Need to Know (Lec 1-3) Flashcards
Structural Anatomy of a Muscle (6)
Epimysium Fascicle Perimysium Muscle Fibers Endomysium Inscriptions
Proteins of a Muscle Fiber (2)
Myosin (thick)
Actin (thin)
Myosin
protein for thick filaments
-located in this order: A-band> H-zone> M-line
Actin
protein for thin filaments
- located in I-band > A-band
- composed of 3 proteins
Muscle Fiber Types (3)
Type 1 Slow Twitch ST
Type 2 Fast Twitch FTa
Type 2 Fast Twitch FTx
Actin Proteins (3)
Actin
Tropomyosin
Troponin
Type 1 Slow Twitch ST
- 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)
Type 2 Fast Twitch FTa
- 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
Type 2 Fast Twitch FTx
- 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
Sodium-Potassium Pump
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
Sliding Filament Theory (1-4)
- Actin Potential (ACH released from Motor nerve)
- Sodium rushes into cell > (Action Potential)
- That causes Ca++ to be released from sarcoplasmic reticulum
- Ca++ binds troponin
Sliding Filament Theory (5-8)
- Troponin moves Tropomyosin
- Tropomyosin uncovers myosin binding site on Actin
- Myosin binds Actin (cross-bridge)
- Myosin pulls Actin chain along in one direction
Sliding Filament Theory (9-11)
- Sacromere shortens (Z-disks move closer together)
- Whole fiber shortens (Muscle Contraction!)
- Ca++ ATPase pumps restore Ca++ to sarcoplasmic reticulum (Muscle Relaxation)
Orderly Recruitment of Muscle Fibers
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
Size Principle of Muscle Fibers
order of recruitment of motor units directly related to size of a-motor neuron
Development of Action Potential (6)
- Resting membrane potential (-70 mV)
- Depolarization (+40mV)
- Overshoot (Na+ channels open and Na+ moves out of cell, beginning repolarization)
- Repolarization
- Afterhyperpolarization ( additional K+ moves out of the cell, hyperpolarizing it.
- Cells return to RMP
Muscle Spindles
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
Golgi Tendon Organs (GTO)
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
Mechanisms of Muscular Strength Gains (11)
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
Neural Control of muscular strength gains
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
Muscle Hypertrophy
main factor in muscle strength gains after neural control
Increase in muscle size
Chronic Hypertrophy
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
Autogenic Inhibition
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
Fiber Hypertrophy
caused by increases in:
- myofibrils
- actin, myosin filaments
- sarcoplasm
- connective tissue
Fiber Hypertrophy cont.
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)
Fiber Hyperplasia
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
Mechanisms for Hypertrophy (3)
Chronic Muscle Hypertrophy
Fiber Hypertrophy
Fiber Hyperplasia
How are fiber types altered with resistance training?
- increase in static strength, cross-sectional area
- decrease in percent of type 2 FTx, increase percent type 2 FTa
