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Anatomny > Skeletal Muscle Tissue chapter 9 > Flashcards

Skeletal Muscle Tissue chapter 9 Flashcards

1
Q

Muscle Tissue

A

is one of the four primary tissue types

  • converts the chemical energy of ATP into mechanical energy
  • muscle contraction
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2
Q

Important functions of skeletal muscle include

A

-movement

  • contractions pull on tendons to move the bones of the skeleton

-maintain posture

  • constant tension maintains body position

-guard openings to the digestive and urinary systems

  • support soft tissues
  • protect and support visceral organs
  • thermoregulation
  • heat generation from muscle contraction
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3
Q

Skeletal muscles are comprised of layers muscle fibers an connective tissue:

A

epimysium is an exterior collagen layer covering muscle

  • blends between muscles and other tissue

perimysium is a dividing layer of connective tissue surrounding bundles of cells called a fascicle

  • allows for blood vessels and nerves to penetrate muscle tissue

endomysium is a thin areolar tissue layer around each muscle fiber

  • contains capillaries, terminal axons, and myosatellite cells
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4
Q

Endomysium, perimysium, and epimysium form connective tissue attachments to bone

A

form tendons/aponeuroses that merges into periosteum as perforating fibers

  • tendons attach at points; aponeuroses attach broad areas
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5
Q

Stress will break a bone before

A

pulling the tendon/aponeurosis loose

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6
Q

connective tissue

A
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7
Q

Skeletal muscle

A

are long, striated muscles attached to bones containing multiple nuclei that develop via fusion of myoblasts

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8
Q

Muscle Fibers

A

sarcolemma
cell membrane of muscle fiber that holds sarcoplasm
stores glycogen and myoglobin

myofibrils
subdivision of muscle fibers responsible for contraction
exhibits alternating light and dark striations due to overlapping arrangement of myofilaments (actin and myosin)

sarcoplasmic reticulum
surrounds myofibril and forms terminal cisternae (to store and concentrate Ca2+)

transverse tubules (T tubules)
transmits action potential allowing whole fiber to contract simultaneously
triad is 1 T tubule and 2 terminal cisternae

sarcomere

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9
Q

Skeletal Muscle Fibers

A
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10
Q

Sarcomeres

A

are the basic functional, contractile units of muscle

  • comprised of myofilaments (-fibrils) that form striations with muscle fibers
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11
Q

3 types of myofilaments

A

myosin (thick)
arranged in a bundle with heads directed outward in a spiral
interact with actin to form cross-bridges that pivot to produce motion

actin (thin)
intertwined strands of (G) actin with an active site

Ca2+ binds to actin receptors causing a shape change in troponin-tropomyosin complex that exposes active sites
active sites bind to myosin

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12
Q

Muscle contraction is caused by the interactions of

A

myosin and actin filaments

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13
Q

Sarcomeres and Striations

A

Actin and myosin are abundant and highly organized in sarcomere of muscle tissue

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14
Q

Lines and Bands of actin and myosin

A

M line and Z line
M line is center of A band (midline of sarcomere)
Z disc is center of I band (ends of sarcomere)

A band
dark region consisting of thick filaments

I band
light region consisting of thin filaments

H band (zone)
area around M line that has only thick filaments

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15
Q

Sliding filament theory

A

thin filaments of sarcomere slide towards M line in between thick filaments

  • width of A band stays same; H and I bands get smaller
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16
Q

In muscle contractions, sarcomeres are pulled towards center; that is,

A

Z lines shorten the I band to produce tension

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17
Q

Neuromuscular junction

A

is the location of neural stimulation; functional connection between nerve fiber and muscle cell

