two primary functions of the musculoskeletal system
movement and stability
storage of minerals
What is the name of the connection btwn the nervous system and the skeletal system?
neuromuscular junction
name the three types of muscle tissue, whether they are under voluntary or involuntary control, and which nervous systems control each type
skeletal muscle: voluntary, somatic
cardiac: involuntary, autonomic (heart beating)
smooth muscle: involuntary, autonomic (digestion)
functions of the skeletal system
support and protect the body
aid in movement
store nutrients
produce blood cells
functions of the muscular system
bodily movements
stability
internal movement of substances within the body
smooth muscle
contains spindle-shaped, NON-STRIATED, UNI-NUCLEATED fibers
occurs in walls of internal organs
INVOLUNTARY
cardiac muscle
has STRIATED, branched, UNI-NUCLEATED fibers
occurs in walls of the heart
INVOLUNTARY
skeletal muscle
has STRIATED, tubular, MULTI-NUCLEATED fibers
usually attached to the skeleton
VOLUNTARY
connective tissue connecting the musculoskeletal system
ligament: short band of tough, flexible, fibrous connective tissue that connects TWO BONES or cartilage, holding together a joint
tendon: connective tissue attaching MUSCLE TO BONE; when a muscle contracts to move a joint, it is the tendon that pulls on the bone
cartilage: soft cushioning substance that covers the ends of bones; acts as shock absorber and prevents friction btwn bones
skeletal muscle movement
when a muscle contracts it shortens (usually)
tension is placed on tendons connecting muscle to bone
the tension moves the bone at a joint
movement of the bone is toward the point of tendon insertion
flexor
muscles DECREASE the angle btwn two bones at a joint
extensor
muscles INCREASE the angle btwn two bones at a joint
antagonist vs agonist muscles
antagonist: flexors and extensors that act on the same joint to produce opposite actions; ex. triceps in a bicep curl
agonist: muscle is the prime mover of any skeletal movement; ex. quadriceps when straightening the leg
"layers" of muscle tissue from superficial to deep
muscle --> fascicle --> muscle fiber/myofiber/myocyte/muscle cell, --> myofibril --> myofilament
sarcolemma
specialized plasma membrane that surrounds ONE MUSCLE CELL
muscle cell/fiber/myofiber/myocyte
each fiber has densely packed subunits called MYOFIBRILS that run the entire length of the muscle fiber/cell as well as the entire muscle
myofibrils are composed of thick and thin MYOFILAMENTS called actin and myosin (proteins that pull on each other to cause contractions)
nuclei shoved to the side bc myofibrils fill up most of the cell space
sarcomere
unit of contraction
z-line to z-line
many sarcomeres repeated over the length of the muscle fiber=> myofibril
"parts" of sarcomeres
I bands, A bands, H zones, and z-lines/discs
I band
LIGHT in color
contain only THIN filaments; primarily of the protein ACTIN
A band
DARK in color
contain all of the THICK filament composed of protein called MYOSIN with some thin overlap
H zones
center of the A band with NO THIN filament overlap
Z disc/lines
dark lines found in the center of each I band; end/beginning of sarcomere
darkest area of sarcomere
where there is overlap of both myosin (thick filaments) and actin (thin filaments)
M lines
found in the center of each A BAND
help hold down thick filaments
titan
elastic filament protein that runs from Z disc to M line and allows ELASTIC RECOIL
holds thick filaments in place; aid in sliding filament theory
sliding filament theory
when a muscle contracts, SARCOMERES SHORTEN; proteins overlap, they do NOT get shorter
A bands move CLOSER together, but NO CHANGE in length of the A band
I bands SHORTEN, and "move closer" to H band; the region of overlap increases
H band shortens or disappears
Z lines/discs are moving in closer together
ONLY ACTIN AND Z-LINES MOVING IN
how do muscles contract? (summary)
actin filaments will slide past myosin filaments
myosin proteins form cross-bridges with the actin filaments, linking the two chains together (and HOLDING your muscle in a CONTRACTED state)
tropomyosin
protein that blocks the myosin binding sites on actin to prevent unwanted contractions
troponin
protein that binds actin to tropomyosin and calcium; moves tropomyosin out of the way to allow binding
role of calcium
when muscle is relaxed, tropomyosin blocks myosin binding sites
when muscle cells are stimulated by a signal from neurons, calcium is released inside the muscle fiber cytoplasm
calcium attaches to troponin, causing a shape change in troponin and tropomyosin; tropomyosin is pushed up and no longer blocking the binding sites on actin
myosin is allowed access to actin and forms CROSS BRIDGES
power stroke
the release of phosphate upon binding cocks the myosin head, producing a power stroke that pulls the THIN filament; keep pulling actin in one direction
cross bridge cycling
resting fiber; cross bridge is not attached to actin; tropomyosin blocking binding sites
