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2.Ex Psy, lecture 7

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winniesmith2's version from 2018-04-16 12:45

Section 1

Question Answer
(objective) Resistance training leads too hypertrophy, neural control and hyperplasia
How does resistance training yield strength gain neuro-muscular changes.
Describe how strength gain can occur without hypertrophy – Normally motor units are recruited asynchronously – Resistance training -> more synchronous recruitment -> strength ↑ • Improved rate of force development.
Describe how Strength gains may also result from greater motor unit recruitment– Neural drive during maximal contraction ↑ – Frequency of neural discharge ↑ – Inhibitory impulses ↓ -> Improved capability to exert steady forces
Describe autogenic inhibition • Normal intrinsic inhibitory mechanisms – Golgi tendon organs (inhibit muscle contraction if tendon tension too high)  Prevent damage to bones and tendons
How can you get around autogenic inhibition Decreasing inhibitory impulses – Training -> Force ↑ – explains superhuman feats of strength.
Mechanisms of muscle strength gain: Other neural factors; co-activation of agonists and antagonists – Normally antagonists oppose agonist force – Reduced co-activation may result in (slight) strength gain
When motor units contract more synchronously muscles increase force more quickly.
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Section 2

Question Answer
Short-term increase in muscle strength – Substantial increase in maximum force – Increase in voluntary neural activation – Neural factors critical in first ~8 to 10 weeks
Long-term increase in muscle strength – Associated with fibre hypertrophy – Net increase in protein synthesis takes time to occur – Hypertrophy major factor after first ~10 weeks
what does hypertrophy mean increase in muscle size
What is transient muscle hypertrophy (after exercise bout)– Due to edema formation from plasma fluid – Disappears within hours
Describe chronic muscle hypertrophy (long term)– Reflects actual structural change in muscle – Fibre hypertrophy (bigger fibres), fibre hyperplasia (more fibres), or both
Muscle hypertrophy is maximised byeccentric training -> force increases.
Concentric training has what effect may limit muscle hypertrophy and strength gains
Why not just always train eccentricallymay not allow enough rest, other muscles may suffer that are used in the sport and not trained.
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Section 3

Question Answer
Why is muscle hypertrophy maximised by eccentric training – Disruption of sarcomere Z-lines -> protein remodeling -> overreaching
What is fibre hypertrophy • More myofibrils • More actin, myosin filaments • More sarcoplasm • More connective tissue
Describe the effect of resistance training on protein synthesis during and after exercise – During exercise: synthesis ↓, degradation ↑ – After exercise: synthesis ↑, degradation ↓
Effect of hormones on fibre hypertrophy – Testosterone facilitates fibre hypertrophy (natural anabolic steroid hormone) – Synthetic anabolic steroids  large increases in muscle mass
How can you alter genetics to increase fibre hypertrophy cause , mutation in myostatin gene (Belgian blue cows) for example.
What is fibre hyperplasia fibre splitting, each half grows to size of parent fibre. – may also contribute (some evidence in animal studies, very little evidence in humans)
What do satellite cells do fuse damage to myofibre, or alignment and fusion to produce new myofibres (hyperplasia)
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Section 4

Question Answer
what may also increase muscle strength fibre type alterations
A training regimen may not outright change fibre type, but– Type II fibres become more oxidative with aerobic training – Type I fibres become more anaerobic with anaerobic training
Fibre type conversation is possible under certain conditions: conditions for Type 1 -> 11a– High-intensity treadmill or resistance training: Type I  Type IIa
Fibre type conversation is possible under certain conditions: conditions for decrease 11x and increase 11a– Heavy resistance training programme
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Section 5

Question Answer
Describe exercise and muscle damage Sarcomere Z‐disks: anchoring points of  contact for contractile proteins – Transmit force when muscle fibres contract – Z‐disk, actin/myosin damage after eccentric work
Describe Delayed-onset muscle soreness (DOMS) 1-2 days after exercise • Muscle strain (range: stiffness  severe, restrictive pain)
What is the major causse of DOMSeccentric contractions – Level run pain < downhill run pain – Cycling: mostly concentric  mostly no DOMS – Not caused by increases in blood lactate concentrations
What indicates DOMSmuscle enzymes in blood (e.g., creatine kinase) – Suggests structural damage to muscle membrane (leak) – Index of degree of muscle breakdown
What causes the muscle sorenessWhite blood cells (neutrophils, macrophages) defend body against foreign materials and pathogens, clean up altered/destroyed cells • Muscle damage -> inflammation -> pain – Damaged muscle cells attract neutrophils – Neutrophils release attractant chemicals, radicals – Released substances and swelling stimulate pain nerves – Macrophages remove cell debris
Describe effect on DOMS on performanceDOMS-> decreased muscle force generation. Loss of strength; – Physical disruption of muscle / Loss of contractile protein – Failure in excitation-contraction coupling (appears to be most important)
How do you reduce DOMS (strategies)– Minimize eccentric work early in training – Start with low intensity training and gradually increase throughout session
If I’m a beginner in any of the following, which activity will likely result in the most severe DOMS? squash or playing football (most eccentric components).
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