skeletal muscle physiology Flashcards
muscle characteristics
- elastic - return to original shape after contraction
- contractile - can shorten and thicken
- extensible - stretch when pulled
- excitable - respond to stimuli
muscle function
- movement
- posture, facial expression
- heat production
- protection of viscera
neuromuscular junction
- each muscle fiber innervated by only one neuron
- a single motor neuron + all muscle fibers it innervates = a motor unit
structure of motor unit
- presynaptic cell with ACh in vesicles
- postsynaptic cell (muscle) membrane (sarcolemma)- specialized region ACh receptors
- two membranes separated by synaptic cleft
function of a motor unit
- AP reaches axon terminal and synaptic end bulb of neuron
- Ca++ enters via voltage gates - causes exocytosis of ACh
- ACh binds to ACh receptors on motor end plate
- chemical gates open and Na enters - end plate potential
- EPP causes opening of Na+ voltage gates on adjacent sarcolemma
what happens in a relaxed muscle
- tropomyosin covers myosin binding sites on the actin
- the myosin head is activated
myosin head activation
ATP - ADP +Pi + energy
steps of myosin head activation
- excitation of muscle fibre
a. sarcolemma depolarized
b. AP propagates down T-tubules to deep within fibre - excitation-contraction coupling
c. AP in T-tubules cause release of Ca from terminal cisternae of SR by mechanically gated channels
d. Ca binds to troponin
e. troponin-tropomyosin complex moves exposing myosin binding sites on actin - contraction (mechanical event)
f. activated myosin heads attach to binding sites on actin
g. energy stored in myosin head is released
h. ATP attaches to myosin head, causing its release from actin
I. myosin head reactivates
j. if Ca in cytosol remains high, these steps repeat
sliding filament mechanism
- sarcomeres shorten
- myofibrils shorten muscle shortens
- thin (actin) and thick (myosin) myofilaments remain the same length
relaxation
steps:
1. ACh broken down by AChE on motor end plate (facing cleft)
2. SR actively takes up Ca++
3. ATP binds to and releases myosin heads
4. tropomyosin moves back to cover myosin binding sites on actin
what is ATP necessary for
- cross bridge release (ATP not broken down)
- activation of myosin
3/ pump Ca into SR - fibre Na/K ATPase activity
Rigor Mortis
- myosin heads still activated even after death can bind to actin
- ATP production gradually stops (no O2)
- starts 3 hours after death
flaccid paralysis
a. myasthenia gravis
b. curare poisoning
botulism
- improper canning
- prevents exocytosis of ACh
- used to control uncontrolled blinking , crossed eyes
- cosmetic - botox (wrinkles, sweating)
substances resulting in muscle contractions
a. nicotine
- binds to receptors + mimics ACh effect
- muscle spasms
b. black widow spider venom
- massive release of ACh - stops breathing
muscle tension
= force exerted by a muscle or muscle fibre determined by # of cross bridges formed
in a fibre
what effects the number of cross bridges formed
- frequency of stimulation
- fibre length
- size of fibre
- fatigue
periods of a single stimulus
a) 1 stimulus = 1AP (lasts 1-2 msec)
b) latent period (2 msec)
- processes associated with excitation and excitation contraction coupling
c) contraction period (10-100 msec) increase tension
- cross bridge formation + sliding filaments
- lots Ca++ released from SR on stimulation but taken back rapidly
d) relaxation - decrease in tension
- Ca++ pumped into SR; ATP releases myosin
frequency of stimulation
a. single stimulus - produces a twitch (weak contraction and relaxation)
b. 2nd stim. arrives before complete relaxation from 1st
c. rapid sequence of stimuli
- tension increases further
- partial relaxation between contractions
d. high frequency of stimuli
- no relaxation between contractions
- highest tension, all troponin saturated with Ca++
fibre length
a. resting fibre length is optimum
b. decrease tension if shorter or longer when stimulated
size of fibre
- thicker = more myofibril
- thicker = more tension
- increase with e.g. exercise = testosterone
fatigue
- muscle does not contract well
- reduced max tension
how to fibre types in a muscle differ
- fast - contract/ relax rapidly - white (little myoglobin)
2. slow - contract, relax slowly -red (more myoglobin)
in a whole muscle how is tension affected
- number of fibres contracting
- - small motor units recruited first, then larger ones added when tension is needed - # fibres/motor unit
- more fibres = increase tension
- muscle size
- larger = more fibres - fatigue
muscle tone
- low level of tension in a few fibres that develops as different groups of motor units are alternately stimulated over time.
- gives firmness to muscle
types of whole muscle contraction ex: lifting a book
- isotonic
- muscle changes length
- uses ATP
- flexion at the elbow - isometric
- muscle length constant
- tension less than required to move load
- uses ATP
- tension increases
what happens during resting conditions
a) fatty acids used to produce ATP
b) storage of:
I) glycogen
ii) creatine phosphate
iii) little ATP
what happens during short term exercise ex: sprinting
- primarily anaerobic
a) use available ATP
b) creatine phosphate used to produce ATP
c) creatine glycogen - glucose - pyruvic acid - anaerobic pathway - lactic acid
what happens during long term exercise (1min to hours)
- ATP - from aerobic pathway
- glucose (from liver)
- fatty acids, used more as exercise continues
- O2 sources: blood hemoglobin + muscle myoglobin`
types of muscle fatigue
1) physiological fatigue
- inability to maintain tension
- fatigue decreases ATP use
2. psychological fatigue
- failure of CNS to send commands to muscles - probably due to lactic acid
why cant cross bridges not release ATP in physiological fatigue
a) depletion of energy supplies
b) build-up of end products
EPOC
excess post-exercise O2 consumption
- recovery O2 consumption (deep rapid breathing)
- also increases in body temp from exercise = increases O2 demand
what is O2 used for in EPOC
- replenish stores of glycogen
- convert lactic acid to:
- pyruvic acid - krebs
- glucose in liver