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18
Q

3 parts of neromusclar junctions

A

synaptic knob
swollen end of nerve fiber (contains acetylcholine - ACh)

motor end plate and junctional folds (sarcolemma)
increases surface area for ACh receptors
contains acetylcholinesterase (AChE) that breaks down ACh and causes relaxation

synaptic cleft
gap between nerve and muscle cell

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19
Q

Skeletal muscle must be stimulated by a nerve or

A

it will not contract

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20
Q

Neuromuscular Junction: Neural Stimulation steps

A
  1. Neural action potential reaches synaptic knob
  2. Synaptic terminal releases acetylcholine (Ach) into the cleft
  3. Acetylcholine (Ach) :binds to receptors on junctional folds of sarcolemma to propagate action potential
  4. Ach is removed by acetylcholinesterase (AChE)Action potential causes Na+ (in extracellular fluid) to travel to T tubule

-Ca2+ from terminal cisternae is released causing actin-myosin interaction

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21
Q

Muscle function is a repeating cycle of

A

contraction and relaxation

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22
Q

Activation encompasses

A

excitation
neural stimulation leads to action potentials in muscle fiber

excitation-contraction coupling
action potentials on the sarcolemma activate myofilaments

contraction
shortening of muscle fiber

relaxation
return to resting length

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23
Q

Muscle contraction is ____; muscle relaxation is____

A

active; passive

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24
Q

Excitation

A

is the process leading to an action potential in the muscle fiber

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25
Q

Steps in excitation:

A

-nerve stimulus arrives at synaptic knob
causes Ca2+ to allow release of Ach

-Ach diffuses across cleft and binds to receptors on sarcolemma
receptors change shape and allow Na+ and K+ to cross plasma membrane

-Na+/K+ movements alter resting membrane potential (-90mV) and create an action potential
muscle fiber is now excited

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26
Q

Excitation-Contraction Coupling

A

refers to the activation of the myofilaments

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27
Q

Steps of excitation-contraction coupling:

A

-action potential spreads to T tubules

  • terminal cisternae of SR release stored Ca2+ into sarcoplasm
  • Ca2+ binds to troponin-tropomyosin molecules of actin causing a shape change

-active sites on actin are exposed

  • actin-myosin cross bridges can now form
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28
Q

Contraction

A

refers to the development of tension in the muscle fiber

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29
Q

Steps in contraction:

A
  • myosin head, using ATP, activates and “cocks” into extended position
  • myosin binds to actin and a cross bridge is formed
  • myosin head flexes, pulling actin filament towards H zone
  • referred to as power stroke
  • myosin binds to new ATP and process repeats
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30
Q

Myosin heads contract sequentially so as to not allow actin to

A

slide back to the resting position

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31
Q

Relaxation

A

is the process of a muscle “passively” returning to resting length

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32
Q

Steps in relaxation:

A

-nerve stimulation stops
ACh is no longer released and is broken down by AChE

-Ca2+ is actively transported back into cisternae
Ca2+ also dissociates from troponin-tropomyosin causing a shape change

-active sites on actin are blocked
myosin can no longer bind to actin

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33
Q

Rigor mortis

A

is a stiffening of the body beginning 3 to 6 hours after death

  • deteriorating sarcoplasmic reticulum releases Ca2+
  • activates actin-myosin cross bridges so muscle contracts but cannot relax
    • relaxation requires ATP and ATP production is no longer produced after death
34
Q

Fibers remain contracted until

A

myofilaments decay

35
Q

Rigor mortis is a temporary condition lasting about

A

24-48 hrs

36
Q

Tension

A

generated during contraction depends on length of muscle before it was stimulated

  • i.e. thick filaments are overly contracted and too close to Z discs; can’t slide far
  • weak contraction results
  • i.e. little overlap of thin and thick is too stretched; does not allow for many cross bridges to form
  • weak contraction results
37
Q

Muscle tone

A

Muscle tone (firmness of muscle at rest due to partial contraction) is maintained by the CNS ensuring optimal resting length

  • produces greatest force when muscle contracts
  • increasing muscle tone increases metabolic energy used, even at rest
38
Q

Weak stimuli do not cause

A

muscle contraction
muscle tissue has a threshold
level which the strength or frequency of stimuli will cause a contraction

