KIN 3306: EXAM 2
68 Cards in this Set
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What are the three types of muscle tissue?
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-smooth
-cardiac
-skeletal (voluntary)
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epimysium
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surround entire muscle
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endomysium
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surrounds individual muscle fibers
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perimysium
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surrounds bundles of muscle fibers
(fascicles)
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what is sarcolemma?
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muscle cell membrane
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myofibril
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elongated thread in striated muscle cells
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plasmalemma
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plasma membrane
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sarcomere
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basic contractile unit of a myofibril
-composed of thick and thin filaments (myosin vs actin)
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myosin
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comprises 2/3 of skeletal muscle proteins
-titin filaments stabolize myosin
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three proteins in thin filaments
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-actin
-tropomysosin
-troponin
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tropomyosin
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twists around actin strand
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troponin
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bound at intervals to actin
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phases of muscle contraction
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-action potential/calcium release
-calcium troponin binding; tropomyosin shift
-actin-myosin binding
-myosin power stroke/ATP binding
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Resting membrane potential
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-70mV
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Explain RMP
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caused by uneven separation of charged ions inside (K+) and outside (Na+) the cell
-more ions outside the cell than inside
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what ions are outside the cell during RMP
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(Na+) sodium
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what ions are inside the cell during RMP
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(K+) Potassium
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Sodium Potassium Pumps
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Pumps more positive charge outside. moves Sodium (Na+) out and Potassium (K+) in, but moving 3 Sodium out for every 1 potassium in.
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Muscle Contraction
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1. Action potential of neuron releases acetylcholine when meets neuromuscular jxn
2. Action potential then generated on sarcolemma and throughout T-tubules
3. Sarcoplasmic reticulum releases Ca2+
4. Myosin cross bridges form – result of Ca2+ binding to troponin on act…
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Action Potential occurs when...
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A stimulus of sufficient strength depolarizes the cell-opens Na+ channels, and Na+ diffuses into the cell. (inside becomes positive)
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Excitation- Contraction Coupling (EC Coupling)
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Action potential travels to SR, releasing calcium into sarcoplasm. Calcium binds to Troponin. Troponin moves to Tropomysoin, revealing myosin binding site on actin. Myosin cross bridge bind to actin.
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Muscle Excitation
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Action potential in motor neuron cause release of acetylcholine (ACh) in synaptic cleft. ACh binds to receptors on motor end plate, leads to depolarization that is conducted down transverse rubles, which causes release of Ca+2 from SR.
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Sliding Filament Theory
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muscle contraction=muscle fiber shortening.
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Myosin power stroke
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-myosin bound to actin tilts its head, pulling thin filament towards the center of the sarcomere.
-Process is repeated until Z-disk reaches myosin filaments or until calcium is no longer available.
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Muscle Relaxation
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-calcium pumps return calcium to SR
-ATP is required
-Troponin and Tropomyosin return to original position.
-Thick and Thin filaments return to original positions.
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Fiber type and Performance
(Power Athletes)
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-Sprinters
-mostly fast (70-75%) Fast Twitch (Type 2)
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Fiber type and Performance (Endurance Athlete)
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-Distance runners
-mostly slow (70-80%) Slow Twitch (Type 1)
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Factors of Muscle Force
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# of motor units activated
- Type of units activated (FT or ST)
-Muscle size
-initial muscle length
-joint angle
-speed of muscle action (shortening or lengthening)
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Length-Tension Relationship
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-Optimal sarcomere length = optimal overlap
-Too short or too stretched = little to no force
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Speed-Force Relationship
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- Concentric: max force decreases at higher speeds
- Eccentric: max force increases at higher speeds
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Primary adaptation to Resistance Training?
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increase in a muscle's force-producing ability (muscle strength)
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Two components to increase muscle strength from resistance training.
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- Neural Adaptation: optimization of motor unit recruitment
- Muscle Hypertrophy: muscle enlargement.
