Anat/Phys > Chapter 9: Muscles > Flashcards

Chapter 9: Muscles Flashcards

(55 cards)

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1
Q

What are 4 characteristics of muscle tissue?

A
  1. Excitability (responsiveness or irritability)- ability to receive and respond to stimulus
  2. contractability- ability to shorten forcibly
  3. extensibility- ability to be stretched or extended
  4. elasticity- recoil & resume their shape after stretching
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2
Q

What are 4 functions of muscles?

A
  1. provide movement
  2. maintain posture/ body position
  3. stabilize
  4. generate heat
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3
Q

Sarcolemma

A

plasma membrane beneath the endomysium that surrounds a muscle fiber

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4
Q

sarcoplasm

A

muscle cell cytoplasm, contains many glycosomes, stored glycogen that is converted to glucose during muscle activity and myoglobin, pigment that stores O2

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5
Q

myosin

A
  • responsible for actin based motility- thick filament
  • head has filamentous actin and uses ATP hydrolysis to generate force and to “walk” along the filament
  • contractions depend on myosin and actin
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6
Q

actin

A
  • thin filaments- protein
  • binding sites for myosin found on actin (inhibitor- tropomyosin)
  • make up myofilament with myosin
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7
Q

crossbridge

A

the globular heads of myosin are the business end during contraction, they link thick & thin filaments together, forming crossbridges, and they swivel around their point of attachment
- these crossbridges act as motors to generate tension developed by a contracting muscle cell

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8
Q

tropomyosin

A

-rod-shaped protein(polypeptide) that helps stabilize actin and in relaxed muscles, blocks they binding site for myosin on actin

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9
Q

troponin

A

protein found in thin filaments that helps control myosin

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10
Q

sarcoplasmic reticulum

A
  • along with t-tubules are sets of intracellular tubules in skeletal muscle fibers.
  • SR is an elaborate smooth endoplasmic reticulum
  • the interconnecting tubules surround each myofibril like a sleeve
  • most of these tubules run longitudinally along the myofibril communicating at the H-zone
  • GOING TO REGULATE THE INTRACELLULAR LEVELS OF CALCIUM
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11
Q

T-tubules

A
  • at the A-band/ I-band junction, the sarcolemma protrudes into the cell, making an elongated tube (T-transverse)
  • they run between terminal cisternae of the SR forming triads
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12
Q

triads

A

where T- tubules and SR come in contact, there are voltage sensors and gated channels thru which CA2+ can be released

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13
Q

sliding filament model of contraction

A

-during contraction, your thin filaments slide past the thick ones, making actin and myosin filaments overlap more

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14
Q

acetylcholine ACh

A
  • neurotransmitter found in small membraneous sacs ( synaptic vesicles) that are located at axon terminal
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15
Q

depolarization

A
  • a local change in membrane potential, more Na+ enters the cell than K+ leaves, the cell interior becomes more positive and peaks at threshold
  • starts an AP that spreads in all directions across muscle membranes, as it goes along it opens sodium channels
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16
Q

repolarization

A
  • Na+ channels close

- K+ channels open and this lets K+ outside the cell to restore the initial negative charge inside

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17
Q

refractory period

A
  • cell can’t be stimulated again until it is repolarized

- ATP dependent Na+/K+ pumps restore the ionic conditions of the resting cell

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18
Q

nerve impulse and generation of AP across the sarcolemma

A
  • AP arrives at axon terminal at neuromuscular junction
  • ACh is released: binds to receptors on sarcolemma
  • ion permeability of sarcolemma changes
  • local depolarization (end plate potential) ignites AP in sarcolemma
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19
Q

Excitation-Contraction Coupling

A
  • AP travels across the entire sarcolemma
  • AP travels along T-tubules
  • SR releases Ca2+, Ca2+ binds to troponin: myosin- binding sites on actin exposed
  • myosin heads bind to actin(crossbridges); contraction begins
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20
Q

muscle tension

A

-force that is exerted by the contracting muscle on an object

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21
Q

load

A

-force exerted by the object to be moved, on the muscle

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22
Q

isotonic contraction

A

-isotension overcomes the load, the load is lifted, you can measure shortening of the muscles