cross bridge binds to actin
Phosphate intermediate is released from myosin head, causing a shape change in myosin
power stroke causes filaments to slide; ADP is released; myosin head is still bound to actin
a new ATP bind to myosin head, allowing it to release from actin
ATP is hydrolyzed snd phosphate binds to myosin causing cross bridge to return to its original orientation
process only happens if calcium is present to move tropomyosin from blocking binding sites*
function of sarcoplasmic reticulum (SR)
calcium storage and control
SR calcium control
stores calcium when muscle is at rest
when muscle fiber is stimulated, calcium diffuses out of calcium release channels
at the end of a contraction, calcium is actively pumped back into the SR
transverse tubules
narrow membranous tunnels formed from the sarcolemma
open to the extracellular environment
ABLE TO CONDUCT ACTION POTENTIALS
closely situated next to terminal cisternae of SR --> faster stimulation of SR from sarcolemma
stimulating a muscle fiber
acetylcholine (Ach) is released from the motor neuron, binds to Ach receptors in sarcolemma, Na+ enters muscle cell through channels
causes local membrane depolarization of sarcolemma (end plate potential), that stimulates voltage-gated channels
end plate potentials are generated and conducted along transverse tubules
voltage-gated calcium channels (VGCaC) in transverse tubules change shape and mechanically cause calcium channels in SR to open
calcium is released into the cytoplasm and can bind to troponin to push tropomyosin out of the way and stimulate a muscle contraction
relaxing a muscle fiber
end plate/action potentials cease
calcium release channels close
calcium-ATPase pumps move calcium back into SR through active transport
no more calcium is available to bind to troponin
tropomyosin moves to block the myosin heads from binding to actin
why does rigor mortis occur?
no longer making ATP, therefore the body is no longer pumping calcium into SR, allowing to stay bound to troponin to move tropomyosin out if the way for myosin to bind to actin --> contractions
no more ATP to release myosin from actin, so the body is stuck in a contracted state
myasthenia gravis
autoimmune disorder where the body makes antibodies that improperly recognize and block Ach receptors in the sarcolemma
result: severe muscle weakness
treatment: therapies with reversible inhibitors of acetylcholinesterase (AChE)- enzyme that breaks down Ach
latrotoxin
causes increased release of Ach vesicles --> increased muscle contraction
motor unit
single motor neuron and all the muscle fibers it innervates
all the muscle fibers in a motor unit contract AT ONCE
the more innervated the motor unit, the stronger the contraction (different muscles require different amount of power- ex. eyelid vs quad)
finer muscle control requires many smaller motor units (ex. eye lid, lots of control-neuron:muscle fiber ratio 1:4)
larger, stronger muscles may have motor units with 1: several hundred ratio (ex. quad- many more muscle fibers contracting from one neuron- less control)
graded contractions
varied contraction strength of overall muscle due to DIFFERENT numbers of motor units being stimulated
add up based on load
neuromuscular junction
site where a motor neuron stimulates a muscle fiber
one motor unit has many neuromuscular junctions
motor end plate
area of the muscle fiber sarcolemma where a motor neuron stimulates it using the NT Ach
further contracting strength comes from...
increased FREQUENCY of stimulation: increases contraction strength of a motor unit (fire more rapidly)
motor unit recruitment: if a stronger contraction is needed, MORE motor units will fire to cause more cells to contract
twitch
a stimulation of a muscle fiber/cell
small, single stimulation
ONE muscle fiber is a part of only ONE motor unit
has a latent period after stimulus and before contraction phase
latent phase
time between action potential and contraction
occurs bc there are many steps that must occur before contraction happens
action potential always releases same amount of calcium, therefore there is the same amount of contraction or strength
muscle contractions
twitch: small, single stimulation
summation: twitch + twitch (before relaxation)
unfused (incomplete) tetanus: summation of many twitches
fused (complete) tetanus: stimulation with no relaxation- max amount of force your muscles can provide; all the muscle fibers are contracted to their full length (myosin and actin have slid their max)
motor unit recruitment
asynchronous activation of motor units: some motor units START to twitch when others RELAX
produces continuous contraction of the whole muscle recruitment of additional motor units makes muscle contractions stronger
certain motor units are preferred (small forces = small motor units; large forces = large motor units)
are both temporal and spatial summation possible with skeletal muscle cells?