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Neural Adaptation
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-synchronization of Motor Unit Recruitment (Summation)
-increase motor neuron firing Frequency (rate-coding)
-decrease inhibitory signals from Golgi Tendon organ
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Muscle Hypertrophy
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Transient Hypertrophy: due to fluid accumulation during contraction
Chronic Hypertrophy: structural increase in size
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Primary cause of Chronic Hypertrophy
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Fiber Hypertrophy
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Two neural factors involved in muscle strength
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-Recruit more motor units (Summation)
-Increase frequency (rate-coding)
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Muscle Strength Gains Over Time:
Early and Long-term
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Early gains: alterations of neural control of trained muscles (Neural adaptation)
Long-Term gains: Increase muscle size (Hypertrophy)
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T or F: Increase in muscle size results primarily from individual fibers getting larger
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True
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Cellular mechanisms of Hypertrophy
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- Larger fiber CSA (cross-sectional area)>increase # of myofibrils.
-Myofibrils reach critical size they split longitudinally.
-Accompanied by increase in SR, t-tubules.
-Increase protein synthesis > Increase # of myofibrils.
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What is (RPS)?
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-Increased rates of protein synthesis (RPS)
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What is (RPD)?
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-Decreased rates of protein degradation (RPD)
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Explain the balance of RPS and RPD in Stable Muscle Mass.
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Rate of protein synthesis = Rate of protein degradation.
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Explain the balance of RPS and RPD in Muscle Hypertrophy.
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Rate of protein synthesis is greater than rate of protein degradation.
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Explain the difference of RPS and RPD in Muscle Atrophy.
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Rate of protein synthesis is lower than Rate of protein degradation.
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T or F: Resistance Training leads to increase in Protein Synthesis?
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True
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T or F: Net increase of muscle proteins leads to fiber enlargement?
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True
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What are Satellite Cells?
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"myogenic stem cells" that are available to maintain a relatively constant nucleus to muscle mass ratio (myonuclear domain)
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What maintains a relatively constant nucleus to muscle mass ratio?
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Satellite Cells
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Role of Satellite cells in muscle hypertrophy:
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inactive until needed for growth or repair of myofiber. When stimulated, initiate steps of myogenesis. Fuse to existing fibers (Hypertrophy) or fuse together forming new fibers (Hyperplasia)
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Muscle response to resistance training.
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-primarily from increase in fiber size (fiber hypertrophy)
-minor contribution from fiber hyperplasia (forming new fibers) : New fibers form, Fusion of satellite cells, Fiber split
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T or F: Training can change the properties of existing fibers. If yes, which type?
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True, This typically occurs in the intermediate (Type 2a fibers)
-Type 2x to Type 2a
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If properties of existing fibers change, how long does it usually take?
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15-20 weeks
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T or F: Some training interventions may induce fiber type conversion (Type 2a to Type 1)
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True, but rarely happens.
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What are the causes of Muscle Atrophy?
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-Immobilization/ Inactivity
-Detraining
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T or F: 25% of previous gains lost in first week?
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True, All adaptations lost in half the time it took to gain them.
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T or F: In Muscle Atrophy, changes start to occur within 6-h, Decrease in RPS, 4-5% strength decrease per day in 1st week.
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True, they are all correct.
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Sarcopenia
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loss of muscle mass and atrophy with age
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what muscle fibers are affected in sarcopenia?
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fast twitch
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causes of sarcopenia
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-increase in protein degradation
-decrease in body's repair mechanisms
-increase in oxidative damage
-genetic predisposition
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what is the pain felt immediately after exercise is called?
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acute muscle soreness
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what causes acute muscle soreness?
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-accumulation of acid (H+)
-tissue edema (transient hypertrophy)
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What is DOMS
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delayed onset muscle soreness
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what causes DOMS
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-eccentric muscle contraction- induced damage and subsequent immune system response
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key phases of DOM
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-structural damage
-immune system response
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what are the 6 stages of DOM
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1. eccentric contraction causes structural damage to the muscle fiber
2. calcium homeostasis is disrupted resulting in further in further muscle fiber degradation
3. intracellular contents and immune products stimulate nerve endings
4. immune system activation causes additional delayed…
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how do you treat DOMS
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-time
-rest from activity
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what are some general training principles?
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1. progressive overload (increase intensity and volume to continue gaining)
2. variation
-periodization
-one or more aspects of the training program should be altered over time to maximize effectiveness of training
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what are the three types of resistance training?
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1. isometric of static (constant length)
2. dynamic of isotonic (constant load)
3. isokinetic (constant speed)
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KIN 3306: CHAPTER 9