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23
Q

isometric contraction

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A

getting muscle tension but the load isn’t moved

24
Q

motor unit

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A

motor neuron and all of the muscle fibers it supplies

25
recruitment
- multiple motor unit summation | - higher voltage shocks, they are all calling more muscle fibers into play
26
threshold stimulus
-the stimulus in which you first observe a contraction
27
maximum stimulus
- strongest stimulus that produces increased contractile force, activates ALL motor units
28
size principle
-smallest motor neurons are excited first, bigger ones are only excited when a powerful contraction is needed
29
1. 6 seconds of exercise Short term
- ATP stored in muscles is used first
30
2. 10 seconds of exercise short term
- ATP is formed form creatine phosphate and ADP - creatine phosphate is high energy molecule stored in muscle - creatine phosphate + ADP= (cat. creatine kinase) creatine + ATP - stored ATP + CP provides for 14-16 seconds of muscle contraction
31
3. 30-40 seconds to end of short term exercise
-glycogen stored in muscles is broken down to glucose, which is oxidized to generate ATP a.Glycolysis- initial breakdown of glucose that does not require O2 b. glucose is broken down into pyruvic acid, releasing ATP (then used by muscle) C. normally pyruvic acid enters mitochondria and reacts with O2 to produce ATP via aerobic respiration, but if you are exercising hard pyruvic acid becomes lactic acid d. anaerobic pathway provides much less ATP than aerobic but it acts faster -anaerobic path provides ATP for 30-40 seconds of strenuos activity, but it uses a lot of glucose, lactic acid buildup causes muscle soreness
32
Hours of exercise-long term
-ATP is generated by breakdown of several nutrient energy fuels by aerobic pathway -this pathway uses oxygen released form myoglobin or delivered by hemoglobin, when it ends, the oxygen deficit is paid back -occurs in mitochondria: Glucose + oxygen = CO2 + water + ATP -aerobic provides lots of ATP but its slow and requires oxygen
33
contractures
if you run out of ATP, your muscles will stay contracted | ex. writer's cramp
34
fatigue form short term exercise
- you can get ionin imbalances | ex. K+ collects in the T-tubules, disturbing the membrane potential & halting Ca2+ release form SR
35
fatigue in long term exercise
- if you get damage to the SR this can interfere with Ca2+ release
36
What 4 factors affect the strength of MUSCLE CONTRACTION?
1. number of muscle fibers stimulated 2. size of muscle fibers-the larger the more powerful 3. frequency of stimulation- the more rapidly a muscle is stimulated the greater the force 4. degree of muscle stretch-must be optimal length
37
3 muscle fiber types
1. slow oxidative 2. fast glycolytic 3. fast oxidative
38
slow oxidative fibers
- slow to contract - aerobic respiration - resistant to fatigue - LOW POWER - endurance type: marathon, maintaining posture
39
fast glycolytic fibers
- contract rapidly - anaerobic respiration - tire quickly - contract powerfully - good for short-term, intense or powerful movements, weight lifting , hitting baseball
40
fast oxidative fiber
- contracts rapidly - aerobic respiration - moderate fatigue - moderate power - good for walking, sprinting
41
effects of aerobic training on muscles
1. increases in # of capillaries around a muscle fiber, & # of mitochondria in them, and more productio of myoglobin and may convert fast glycolytic to fast oxidative fibers 2. RESULTS: more efficient muscle metabolism, greater endurance, more strength, more resistance to fatigue
42
effects of resistance training
1. muscle hypertrophy- increase in size if individual muscle fiber, develop more mitochondria, form more myofilaments & myofibrils and store more glycogen 2. RESULTS: increase muscle size and strength but loose increase very quickly if you don't maintain exercise, muscles atrophy-loose muscles at 5% a day
43
longitudinal layer in smooth muscle
- where your muscle fibers are parallel to the long axis of the organ - contraction causes the organ to dilate & shorten
44
circular layer in s. muscle
- fibers run around the circumference of the organ | - contraction causes the organ to elongate
45
peristalsis
-alternating contraction & relaxation of muscles, helps squeeze things through
46
varicosities
these are nerve fibers that supply smooth muscle
47
diffuse junction
- wide synaptic cleft in smooth muscle cells
48
caveolae
-infoldings in the sarcolemma that store Ca+
49
pacemaker cells
-these control the contractile pace for the whole muscle sheet
50
calmodulin
-calcium-binding protein that activates myosin
51
myosin kinase
-enzyme interacts with calmodulin to activate myosin
52
what are 3 special features of smooth muscle contraction?
1. response to stretch - S. muscle has a STRESS-RELAXATION RESPONSE- muscle can increase contraction as it stretches, then it relaxes at its new length - this allows a hollow organ to fill and expand slowly without expelling its contents. ex. stomach 2. Length & tension changes-smooth muscle can stretch a lot more than skeletal muscle because it doesn't have sarcomeres. Skeletal muscles, constrictive, can only stretch 60% of its resting length, S. muscle can stretch 150% 3. Hyperplasia- s. muscle can divide to increase their numbers ex. uterus during pregnancy
53
visceral single unit S. muscle
- have opposing sheets, are innervated with varicosities - contract as a unit - respond to chemical stimuli - typical type, found in visceral- walls of hollow organs, except heart
54
multiunit S. muscle
- have structurally independent muscle fibers - supplied by nerves with motor units - respond to neural stimuli with graded contractions that involve recruitment - occur in airways to the lungs, large arteries and some of internal eye muscles
55
what is muscular dystrophy?
- Duchenne muscular dystrophy-sex-linked recessive disease - diagnosed at early childhood and only live into 20s a. DMD is caused by lack of protein DYSTROPHIN, that links the cytoskeleton to the extracellular matrix and helps stabilize the sarcolemma b. the sarcolemma tears, allowing excess calcium to enter, damaging the fibers - eventually apoptosis occurs and muscle mass is lost c. there is no cure for DMD, but animal testing is underway for processes which will allow the body to produce dystrophin
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