39
Q

After threshold is reached, a latent period of no contraction follows:

A
  • time required for excitation, excitation-contraction coupling, and internal tension to build
  • i.e., the contraction cycle has not begun
40
Q

Contraction (external tension)

A

followed by relaxation occurs
-Ca2+ is released (cross-bridges form) and tension peaks but Ca2+ is quickly reabsorbed (cross-bridges detach)

  • contraction phase is shorter than relaxation phase
41
Q

Twitch

A

is a single stimulus (latency)–contraction-relaxation sequence:

42
Q

twitch is a single stimulus (latency)–contraction-relaxation sequence:

A
  • treppe (staircase phenomenon) - faster stimuli produce stronger twitches
  • rare for skeletal muscles
  • wave summation - higher frequency stimuli arrives before muscle relaxes and recovers gradually producing more tension
  • incomplete tetanus (sustained, fluttering peak tension) is a form of wave summation
  • complete tetanus is when twitches fuse into a prolonged, continuous contraction
  • maximum frequency stimulation gives muscles no time to relax
  • rarely occurs in the body
43
Q

Motor unit

A

is a motor neuron and all the muscle fibers it innervates; dispersed within muscle causing weak contractions over wide area

44
Q

2 motor units

A
  • small motor units
  • fine control units and may contain as few as 20 muscle fibers per nerve fiber
  • eye and hand muscles
  • large motor units
  • strength control units and may contain 200 or more muscle fibers per nerve fiber
  • gastrocnemius muscle (1000 fibers per nerve fiber)
45
Q

Muscles contain multiple motor units to sustain long term contraction; motor units alternate

A

to prevent fatigue (asynchronus motor unit summation)

46
Q
A

Motor Units

47
Q

Isotonic and Isometric Contractions

A

Muscle contraction does not always change the muscle length but tension will always develop

48
Q

Types of tension development:

A

isotonic muscle contraction develops tension while changing muscle length

  • tension while shortening is concentric (isotonic) contraction
  • muscle tension > resistance*
  • tension while lengthening is eccentric (isotonic) contraction
  • muscle tension < resistance*

isometric muscle contraction develops tension without changing length

  • important in postural muscle function and antagonistic muscle joint stabilization
49
Q
A

Isometric and Isotonic Contractions

50
Q

ATP, CP and Pyruvic Acid ATP

A

Sustained muscle contraction uses a lot of ATP (adenosine triphosphate)
-muscles store enough energy via CP (creatine phosphate) to start contraction

  • must manufacture more ATP as needed
    • mitochondria are responsible for the production of ATP
51
Q

Glucose is metabolized into

A

ATP

52
Q

Different mechanisms synthesize ATP depending on

A

exercise duration

53
Q

Cells produce ATP in 2 ways:

A

glycolysis

aerobic metabolism

54
Q

glycolysis

A
  • breaks down glucose from glycogen stored in skeletal muscles when stored ATP is exhausted
  • produces 2 ATP and 2 pyruvate molecules per glucose molecule; a lactic acid byproduct is also produced

>>>>lactic acid is the “feel the burn” of exercise

55
Q

aerobic metabolism

A
  • mitochondria utilize pyruvate, O2, ADP to enzymatically synthesize ATP
  • produces net 34 ATP per glucose molecule (17 per 1 pyruvate molecule created by glycolysis)

>>>primary source of ATP for resting muscles

56
Q

Active muscles utilize glycolysis (approximately 10 mins) until oxygen consumption allows

A

aerobic respiration to resume

57
Q

Citric acid cycle

A

to remove and deliver H+ from organic molecules to the ETS (via coenzymes NAD/FAD)

  • 2-carbon molecule (acetate) is attached to coenzyme A, forming acetyl-CoA
  • acetyl group is removed and attached to a 4-carbon molecule forming citric acid
  • 1 ATP is produced for each processed acetyl group
58
Q

ETS function

A

to transfer (e-) from H+ (oxidation) creating a concentration gradient which results in the production of ATP

