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Phys 1412 > Topic 10: Skeletal Muscle Physiology > Flashcards

Topic 10: Skeletal Muscle Physiology Flashcards

1
Q

Muscle Characteristics

A
  • excitable – respond to stimuli and produce action potentials
  • contractile – can shorten, thicken
  • extensible – stretch when pulled
  • elastic – return to original shape after contraction or extension
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2
Q

Muscle Functions

A
  • movement – e.g. walking, breathing
  • posture, facial expression
  • heat production ⇒ 37°C
  • protection of viscera – body wall
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3
Q

Neuromuscular Junction

A
  • each muscle fiber (cell) innervated by only 1 neuron
  • axon of motor neuron branches to innervate several muscle fibers (1 neuron ⇒ ~150 fibers within same whole muscle)
  • a single motor neuron and ALL the muscle fibers it innervates = a motor unit
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4
Q

Neuromuscular Junction Structure

A
  • presynaptic cell (neuron) with ACh (nt) vesicles
  • postsynaptic cell (muscle) membrane (sarcolemma) - specialized region with ACh receptors (= motor end plate)
  • two membranes separated by synaptic cleft
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5
Q

Neuromuscular Junction Function

A
  • AP reaches axon terminal and synaptic end bulb of neuron
  • Ca2+ 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 = a depolarizing GP)
  • EPP causes opening of Na+ voltage gates on adjacent sarcolemma ⇒ AP (AP has same properties/channels as on a neuron) – propagates along sarcolemma
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6
Q

Neuromuscular Junction Note

A
  • 1 AP (neuron) →1 EPP → 1 AP (always!)
    i. e. always a critical stimulus because:
  • lots of ACh released
  • motor end plate has many receptors ∴ to inhibit skeletal muscle must inhibit motor neuron
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7
Q

In a relaxed muscle

A
  • tropomyosin covers myosin binding sites on the actin

- the myosin head is activated

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8
Q

Myosin Head Activation

A
  • ATP (on head) breaks down to ADP (on head) and energy (stored in head)
  • once actin binding sites on actin are exposed, myosin binds
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9
Q

Excitation of muscle fiber (electrical event)

A
  • Sarcolemma depolarized - EPP ⇒ AP

- AP propagates down T-tubules to deep within fiber

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10
Q

Excitation-contraction coupling (electrical to mechanical event)

A
  • AP in T-tubules cause release of Ca2+ (coupling agent) from terminal cisternae of sarcoplasmic reticulum (SR) via mechanically gated channels
  • Ca2+ binds to troponin
  • Troponin-tropomyosin complex moves, exposing myosin binding sites on actin
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11
Q

Contraction (mechanical event) = Sliding Filament Mechanism

A
  • Activated myosin heads attach to binding sites on actin (cross bridge formation)
  • Energy stored in myosin head is released - myosin head pivots (= POWER STROKE), ADP + Pi are released. Actin slides over myosin toward center of sarcomere (M line)
  • ATP attaches to myosin head, causing its release from actin + unpivot = RECOVERY STROKE
  • Myosin head reactivates (ATP ⇒ ADP + Pi)
  • If Ca2+ in cytosol remains high these steps repeat
  • cycle repeats many times to shorten the sarcomere
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12
Q

Sliding Filament Mechanism – Sarcomere

A 
Sarcomeres shorten
-H zone, I band shorten
-A band = same length
Myofibrils shorten ∴ muscle shortens
thin (actin) and thick (myosin) myofilaments remain the same length
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13
Q

Muscle Fiber Relaxation Steps

A
  • ACh broken down by AChE on motor end plate (facing cleft) produces acetic acid (Krebs cycle) and choline
  • SR actively takes up Ca2+ (Ca2+-ATPase)
  • ATP binds to and releases myosin heads
  • Tropomyosin moves back to cover myosin binding sites on actin
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14
Q

Muscle Fiber Relaxation ATP necessary for

A
  • cross bridge release (ATP not broken down)
  • activation of myosin (ATP ⇒ ADP + Pi)
  • pump Ca2+ into SR
  • fiber Na+/K+-ATPase activity
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15
Q

