Topic 10 Flashcards
Excitable muscle
respond to stimulus by producing action potentials
Contractile muscle
can shorten, thicken
Extensible muscle
stretch when pulled
Elastic muscle
return to regional shape after contraction or extension
4 muscle functions
- movement
- posture, facial expression
- heat production
- protection of viscera
Each muscle fibre innervated by only..
1 neuron
Axon of motor neuron branches to..
innervate several muscle fibres. 1 neuron is about 150 fibres within the same whole muscle
Motor unit
single motor neuron and ALL the muscle fibres it innervates
Neuromuscular junction structure
- presynaptic cell (neuron) with ACh (nt) in vesicles
- postsynaptic cell (muscle) membrane (sarcolemma) specialized region with ACh receptor (=motor end plate)
- two membranes speared by synaptic cleft
Neuromuscular junction function first step
AP reaches axon terminal and synaptic end bulb of neuron
Neuromuscular junction function second step
Ca enters via voltage gates and causes exocytosis of ACh
Neuromuscular junction function fourth step
chemical gates open and Na enters so end plate potential (EPP= depol. GP)
Neuromuscular junction function fifth step
PP causes opening of Na voltage gates on adjacent sarcolemma which creates an AP and propagates along sarcolemma
1 AP neuron equals..
1 EPP and 1 AP always!
In a relaxed muscle ..
tropomyosin covers myosin binding on the actin and the myosin head is activated
Myosin head activation 3 steps:
- excitation of muscle fibre (electrical event)
- excitation-contraction coupling (electrical to mechanical event)
- contraction (mechanical event) = sliding filament mechanism
Excitation of muscle fibre
a) sarcolemma depolarized - EPP –> AP
b) AP propagates down t-tubules to deep within fibre
Excitation-contraction coupling
c) AP in t-tubules cause release of Ca (coupling agent) from terminal cisterna of sarcoplasmic reticulum (SR) via mechanically gated channels
d) Can binds to troponin
e) troponin-tropomyosin complex moves, exposing myosin binding sites on actin
Contraction = sliding filament mechanism
f) activated myosin heads attach to binding sites inaction (cross bridge formation)
g) energy stored in myosin head released -myosin head pivots (=POWER STROKE), ADP+Pi are released. Actin slides over myosin toward centre of sarcomere
h) ATP attachés to myosin head, causing its release from actin + pivots = RECOVERY STROKE
i) myosin head reactivates (ATP –> ADP + Pi)
j) if Ca in cytosol remains high, these steps repeat (as many times to shorten the sarcomere)
Sliding filament mechanism 3 steps
- sarcomeres shorten: H zone, I band shorten. A band = same length
- Myofibrils shorten = muscle shortens
- thin actin and thick myosin my-filaments remain same length
Relaxation 4 steps
- Act broken down by AchE on motor end plate (facing cleft)
- SR actively takes up Ca (Ca ATPase)
- ATP binds to and release myosin heads
- tropomyosin moves back to cover myosin binding sites on actin
ATP necessary for 4 reasons
- cross bridge release (ATP not broken down)
- activation of myosin (ATP –> ADP + Pi) + power stroke
- pump Ca into SR
- fibre Na K ATPase activity
Rigor Mortis (stiffness of death)
- myosin heads still activated even after death and can bind to actin
- ATP production gradually stops (no O2)
- starts 3 hrs after death (max 12 hrs)
- gradually subsides over days as cells break down
Extracellular Ca as clinical application
-stabilizes Na+ voltage gates (keeps them closed in the absence of APs) ∴ if extracellular Ca++ low (pregnancy, lactation) – gates open & Na+ enters fibre → cramps (contractions)
Conditions/substances resulting in flaccid paralysis:
- myasthenia gravis
- curare poisoning
- botulism
Myasthenia gravis
decrease in Ach receptors (autoimmune). use AchE inhibitors to increase binding to remaining receptors
Curare poisoning
prevents Act from binding to receptors (was used in surgery)
Botulism
- improper canning= clostridium botulinum
- prevents exocytosis of Ach
- used to control blinking, cross eyes