we see temporal (being close to temporal) but do not really see spatial
to achieve similar outcome to spatial in skeletal muscle cells is motor unit recruitment
velocity and force of muscle contractions
for muscle to contract, they must generate force that is GREATER than the opposing forces
the greater the FORCE, the SLOWER the contraction
isometric contraction
-muscle is working, but holding a pose (planks or yoga)
muscle does NOT change length
muscle tension is LESS than resistance
muscle can't shorten because the load is too great
still contracting but no movement occurs
isotonic contraction
muscle is working and movement occurs
muscle changes length (shortens or lengthens)
amount of power stays the same
muscle tension is greater than resistance
muscle fibers SHORTEN when the TENSION produced is just GREATER than the load
types of isotonic contractions
concentric contraction: muscle fiber SHORTENS when force is GREATER than load
eccentric contraction: muscle may actually LENGTHEN, despite contraction, if the load is too great ( allow you to lower a weight gently after full contraction)
factors that increase the force of skeletal muscle contraction
high frequency of stimulation (temporal summation and tetanus)
large number of muscle fibers recruited
large muscle fibers: if have larger fibers, you have more (contractile) myofilaments, and therefore have more sliding filaments
muscle and sarcomere stretched to slightly over 100% of resting length (length-tension relationship)
length-tension relationship
there is an ideal length of the sarcomere, where the length is just long enough to support the correct amount of muscle tension for contraction to occur
sarcomeres at resting length: optimal sarcomere operating length is 80-120% of resting length; tension is maximal (amount of actin and myosin overlap that is desired- give a little more contraction and generate more tension)
sarcomeres greatly shortened: actin collisions, no room to slide (already so close to z-lines)
sarcomeres excessively stretched: myosin can't bind to actin bc too far apart
what affects how fast muscles can contract and how long they can continue to contract until failure?
muscle type, load, and recruitment
metabolism and muscle contractions
muscle cells use energy from various sources over time
stored ATP: used up very quickly (within seconds)
creatine phosphate ( within seconds)
anaerobic metabolism: doesn't require oxygen and uses glycolysis for ATP production (within minutes)
aerobic metabolism: oxidative phosphorylation (within minutes or hours)
types of skeletal muscle fibers
slow twitch (1) and fast twitch (2)
slow twitch fiber
slow oxidative fibers
slowest velocity of contraction; long distance runner
go through krebs cycle and ETC to create ATP, therefore takes longer
slow bc need ATP for every myosin to release from actin
ex. soleus muscle
fast twitch fibers
fast oxidative fibers: middle ground, mixed oxidative and glycolytic production, middle distance runner
fast glycolytic fibers: fastest velocity of contraction, use of glycolysis for ATP production, ex. eyelid, sprinter
what determines the cross bridge cycle rate?
the rate of ATP production: if can make ATP faster, can go through cross bridge cycle faster
glycolytic vs oxidative muscle fibers
glycolytic: ATP production through glycolysis, few mitochondria, large fiber diameter, small capillary supply (not as reliant on oxygen), few myoglobin (anaerobic), fast fatigue rate (lactic acid build up)
oxidative: ATP production through oxidative phosphorylation in mitochondria, many mitochondria, small fiber diameter, large capillary supply (relies on presence of oxygen), many myoglobin (aerobic), slow fatigue rate (lactic acid build up)
inactivation of which protein(s) in a myofiber would result in an increased muscle contraction?
acetylcholinesterase, tropomyosin, calcium- ATPase pump
which protein provides elasticity to allow a sarcomere to recover from a contraction?
titin
Which part(s) of a sarcomere would you expect to shrink or disappear during a contraction?
H bands and I bands
Which step of the cross-bridge cycle allows for the filaments to slide past one another during a contraction?
myosin releasing Pi
Which of these events take place during stimulation of both neurons and muscle cells?
-opening of VGKC
opening of VGNaC
opening of VGCaC
release of Ach from synaptic vesicles
true or false: The calcium that binds troponin and the calcium that stimulates synaptic vesicle release come from the same intracellular source.
false