Clinical Applications

A

Botulism, Rigor Mortis, Myasthenia gravis, Curare Poisoning, Nicotine, Black Widow Spider Venom

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16
Q

Botulism

A
  • improper canning - Clostridium botulinum
  • prevents exocytosis of ACh - flaccid paralysis
  • medical - treat uncontrolled blinking, crossed eyes
  • cosmetic – Botox (wrinkles, sweating)
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17
Q

Rigor Mortis

A
  • “stiffness of death”
  • intracellular Ca++ ⇑ from ECF, SR (there is leakage) ⇒ binding sites exposed (crossbridges) ⇒ myosin heads not released from actin (no new ATP produced)
  • starts ~ 3 hrs after death, max at about 12h
  • gradually subsides over days as cells break down
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18
Q

Myasthenia gravis

A
  • ⇓ in ACh receptors (autoimmune)
  • flaccid paralysis
  • treatment - AChE inhibitors (⇑ binding to remaining receptors)
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19
Q

Curare Poisoning

A
  • prevents ACh from binding to receptors

- flaccid paralysis – was used in surgery

20
Q

Nicotine

A

mimics ACh effect (binds to receptors) – get muscle spasms

21
Q

Black Widow Spider Venom

A

triggers massive release of ACh - muscles continuously contract - stop breathing

22
Q

Muscle Tension

A

= force exerted by a muscle or muscle fiber
-determined by number of cross bridges formed
In a fiber, affected by:
-Frequency of stimulation:
-Fiber Length
-Size of fiber
-Fatigue

23
Q

Frequency of stimulation

A
  • Single stimulus
  • 2nd stim. arrives before complete relaxation from 1st
  • Rapid sequence of stimuli
  • High frequency of stimuli
24
Q

Single stimulus

A

produces a twitch (a weak contraction and relaxation - not normally occurring in skeletal muscles)

  • single stimulus ⇒ 1 AP (lasts 1-2 msec)
  • latent period (~2 msec)
  • -excitation-contraction coupling occurring
  • contraction period (10-100 msec) - ⇑ tension
  • -cross bridge attachment and sliding filaments
  • -a lot of Ca2+ released from SR on stimulation, but taken back rapidly by SR Ca2+-ATPase, so not all myosin heads attach – does not reach maximum possible tension
  • relaxation - ⇓ tension
  • -Ca2+ pumped into SR; ATP releases myosin; etc
25
Q

2nd stim. arrives before complete relaxation from 1st

A
  • muscle AP always completed (refractory period) BUT uptake of Ca2+ by SR is not yet complete (fiber relaxing)
  • 2nd stimulus causes release of more Ca2+, adding to that already in the cytosol ⇒ more myosin heads can attach
  • produces 2nd contraction with ⇑ tension = wave summation (contraction has no refractory period)
26
Q

Rapid sequence of stimuli

A
  • tension increases further (⇑ Ca2+ availability ⇒ wave summation)
  • partial relaxation between contractions produces quivering = incomplete tetanus
27
Q

High frequency of stimuli

A
  • no relaxation between contractions i.e. sustained contraction = complete tetanus
  • all troponin saturated with Ca2+ and fiber warm (ATP synthesis - heat) ⇒ works faster
  • occurs normally in the body
28
Q

Fiber length

A

Resting fiber length is optimum
-allows for a maximum # of cross bridges formed upon stimulation ∴ max tension
⇓ tension if shorter or longer:
-shorter ⇒ thin filaments overlap and interfere with cross bridge attachment (min length = 70% of optimal)
-stretched ⇒ not all myosin heads near actin binding sites (max length = 130% of optimal)

29
Q

Size of fiber

A

thickness = more myofibrils/fiber

  • thicker = more tension
  • ⇑ with e.g. exercise, ♂ = testosterone
30
Q

Fatigue

A
  • muscle does not contract well

- reduced maximum tension

31
Q

Fiber types in a muscle differ

A
  • Fast – contract/relax rapidly - white (little myoglobin)

