, Pi, and free radicals
long-duration exercise
muscle factors:
- accumulation of free radicals
- electrolyte imbalance
- glycogen depletion
central fatigue
- reduced nerve transmission to muscle
- current research suggests that fatigue is related to both central and peripheral factors
muscle cramps
- erratic, involuntary muscle contractions
causes of muscle cramps
- electrolyte depletion theory
- altered neuromuscular control theory
electrolyte depletion theory
sodium loss via sweating causes spontaneous muscle contractions due to loss of normal resting membrane potential
altered neuromuscular control theory
- muscle fatigue causes abnormal activity of the muscle spindle and golgi tendon organ
- leads to abnormal firing of alpha motor neurons
adaptations to resistance training
- neural adaptations responsible for early gains in strength
- evidence that neural adaptations occur
neural adaptations responsible for early gains in strength
strength gains during first 8 weeks of training are largely due to nervous system adaptations
evidence that neural adaptations occur
- muscular strength increases in first two weeks of training without increase in muscle fiber size
- phenomenon of “cross education” - training of one limb results in increases of strength in untrained limb
neural adaptations include:
- increased neural drive
- increased number motor units recruited
- increased firing rate of motor units
- increased motor unit synchronization
- improved neural transmission across neuromuscular juction
training adaptations to muscle mass
- hyperplasia
- hypertrophy
hyperplasia
increased number of fibers
- unclear if hyperplasia occurs in humans
hypertrophy
- increased cross-sectional area of muscle fibers
- hypertrophy is likely the dominant factor in resistance training-induced increases in muscle mass
- hypertrophy due to increased muscle proteins (that is actin and myosin)
- leads to an increase in maximal force generating capacity
muscle soreness
- delayed onset muscle soreness (DOMS)
- eccentric exercise causes more damage than concentric exercise
- slowly begin a specific exercise over 5 to 10 training sessions to avoid DOMS
Delayed onset muscle soreness (DOMS)
- appears 24 to 48 hours after strenuous exercise
- due to microscopic tears in muscle fibers or connective tissue
steps leading to DOMS
- strenuous muscle contraction results in muscle damage
- membrane damage occurs
- calcium leaks out of SR and collects in mitochondria
- results in inflammatory process
- edema and histamines stimulate pain receptors
muscle injury
- repeated lengthening contractions can cause nerve damage to the muscle fiber
- during lengthening contractions, actin filaments are pulled apart in the opposite direction by an external force on the muscle
- streaming of Z-lines
muscle atrophy
- limb immobilization
- changes occur in a matter of hours
- during first 6 hours: decreased rate of protein synthesis and “use it or lose it”
- decreased strength
- affects both type I and II fibers
- muscles can recover when activity is resumed
