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KNS 480 > PNF & Muscular system > Flashcards

PNF & Muscular system Flashcards

1
Q

PNF

A

proprioceptive neuromuscular facilitation: common practice for increasing range of motion for rehabilitation and performance

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2
Q

proposed mechanisms

A
  • autogenic inhibition
  • reciprocal inhibition
  • stress relaxation
  • gate control theory
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3
Q

autogenic inhibition

A

occurs in contracted or stretched muscles; GTOs are activated and trigger a decrease in excitatory signals in the same muscle and causes muscle relaxation

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4
Q

Reciprocal inhibition

A

occurs when the opposing muscle is contracted voluntarily and decreased neural activity is seen in the working muscle due to muscle spindle activation

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5
Q

contract-reflex stretch

A

take muscle into an assisted stretch, hold for 5-10 sec, isometrically contract the stretched muscle for 5-10 sec, relax for 2-3 sec, then stretch again (autogenic)

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6
Q

contract-relax-antagonist contract (CRAC)

A

takes muscles into an assisted stretch, hold for 5-10 sec, isometrically contract the antagonist muscle for 5-10 sec, relax for 2-3 sec, then stretch again
(reciprocal)

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7
Q

skeletal muscle

A

functions: produce movement, maintain posture, generate heat
Actions: pull NOT push

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8
Q

epimysium

A

top layer of connective tissue

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9
Q

perimysium

A

middle layer of connective tissue

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10
Q

endoomysium

A

innermost layer of connective tissue

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11
Q

basement membrane

A

“glue that holds something together” with the connective tissue

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12
Q

sarcolemma

A
  • specialized cell membrane
  • good with action potential
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13
Q

microstructure of muscle

A

myofibrils
> actin (thin filament)
> myosin (thick filament)
sarcomere (functional unit)
> Z line
> M line
> H zone
> A band
> I band
sarcoplasmic reticulum
transverse tubules

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14
Q

satellite cells

A

specialized immune cells that repair damage

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15
Q

neuromuscular junction

A

junction between motor neuron & muscle fiber

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16
Q

motor unit

A

motor neuron and all fibers it innervates

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17
Q

motor end plate

A

pocket formed around motor neuron by sarcolemma

18
Q

neuromuscular cleft

A

short gap between neuron and muscle fiber

19
Q

acetylcholine

A

released from the motor neuron
> causes an end-plate potential (EPP)
> depolarization of muscle fiber

20
Q

muscular contraction

A

explained by two interacting theories
> excitation-contraction coupling
> sliding filament theory

21
Q

energy for energy contraction

A
  • ATP required for muscle contraction
  • release of energy from ATP hydrolysis provides energy required for power stroke
    > myosin ATPase breaks down ATP as fiber contracts
    > ATP, ADP + Pi
    Sources of ATP
    > phosphocreatine (PC)
    > Glycolysis
    > oxidative phosphorylation
22
Q

excitation contraction coupling

A
  • depolarization of motor end plate (excitation) is coupled to muscular contraction
    > action potential travels down transverse tubules and causes release of Ca ++ from SR
    > Ca++ binds to troponin and causes position change in tropomyosin
    —-exposing myosin binding sites on actin
    > strong binding state formed between actin and myosin
    > contraction occurs ( power stroke)
23
Q

Steps for excitation-contraction coupling

A
  1. An action potential travels down an alpha motor neuron and arrives at the
    synaptic knob
  2. The synaptic knob releases acetylcholine (ACh) across the synaptic cleft of the
    neuromuscular junction where it binds to receptors on the sarcolemma of the
    muscle fiber
  3. ACh activation of the sarcolemma opens ion channels, and Na+ moves into the
    fiber
  4. Movement of Na+ ions depolarizes the muscle fiber and sends a depolarization
    wave through the T-tubules
  5. Depolarization of the T-tubules triggers the release of Ca2+ from the sarcoplasmic
    reticulum into the sarcoplasm of the muscle fiber
  6. Excitation-Contraction Coupling Steps
  7. Ca2+ ions bind to troponin, resulting in a shift in position of tropomyosin, exposing
    the myosin binding sites on actin
  8. Crossbridge cycling occurs between actin and myosin to create muscular force
    development until neural stimulation stops
  9. Neural stimulation ceases, stopping ACh release and repolarizing the cell
  10. During repolarization, Ca2+ ions are returned to the sarcoplasmic reticulum and
    troponin and tropomyosin return to their resting positions, blocking the myosin
    binding sites on actin
    Events leading to muscle excitation, contraction, and relaxation
24
Q

sliding filament theory

A

Remember: Myosin binding sites on actin must be exposed for
_CROSSBRIDGE__ formation to occur
1. Myosin head with an attached hydrolyzed ATP (ADP + Pi) is in a resting state
2. Myosin head binds to actin and forms a crossbridge with actin
3. Pi is released from the myosin head and alters the shape of myosin, pulling on
actin and creating a “power stroke”
4. After the power stroke, ADP is released from the myosin head
5. A new ATP binds to the myosin head, releasing the myosin head from actin and
breaking the crossbridge
6. The new ATP is hydrolyzed, allowing the myosin to return to its original resting
state
Exercise and muscle fatigue