- Slow – contract/relax slowly - red (more myoglobin) e.g. postural muscles

32
Q

in a whole muscle, tension affected by

A 
Number of fibers contracting:
-more active motor units = ⇑ tension
-small motor units recruited first, then larger ones added when more tension needed
# fibers/motor unit: 
-more fibers/unit = ⇑ tension
-1 neuron ⇒ 10 fibers (weak) vs 1000 fibers (strong)
Muscle size: 
-larger = more fibers
Fatigue
33
Q

Muscle Tone

A
  • low level of tension in a few fibers that develops as different groups of motor units are alternately stimulated over time
  • gives firmness to muscle
34
Q

Whole Muscle Contraction types

A
  • Isotonic:

- Isometric

35
Q

Isotonic

A
  • muscle changes length
    e. g. flexion at the elbow - tension > weight of forearm
  • tension (relatively constant) exceeds the resistance of the load lifted
  • uses ATP
36
Q

Isometric

A
  • muscle length constant
  • tension less than required to move load
  • tension increases – cross bridges form but no shortening
  • uses ATP
37
Q

Whole Muscle Contraction example

A

Lift a book:

  • muscle = biceps brachii
  • isotonic to lift
  • isometric to hold
38
Q

Muscle Metabolism

A

energy for contraction:

  • During resting conditions
  • During short term exercise (i.e. < 1 minute) e.g. sprinting
  • Long term exercise (1 min to hours)
39
Q

During resting conditions

A 
fatty acids used to produce ATP (aerobic)
storage of:
-glycogen
-creatine phosphate (C~P)
  -ATP + Creatine ⇒ ADP + C~P
40
Q

During short term exercise (i.e. < 1 minute) e.g. sprinting

A

primarily anaerobic

  • use available ATP
  • creatine phosphate used to produce ATP (lasts ~ 15 secs)
    • C~P + ADP ⇒ ATP + creatine
  • muscle glycogen ⇒ glucose ⇒ pyruvic acid ⇒ anaerobic pathway ⇒ lactic acid (lasts ~ 30 seconds
41
Q

Long term exercise (1 min to hours)

A
  • ATP - from aerobic pathway
  • glucose (from liver)
  • fatty acids - used more as exercise continues
  • O2 sources: blood hemoglobin and muscle myoglobin
  • but sometimes anaerobic (discussed under fatigue)
42
Q

Muscle Fatigue types

A
  • Physiological Fatigue

- Psychological Fatigue

43
Q

Physiological Fatigue

A

-inability to maintain tension - not completely understood
-fatigue ⇓ ATP use ∴ protective (if too little, cross bridges can’t release)
Due to:
-depletion of energy supplies e.g. glycogen
-build-up of end products
-failure of APs

44
Q

build-up of end products

A
  • H+ from lactic acid - muscle contraction compresses blood vessels - ⇓O2 to muscle ∴ anaerobic for periods, even in long term exercise
  • Pi (from ATP⇒ADP + Pi) binds to Ca2+
    • less binds to troponin
    • slows the release of the Pi from the myosin – slows cross bridge release from actin
45
Q

failure of APs

A
  • ⇑ [K+] in small space of T-tubules during rapid stimuli ⇒ disturbs MP, stops Ca2+ release from SR
  • long term: neuron runs out of ACh (not usual in healthy person)
46
Q

Psychological Fatigue

A

failure of CNS to send commands to muscles ⇒ probably due to lactic acid

47
Q

Muscles and EPOC

A

EPOC = Excess Post-exercise O2 Consumption
-recovery O2 consumption (deep rapid breathing)
O2 used to:
-replenish stores of glycogen, C~P, O2 on Hb/myoglobin
-convert lactic acid to:
-pyruvic acid ⇒ Krebs
-to glucose in liver
also ⇑ in body temp from exercise = ⇑ O2 demand (faster chemical reactions)

Phys 1412 (12 decks)

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