Resistance/strength training Flashcards
Muscular strength
max force that a muscle group can generate
1 rep max
Muscular endurance
ability to make repeated contractions against submax load
Strength training
high-resistance (6-10 reps till fatigue) = strength increase
low-resistance (35-40 reps till fatigue) = increase endurance
Ageing
loss of muscle mass (sarcopenia)
atrophy type 2 fibres
reduced number of both type 1 and 2 fibres (loss of motor neurons)
resistance training promotes hypertrophy/strength gains in older ind but lower than young
Neural adaptations
early
strength gains during first 8 weeks of training due to nervous system
muscular strength increase first 2 weeks without increase in muscle fibre size
cross education - training of one limb results in increases strength in untrained limb
Early gains
Increased neural drive (measured via EMG)
Increased number of motor units recruited
Increased firing rate of motor units
Increased motor unit synchronization
Improved neural transmission across neuromuscular junction
Increased size of NMJ and vesicles containingACh
Hyperplasia
increased number of fibres
Hypertrophy
increased cross-sectional area of muscle fibres
type II > type I
dominant factor in resistance training-induced increases in muscle mass
due to increased muscle proteins
Muscle adaptations resistance training
increased muscle fibre specific tension in type I
increased calcium sensitivity = greater number crossbridges bound to actin
enables more actin-myosin cross-bridge formation = more force per motor unit
Resistance training protein synthesis
increase protein synthesis and breakdown
muscle growth = protein synthesis > breakdown
slow rate - exceed for 3+ weeks for sig fibre growth
Time course resistance training protein synthesis
increase 50-150% with 1-4h post exercise
elevated 30 to 48h depending on training status
muscle hypertrophy faster in untrained
Factors contribute to muscle protein synthesis increase
mRNA increases = protein synthesis at ribosome
ribosome increase in number and elevate muscle proteins synthesis capacity
activation of protein kinase (mTOR) accelerate protein synthesis
Signaling molecules stimulate mTOR activation
Phosphatidic acid (PA)
Ras homolog enriched in brain (Rheb)
Muscle contractions activate asarcolemmalmechanoreceptor stimulating synthesis of PA.
Contraction-induced activation ofsarcolemmalmechanoreceptors also activatesextracellular signal-regulated kinase (Erk)
-activeErkinhibits TSC2, which is an inhibitor ofRheb.
Hence, resistance training activates mTOR by synthesizing PA andremoving the TSC2 inhibition ofRheb
Time course molecular response resistance training
seconds = increase Rheb and PA
minutes = increase mTOR activation
hours = increase protein synthesis
Resistance training-induced hypertrophy
insulin-like growth factor-1 (IGF-1)
growth hormone
= linked to mTOR activation
single bout exercise = small increase in circulating levels
Satellite cells
stem cells located between sarcolemma and basal lamina
resistance training = activate satellite cells to divide
fuse with adjacent muscle fibres to increase myonuclei
parallel increase - no. myonuclei : size muscle fibre
addition new myonuclei to fibres = required to support increase protein synthesis
increase myofibrillar proteins
myofibre CSA
Genetic influence on hypertrophy
80% ind differbce due to genetic variation
47 diff genes major contributor to muscle mass
hypertrophy-linked genes linked to mTOR pathway - activated via resistance training
high vs low responders - ability to activate specific ‘protein synthesis’ genes in skeletal muscle
Non-responder
low genetic potential for hypertrophy
Moderate-responder
moderate genetic potential for hypertrophy
High-responder
high genetic potential for hypertrophy
Detraining strength training
muscle atrophy (20-30% in 20-30 days)
loss of strength
rate slower than endurance training
recovery rapid (6 weeks) - muscle memory - myonucleui in trained fibre not lost
Muscle protein balance
conservation muscle mass dependent on balance protein synthesis and rates protein degradation
inactive muscle - decrease protein synthesis
increase protein degradation
active muscle - increase protein synthesis
decrease protein degradation
Key mechanism muscle atrophy
increased radical production in muscle fibres (oxidative stress)
decreased protein synthesis
increased protein breakdown
strength vs endurance training
strength training increase muscle fibre
together = impairs strength gains
neural factors - impaired motor unit recruitment
overtraining
depressed protein synthesis - endurance training cell signaling interfere with protein synthesis via inhibition of mTOR by activation of AMPK