25
sliding filament model of MC - Huxley
- swinging lever-arm model - muscle shortening occurs due to the movement of the actin filament over the myosin filament - formation of cross-bridges between the actin and myosin filaments > power stroke - reduction in the distance between Z lines of the sarcomere
26
exercise & muscle fatigue
- defined as a decline in muscle power output Occurs due to: - decrease in muscle force production at crossbridge level - decrease in muscle shortening velocity - cause of muscle fatigue dependent upon exercise intensity that produced fatigue
27
mechanisms of fatigue during heavy, very heavy, and severe exercise (1-10min)
multifactorial range from decreased Ca 2+ release from SR to accumulation of metabolites that inhibit myofilament sensitivity to Ca 2+ > key metabolites that contribute to fatigue include increases in Pi, H+ and free radicals >H+ ions bind to Ca+2 binding sites on troponin-preventing Ca 2+ binding and contraction > both Pi and radicals modify cross-bridge head and reduces number of cross-bridges bound to actin > collectively, these factors act to promote fatigue
28
mechanisms of fatigue during moderate intensity exercise (>60 min)
causes of fatigue during prolonged endurance exercise include increased radical production and glycogen depletion > accumulation of Pi and H+ in muscle do not contribute fatigue during moderate intensity exercise > radical accumulation in muscle fibers modifies cross-bridge head and reduces number of cross-bridges bound to actin > depletion of muscle glycogen reduces TCA cycle intermediates and decreases ATP production via oxidative phosphorylation
29
muscle cramps
- spasmodic, involuntary muscle contractions - associated with prolonged, high-intensity exercise - most not caused by an electrolyte or dehydration balance
30
exercise-associated cramps
likely due to hyperactive motor neurons in the spinal cord > rigorous execrise can alter muscle spindle and golgi tendon organ function resulting in increased excitatory activity of muscle spindles and a reduced inhibitory effect of the golgi tendon organ > passive stretching often relieves this type of muscle cramp
31
muscle cramp help
- sending a strong inhibitory stimulus to the spinal cord to prevent motor neurons from firing - activation of ion channels in the mouth/throat can send inhibitory signals to the spinal cord to inhibit over- active motor neurons and prevent cramping - also oral ingestion of natural spices EX: ginger & capsaicin
32
size principle
the progressive activation of successive recruitment of additional motor units from smallest to largest motor units
33
contractile properties
- maximal specific force production - speed of contraction (Vmax) > regulated by myosin ATPase activity - maximal power output = force x shortening velocity > high force, fast fibers produce high power ouput - fatigue resistance - muscle fiber efficiency > lower amount of ATP used to generate force
34
fiber types
Type 1: endruance Type IIa: both Type IIx: strength power
35
muscle actions
dynamics; concentric (decreases), eccentric (increases) Static; isometric ( no change)
36
muscle twitch
contraction resulting from single stimulus - after stimulation -short latent period exist -corresponds to depolarization of muscle fiber Contraction-calcium released from SR > tension is developed due to crossbridge binding Relaxation -reuptake of calcium into SR > crossbridge detachment - Speed of shortening is greater in fast fibers > SR releases Ca++ at a faster rate > higher ATPase activity
37
force regulation in muscle
**# & types of motor units: more motor units = greater force fast motor units = greater force ** muscle length "ideal" length for force generation increased cross-bridge formation **firing rate of motor neurons > frequency of stimulation --simple twitch -- summation -- tetanus ** contractile history of muscle rested muscle versus muscles exposed to fatiguing exercise warmup exercise results in "post-activation potentiation"
38
aging & muscle loss
sarcopenia: age-related muscle loss - 10% muscle mass lost between age 25-50 years - additional 40% lost between age 50-80 years - loss of fast fibers & gain in slow fibers > resistance training can delay age-related muscle loss
39
muscle force-velocity relationship
> at any absolute force exerted by the muscle, the speed of movement is greater in muscles with a higher percentage of fast-twitch fibers > maximum velocity of shortening is greatest at the lowest force - true for both slow and fast fibers
40
muscle force-power relationship
> at any given velocity of movement, the peak power generated is greater in a muscle with a higher percentage of fast-twitch fibers > the peak power increases with velocity up to movement speed of 200-300 degrees/second > power decreases at higher velocities because force decreases with increasing movement speed

KNS 480 (7 decks)

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