Substances resulting in muscle contractions
- nicotine: binds to receptors and mimics Ach effect. causes muscle spasms
- black widow spider venom: massive release of Ach and stops breathing
Muscle tension
force exerted by a muscle or muscle fibre and determined by # of cross bridges formed
Muscle tension affected by single stimulus
produces a twitch (not normally occurring in skeletal muscle)
Twitch
weak contraction and relaxation
4 steps of single stimulus
- 1 stimulis = 1 AP
- latent period (associated with excitation)
- contraction period: high tension, cross bridge formation + sliding filaments. much Ca release from SR on stimulation, but taken back rapidly by SR CaATPase (not max tension reached)
- relaxation: decrease tension, Ca pumped into SR, ATP release myosin
2nd stimulus arrives before complete relaxation of 1st stimulus
- muscle AP over but uptake of Ca by SR not complete, so second stimulus causes release of more Ca, adding to that already in cytosol (more myosin heads can attach)
- produces 2nd contraction with higher tension (wave summation)
Rapid sequence of stimuli
- tension increases further (high Ca availability so wave summation)
- partial relaxation between contractions produces quivering (incomplete tetanus)
High frequency of stimuli
- no relaxation between contraction contractions (complete tetanus)
- highest tension: all troponin saturated with Ca + fibre warm (ATP synthesis) works faster
- occurs normally in body
Fibre length: resting length
most optimum: max # of cross bridges formed upon stimulation (max tension)
Fibre length: shorter
thin filaments overlap and interfere with cross bridge formation (fewer cross bridges form and decrease tension)
Fibre length: stretched
not all myosin heads near actin binding sites (fewer cross bridges form and decrease tension)
Size of fibre
thicker = more myofibrils/fibre and more tension
2 types of fibres in a muscle
- fast: contract/relax rapidly (white w little myoglobin)
- slow: contract/relax slowly (red w more myoglobin)
In a whole muscle tension is affected by
- number of fibres contracting
- # fibres/ motor unit
- muscle size (more fibres and myofibrils)
- fatigue
Number of fibres contracting
more active motor units = high tension (small motor units recruited first)
Number fibres/motor unit
more fibres/unit = higher tension
Muscle tone
low level of tension in a few fibres that develops as different groups of motor units are alternately stimulated over time (firmness to muscle)
2 types of whole muscle contraction
- isotonic
- isometric
Isotonic
muscle changes length (elbow flex). tension exceeds the resistance of load lifted. uses ATP
Isometric
muscle length starts constant. tension less than required to move load, but tension increases (cross bridges form but no shortening). uses ATP
Muscle metabolism is
energy for contraction
Muscle metabolism during resting conditions
- fatty acids used to produce ATP (anerobic)
- storage of glycogen, creatine phosphate, and little ATP
Muscle metabolism during short term exercise (< 1 min)
- primarily anaerobic
- use available ATP creatine phosphate used to produce ATP
- muscle glycogen –> glucose –> pyrvric acid –> anaerobic pathway –> lactic acid
Muscle metabolism during long term exercise
- ATP from aerobic pathway
- glucose from liver
- fatty acids: used more as exercise continues
- O2 sources: blood hemoglobin and muscle myoglobin
Physiological muscle fatigue
- inability to maintain tension
- fatigue decrease ATP uses (protective)
Physiological muscle fatigue due to..
- depletion of energy supplies
- build up of end products
- failure of APs: increase K in t tubules during rapid stimuli and disturbs MP, stops Ca release from SR
Psychological fatigue of muscle fatigue
failure of CNS to send commands to muscles (due to lactic acid)
EPOC
excess post exercise O consumption
EPOC: O2 used to
- replenish stores of glycogen, C P, O2, on Hb. myoglobin.
- convert lactic acid to pyruvic or glucose
- higher body temp from exercise = higher O2 demand
