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muscle characteristics
excitable — respond to stimuli and produce APs
contractile — can shorten and lengthen
extensible — stretch when pulled
elastic — return to its original shape after contraction/extension
muscle functions
movement
ex. walking, breathing, running
pull on bone across joints to create movement
posture and facial expression
ex. sitting (posture) — muscles are constantly working to keep the body upright
facial muscles are connected to skin, not bones — provides non-verbal communication
heat production
generate heat when contracting
cold → muscles shiver to crank up the heat
protection of viscera
where no thick bones shield
tense up and absorb impact
ex. rectus/transverse abdominus, oblique
motor unit
a single motor neuron and all the muscle fibres it innervates
presynaptic cell
a motor neuron with ACh (nt) vesicles in its axon terminal
postsynaptic cell membrane
a muscle sarcolemma
motor end plate
a specialized region on a sarcomlemma with many ACh receptors that detect signals and trigger contractions
steps of AP on a muscle sarcolemma
AP reaches the axon terminal and synaptic end bulb of a motor neuron
Ca2+ enters via voltage gates, causing exocytosis of ACh
ACh binds to ACh receptors on the motor end plate
chemical gates open and Na+ enters, causing an end plate potential (EPP)
EPP causes opening of Na+ voltage gates on adjacent sarcolemma; AP then propagates along the sarcolemma and down the T-tubules
myofibril
a structure in a muscle fiber that shortens when the muscle contracts
sarcomere
basic structural unit of contraction
myosin
thick filament in a muscle fiber
actin
thin filament in a muscle fiber
steps of muscle fiber contraction
excitation of muscle fiber
i. sarcolemma depolarized → EPP → AP
ACh binds to motor end plate
ii. AP propagates down the T-tubules to deep within the fiber
brings the electrical signal closer to SR (stores Ca2+)
excitation-contraction coupling
i. AP in T-tubules cause the release of Ca2+ from terminal cisternae of the sarcoplasmic reticulum (SR) via mechanically gated channels
“coupling agent” — links electrical (AP) to mechanical (contractions) event
ii. Ca2+ binds to troponin
high concentration inside the SR to low in the cytosol
troponin responds to Ca2+ levels
changes shape when Ca2+ binds, and shifts tropomyosin
iii. troponin-tropomyosin complex moves, exposing myosin binding sites on actin
contraction
i. activated myosin heads attach to binding sites on actin — “cross bridge” formation
ii. energy stored in myosin head is released → myosin head pivots (”power stroke”), ADP + Pi released → actin slides myosin toward center of sarcomere (M line)
thin filament pulled inward
iii. ATP attaches to myosin head → released from actin and unpivots (”recovery stroke”)
myosin head gets back to its position
iv. myosin head reactivates — ATP → ADP + Pi
v. if Ca2+ in cytosol remains high, these steps repeat
power stroke
the movement of the myosin head pulling actin filaments during muscle contraction
recovery stroke
the process of the myosin head reattaching to actin after a movementduring muscle contraction
sliding filament mechanism
sarcomeres shorten
H zone and I band shorten
A band is same length
myofibrils shorten → muscle shortens
thin (actin) and thick (myosin) myofilaments remain the same length
steps of muscle fiber relaxation
ACh broken down by AChE on the motor end plate (facing cleft)
SR actively takes up Ca2+ (using Ca2+ ATPase)
ATP binds to and releases myosin heads
tropomyosin moves back to cover myosin binding sites on actin
things that ATP is necessary for
cross bridge release — not broken down
activation of myosin (ATP → ADP + Pi)
pump Ca2+ into SR
fiber Na+/K+ ATPase activity
botulism
a rare but potentially fatal illness caused by botulin toxin produced by the bacterium Clostridium botulinum, due to improper canning
prevents exocytosis of ACh, causing flaccid paralysis
medical application: used to treat uncontrolled blinking and crossed eyes
cosmetic application: used to reduce wrinkles and sweating
rigor mortis
a condition that occurs after someone passes where muscles stiffen up
intracellular Ca++ increase from ECF and SR (leakage) → binding sites exposed (cross bridges form) → myosin heads not released from actin (no new ATP produced)
starts ~3 hrs after death, max ~12 hrs
gradually subsides over days as cells break down
myasthenia gravis
an autoimmune disorder that leads to flaccid paralysis
decrease in ACh receptors (blocked/destroyed by antibodies) → ACh can’t bind effectively
treatment: AChE inhibitors → increase ACh binding to remaining receptors
curare poisoning
a condition caused by the use of curare, a plant-based toxin, that results in flaccid paralysis
prevents ACh from binding to receptors
was used in surgery to temporarily paralyze a patient during procedure