  • cytochromes pass (e-) to generate energy that pumps H+ out of mitochondrial interior
  • diffusion of H+ powers attachment of high-energy phosphate to ADP (phosphorylation) using ATP synthase

-(e-) transferred to oxygen, eventually forming water

59
Q
A

ATP Production

60
Q

Fatigue

A

causes muscles to become progressively weaker; causes include:

  • ATP synthesis declines as glycogen is consumed
  • lactic acid inhibits enzyme function
  • lowers pH causing decreased Ca2+ troponin binding

After exercise, the body needs more O2 than

61
Q

After exercise, the body needs more O2 than usual to normalize metabolic activities resulting in

A

oxygen debt

62
Q

oxygen debt

A
  • replenishes O2 reserves
  • replenishes ATP and CP resting levels
  • reoxides lactic acid into pyruvic acid
  • pyruvic acid is converted back to glucose to be stored
  • serves metabolic rate
  • active muscles produce heat and raise body temperature and consume extra oxygen
63
Q

Muscle Fiber types

A

Slow-twitch Fibers

Fast Twitch Fibers

64
Q

Slow-twitch fibers

A

have more mitochondria, myoglobin and capillaries (aerobic respiration)

  • small diameter; slow contractions and are resistant to fatigue
  • soleus and postural muscles of the back
65
Q

Fast-twitch fibers

A

Fast-twitch fibers have enzymes for glycogen-lactic acid systems (anaerobic fermentation)

  • large diameter; quicker/more forceful contractions; not resistant to fatigue
  • extraocular eye muscles, gastrocnemius and biceps brachii
66
Q

Intermediate fibers

A

are similar to fast-twitch fibers but more have capillaries; more fatigue resistant

67
Q

All muscles contain all fiber types;

A

proportions are genetically determined

68
Q
A

Slow vs. Fast Fibers

69
Q

Muscle Performance

A

is a measure of strength and conditioning
strength depends on:

  • muscle size and fascicle arrangement

-length of muscle at start of contraction
>>length-tension relationship

  • # of motor units utilized
70
Q

conditioning depends on:

A
  • resistance training (weight lifting)

stimulates cell enlargement due to synthesis of more myofilaments

  • endurance training (aerobic exercise)

produces an increase in mitochondria, glycogen and density of capillaries

71
Q

Muscle performance ultimately depends on the types of

A

muscle fibers and to lesser extent physical conditioning

72
Q

Hypertrophy:

A

muscle growth from heavy training

  • increases diameter of muscle fibers and number of myofibrils
  • increases mitochondria and glycogen reserves
73
Q

Atrophy:

A

-muscle shrinkage from lack of exercise

  • reduction in diameter of muscle and number of myofibrils
  • nominal decrease in mitochondria
74
Q

Muscles become flaccid when inactive for days or weeks;

A

what you don’t use, you lose

75
Q

Cardiac Muscle Cells

A

are involuntary, thick with a single large nucleus and notched ends

-have less developed SR with no cisternae but have wide T tubules

-use aerobic respiration
resistant to fatigue but very vulnerable to interruptions in oxygen supply

-intercalated discs
link heart cells mechanically (desomosomes), chemically and electrically (gap junctions)
heart functions as a single fused mass of cells

-demonstrate automaticity

76
Q
A

Structure of Cardiac Cells

77
Q

Smooth Muscle

A

are involuntary, spindle-shaped cells with a single central nucleus

  • no striations, sarcomeres or Z discs
  • SR is scanty and there are no T tubules
  • Ca2+ for contraction comes from extracellular fluid
  • disorderly arrangement of actin and myosin filaments
  • dense bodies transmit contraction from cell to cell
  • nerve supply is autonomic (if present)
  • releases either ACh or norepinephrine
78
Q

Myofilaments are scattered so resting length is not related to tension development; functions

A

over a wide range of lengths (plasticity)

79
Q
A

Smooth Muscle

80
Q
A

Anatomny (6 decks)

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