Need to Know (Lec 1-3) Flashcards

1
Q

Structural Anatomy of a Muscle (6)

A
Epimysium
Fascicle
Perimysium
Muscle Fibers
Endomysium
Inscriptions
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2
Q

Proteins of a Muscle Fiber (2)

A

Myosin (thick)

Actin (thin)

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3
Q

Myosin

A

protein for thick filaments

-located in this order: A-band> H-zone> M-line

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4
Q

Actin

A

protein for thin filaments

  • located in I-band > A-band
  • composed of 3 proteins
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5
Q

Muscle Fiber Types (3)

A

Type 1 Slow Twitch ST
Type 2 Fast Twitch FTa
Type 2 Fast Twitch FTx

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6
Q

Actin Proteins (3)

A

Actin
Tropomyosin
Troponin

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7
Q

Type 1 Slow Twitch ST

A
  • high oxidative capacity and resistance to fatigue
  • low anaerobic and contractile speed
  • slow myosin ATPase activity
  • Low sarcoplasmic reticulum development
  • Low motor unit strength
    (i. e. marathons, walking)
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8
Q

Type 2 Fast Twitch FTa

A
  • moderately high oxidative capacity and resistance to fatigue
  • high anaerobic (glycolytic) capacity and contractile speed
  • fast myosin ATPase activity
  • high sarcoplasmic reticulum development (Ca++ is delivered quicker and more efficiently)
  • motor unit strength
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9
Q

Type 2 Fast Twitch FTx

A
  • low oxidative capacity (sometimes none) and highly fatigue prone
  • highest anaerobic (glycolytic) capacity and contractile speed and motor unit strength (better anaerobic activities, more explosive actions, less endurance)
  • fast myosin ATPase activity
  • high sarcoplasmic reticulum development
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10
Q

Sodium-Potassium Pump

A

an enzyme called Na+ - K+ - ATPase that maintains the resting membrane potential in disequilibrium at -70 mV
-moves 2 K+ in and 3 Na+ out, uses 1 ATP

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11
Q

Sliding Filament Theory (1-4)

A
  1. Actin Potential (ACH released from Motor nerve)
  2. Sodium rushes into cell > (Action Potential)
  3. That causes Ca++ to be released from sarcoplasmic reticulum
  4. Ca++ binds troponin
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12
Q

Sliding Filament Theory (5-8)

A
  1. Troponin moves Tropomyosin
  2. Tropomyosin uncovers myosin binding site on Actin
  3. Myosin binds Actin (cross-bridge)
  4. Myosin pulls Actin chain along in one direction
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13
Q

Sliding Filament Theory (9-11)

A
  1. Sacromere shortens (Z-disks move closer together)
  2. Whole fiber shortens (Muscle Contraction!)
  3. Ca++ ATPase pumps restore Ca++ to sarcoplasmic reticulum (Muscle Relaxation)
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14
Q

Orderly Recruitment of Muscle Fibers

A
minimum number of motor units needed
-First: smallest (type 1) motor units
-Next: mid-sized (type 2 FTa) motor units
-Last: largest (type 2 FTx) motor units
Recruited in same order everytime
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15
Q

Size Principle of Muscle Fibers

A

order of recruitment of motor units directly related to size of a-motor neuron

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16
Q

Development of Action Potential (6)

A
  1. Resting membrane potential (-70 mV)
  2. Depolarization (+40mV)
  3. Overshoot (Na+ channels open and Na+ moves out of cell, beginning repolarization)
  4. Repolarization
  5. Afterhyperpolarization ( additional K+ moves out of the cell, hyperpolarizing it.
  6. Cells return to RMP
17
Q

Muscle Spindles

A

Detects stretch of a muscle

  • sensory neurons conduct action potentials to the spinal cord
  • sensory neurons synapse with alpha motor neurons
  • stimulation of alpha motor neuron causes the muscle to contract and resist being stretched
18
Q

Golgi Tendon Organs (GTO)

A

Detects tension applied to a tendon

  • sensory neurons conduct action potentials to the spinal cord
  • sensory neurons synapse with inhibitory interneurons that synapse with alpha motor neurons
  • inhibition of the alpha motor neurons causes muscle relaxation, relieving the tension applied to the tendon
19
Q

Mechanisms of Muscular Strength Gains (11)

A
Neural Control
Motor Unit Recruitment
Motor Unit Rate Coding
Autogenic Inhibition
Muscle Hypertrophy (chronic hyp., fiber hyp., fiber hyperplasia)
Neural Activation
Atrophy
Inactivity
Immobilization
Detraining
Fiber Type Alterations
20
Q

Neural Control of muscular strength gains

A

main factor in muscle strength gain
Strength gains cannot occur without neural adaptations
-strength gains can occur without hypertrophy
-property of motor system, not just muscle
Co-activation of agonists and antagonists
Morphology of neuromuscular junction

21
Q

Muscle Hypertrophy

A

main factor in muscle strength gains after neural control

Increase in muscle size

22
Q

Chronic Hypertrophy

A

long term bout

  • maximized by high velocity eccentric training
  • disrupts sacromere z-lines (protein remodeling)
  • reflects actual structure change to muscle
  • includes both fiber hypertrophy and fiber hyperplasia
  • concentric training may limit muscle hypertrophy
23
Q

Autogenic Inhibition

A

Normal intrinsic inhibitory mechanisms
-GTO
-inhibit muscle contraction if tendon tension if too high
-prevents damage to bones and tendons
Training can decrease inhibitory impulses
-muscle can generate more force
-may also explain superhuman feats of strength

24
Q

Fiber Hypertrophy

A

caused by increases in:

  • myofibrils
  • actin, myosin filaments
  • sarcoplasm
  • connective tissue
25
Q

Fiber Hypertrophy cont.

A

resistance training increases protein synthesis

  • muscle protein content is always changing
  • during exercise: synthesis decreases, degradation increases (damage to muscle)
  • after exercise: synthesis increases, degradation decreases (recovery)
26
Q

Fiber Hyperplasia

A

an increase in the total number of fibers within a muscle

  • contributes to overall hypertrophy
  • can occur through fiber splitting
  • occurs through satellite cells
  • assists in skeletal muscle regeneration
  • activated by stretch and injury
  • after activation: cells proliferate, migrate and fuse
27
Q

Mechanisms for Hypertrophy (3)

A

Chronic Muscle Hypertrophy
Fiber Hypertrophy
Fiber Hyperplasia

28
Q

How are fiber types altered with resistance training?

A
  • increase in static strength, cross-sectional area

- decrease in percent of type 2 FTx, increase percent type 2 FTa