nicotine
a drug that mimics ACh effects and binds to receptors, producing muscle spasms/twitching
stronger, longer-lasting contractions
chronic use → too much ACh in body → body compensates → less ACh + receptors (due to too much stimulation) → rely on nicotine → addiction
quit → reverse but takes time → withdrawals
black widow spider venome
a substance that triggers a massive release of ACh causing muscles to continuously contract andcant relax, may lead to a person to stop breathing
causes spasmic paralysis
muscle tension
the force exerted by a muscle or muscle fiber
determined by the number of crossbridges formed — more cross bridges = higher force/tension
wave summation
the process by which muscle contractions can increase strength by utilizing successive stimuli to enhance tension
incomplete tetanus
a state of partial muscle contraction resulting from rapid successive stimuli that do not allow the muscle to completely relax, leading to a sustained but not maximal contraction
complete tetanus
a condition where a muscle remains fully contracted due to a high frequency of stimulation, resulting in maximum tension without relaxation
factors that affect muscle tension in a fiber
frequency of stimulation
a. single stimulus
b. 2nd stimulus arrives before relaxation from 1st → wave summation
c. rapid sequence of stimuli → incomplete tetanus
d. high frequency of stimulu → complete tetanus
fiber length
resting fiber length is optimal
tension decreases if shorter/longer
size of fiber
thicker = more myofibrils/fibers = more crossbridges form = more tension
fatigue
reduced max tension
fast fibers
a type of muscle fiber that contracts and relaxes quickly
appear white, has little myoglobin
great for speed, quick and powerful bursts — ex. sprinting, weight lifting
ex. white meat in chicken — breasts and wings
slow fibers
a type of muscle fiber that contracts and relaxes slowly, sustaining contractions longer
appear red, have a lot of myoglobin
ex. postural muscles
great for endurance activities — ex. marathon running
ex. dark meat in chicken — legs
factors that affect muscle tension in a whole muscle
number of fibers contracting
more active motor neurons = more tension
number of fibers per motor unit
more units/fiber = more tension
muscle size
larger = more fibers = more tnesion
fatigue
size principle
a principle that states that muscle fibers are recruited from smallest to largest based on the force needed
muscle tone
low level of tension in a few fibers that develops as different groups of motor units are alternately stimulated over time
gives firmness to muscles
small amt of tension even when muscle is relaxed
isotonic contraction
a type of whole muscle contraction in which the muscle changes length while generating force, maintaining constant tension
trension exceeds the resistance of a load lifted
uses ATP
isometric contraction
a type of whole muscle contraction where the muscle generates tension without changing length, maintaining an equal force against a load
when a load doesn't budge because the force isn't enough to move it
there isn’t enough strength to overcome resistance
still uses ATP because crossbiedges are still actively working
muscle metabolism during resting conditions
fatty acids used to produce ATP — aerobic
storage of:
glycogen
creatine phosphate (C~P)
ATP + creatine → ADP + C~P
little ATP
muscle metabolism during short-term exercise
primarily anaerobic
use available ATP
last 4-6 secs
creatine phosphate (system) used to produce ATP
C~P + ADP → ATP + creatine
lasts ~15 secs
C~P is a high-energy molecule
muscle glycogen → glucose → pyruvid acid → anaerobic pathway → lactic acid
lasts ~30 secs
muscle metabolism during long-term exercise
ATP — from aerobic pathway
glucose — from liver
fatty acids — more as exercise continues
O2 sources: blood hemoglobin + muscle myoglobin
but sometimes anaerobic
physiological muscle fatigue
a type in muscle fatigue that results from the inability to maintain tension
lowers ATP use
factors of physiological muscle fatigue
depletion of energy supplies — ex. glycogen
build-up of end products
a. H+ from lactic acid
muscle contraction compresses blood vessels → ↓ O2 to muscle
ATP production is anaerobic for periods, even in long-term exercise
can inhibit hydrolysis (no ATP)
b. Pi (from ATP → ADP + Pi) binds to Ca2+
less binds to troponin
slows release of Pi from myosin → slows cross bridge release from actin
weakens contraction
everything still work but not as efficient
failure of APs (in muscle fiber)
increase [K+] (build up) in small spaces of T-tubules during rapid stimuli → disturbs MP → stops Ca2+ release from SR
membrane doesn't repol properly, voltage channels wont behave properly → no contractions even if NS sending signal
long term: neuron runs out of ACh
psychological fatigue
a type of psycholocial0n hiwch