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Hypertrophy
increase in muscle SIZE
Atrophy
Decrease in muscle SIZE
Neural Control of Strength Gains
recruitment of motor units
increased frequency of discharge from the alpha-motor neuron
Autogenic inhibition (GTOs)
Reduction in coactivation of agonist and antagonist muscles
Recruitment of motor units
increased number of motor units recruited from increased neural drive
Synchronicity of motor unit recruitment is improved - motor action potential sync
In first few weeks of resistance training, what type of gains occur?
neural gains: better muscle coordination, stability, control
Recruiting more motor units means
increase of muscle force production - strength
Resistance Training affect on muscles:
Type I & II:
produce more force
more action neural gains protentional
more frequent nerve impulses
GTO
Golgi Tendon Organ
Measures amount of tension being applied through muscle
Transient Hypertrophy
temporary/short-term
Chronic Hypertrophy
increase in muscle size after long-term resistance training
Net increase in muscle protein synthesis
more myofibrils
more actin & myosin myofilaments
more sarcoplasm
more connective tissue
Fiber Hypertrophy
net increase in muscle protein synthesis
facilitated by post-exercise nutrition
Testosterone plays a role in
promoting muscle growth
Is there a specific workout to induce fiber hypertrophy?
eccentric training
Fiber Hyperplasia
muscle fibers can split in half w/ intense weight training (cat research)
each half then increases to the size of the parent fiber
conflicting study results may be due to differences in the training load or mode
Early gains in strength are influenced by:
neural factors
Long-term strength increases are influenced by:
muscle hypertrophy
Neural adaptations always accompany
strength gains
Neural mechanisms leading to strength gains include
increased frequency of stimulation
recruiting more motor units
more synchronous recruitment of muscle fibers
decreased coactivation of agonist/antagonist
Chronic muscle hypertrophy reflects
actual structural changes in the muscle
Immobilization
decreased rate of protein synthesis
decreased strength (3-4% per day)
decreased cross-sectional area
decreased neuromuscular activity
affects both type I and type II fibers, with greater effect in type I
muscles can recover when activity is resumed
Cessation of Training
decreased strength
little change in fiber cross-sectional area
maintenance training is important to prevent strength losses
Fiber type alterations with resistance training
results from cross-innervation or chronic stimulation
type IIx to IIa
type I to IIa
Acute muscle soreness
results from accumulation of end products of exercise in muscles/edema
usually disappears within minutes or hours after exercise
Delayed-Onset Muscle Soreness (DOMS)
soreness felt 12-48 hours after strenuous exercise
Armstrong’s model
May be caused by inflammatory reaction inside damaged muscles
Armstrong’s model
structural damage
impaired calcium homeostasis leading to necrosis
accumulation of irritants
increased macrophage activity
Exercise-induced muscle cramps
decreases in Golgi tendon organ
Increases in muscle spindle activity
Loss of strength is due to:
physical disruption in muscle
failure within excitation-contraction process
loss of contractile proteins
Reducing Muscle Soreness
reduce the eccentric component of muscle action during early training
start at low intensity then gradually increase it
begin with high-intensity, exhaustive bout eccentric-action exercise
Muscle Soreness Key points
acute muscle soreness occurs late in exercise bout and during immediate recovery period
DOMS occurs 12-48 hours after exercise
occurs mostly eccentric muscle action
causes include structural damage to muscle cells and inflammatory reactions within the muscles
muscle soreness may be an important part of maximizing the resistance training response.