Muscle Atrophy and Strengthening

Skeletal muscle physiology

Muscles convert chemical energy into mechanical energy via the breakdown of ATP into ADP and P to produce muscle contraction
This is activated and controlled by the nervous system and requires ongoing chemical energy supply (ATP and glucose)
Able to maintain and repair own cells
Myosin is thick and actin is thin filament - contraction occurs when actin slides over myosin towards the centre of the sarcomere, shortening it
Neuromuscular junction is the synaptic connection between the terminal end of a motor nerve and a muscle, it is the site for transmission of action potential form a nerve to a muscle

Type 1 muscle fibres

Slow oxidative
Slow contraction speed, low force output, high fatigue resistance, suitable for endurance, primarily aerobic - rely on O2, high mitochondrial density, red due to high myoglobin content

Type 2a muscle fibres

Fast oxidative glycolytic
Moderate contraction speed, intermediate force, moderate fatigue resistance, endurance and power, aerobic and anaerobic, moderate mitochondrial density, adapt to energy demand

Type 2b muscle fibres

Fast glycolytic
Fast contraction speed, high force output, low fatigue resistance, short and explosive power bursts, primarily anaerobic, glycogen for energy, low mitochondrial density

Muscle strength

The ability of a muscle to generate a force
Factors affecting this; type of contraction, frequency of firing of units, psychological factors, angle of pull, CSA of muscle, age, fitness, length/tension relationship, neural factors, length of lever arm, strength and stiffness of connective tissues, speed of contraction, genetics, number of motor units activated

Muscle power

The ability to exert force in the shortest period of time

Muscle endurance

The ability of a muscle to carry out repeated contractions over a period of time

Measurements of strength

Circumferential measurements is an indicator of atrophy - but is not sensitive of strength gains
Ultrasound scan used mainly in research
Dynamometers and isokinetic measure strength

MRC strength scale

0 = no contraction
1 = flicker, observed/palpated
2 = full range of motion with gravity counterbalanced
3 = full range of motion against gravity with hold
4 = full range of motion against gravity with minimal resistance
5 = full range of motion against maximum resistance - full function

Muscle atrophy

Loss of skeletal muscle mass
Typically due to lack of muscle stimulation (disuse atrophy)
Characterised by weakening, shrinking and decreasing muscle mass and cross sectional area of muscle fibres
Results in reduction in force production, easy fatigue, decreased exercise capability and reduced quality of life

Causes of muscle atrophy

Disuse, bedrest, non-weight bearing, splinting, neurological disruption, pathology, ageing, malnutrition

Physiology of disuse

Lack of muscle contraction due to lack of stimulation
Protein loss of cell apoptosis
Protein degradation exceeds protein synthesis
Type 1 muscle fibres affected more than type 2 muscle fibres

Physiology of muscle strengthening

Neural activation (0-2 weeks)
Muscle fibre hypertrophy (6-8 weeks)
Cellular and circulatory adaptations (10-12 weeks)

Neural activation

Enhanced neuromuscular coordination and utilisation of previously redundant motor units
More motor units are recruited within a given muscle and a stronger contraction of the muscle is therefore produced
Occurs before other physiological and physical changes that result from strength training
Neural activation is an important component of strengthening very weak muscles after a period of diuse
Main action of strengthening if effects seem to be happening in real time

Muscle hypertrophy

An increase in cross sectional area of muscle fibres
Muscle increases in size and strength - increased cross sectional area accounts for 40% of increase in strength, remaining 60% attributed to increased neural activation and other changes occurring within the muscles
Primarily occurs in type 2 muscle fibres - greater potential growth due to high capacity for protein synthesis
Later adaptation to strengthening (6-8 weeks onwards)
Satellite cells reside in muscle fibres - they become activated as a result of tissue damage (repair mechanism) - muscle injury or microdamage as a result of supra-normal muscle exercise
Trigger a process of hypertrophy which increases the cross sectional area of the muscle

Process of muscle hypertrophy

Mechanical overload on the muscle leads to microdamage to the muscle fibres
Triggers release of growth-promoting factors (anabolism)
Satellite cells are activated, proliferate, differentiate and fuse with existing muscle fibre nuclei
Fusion creates more nuclei leading to more protein synthesis
More protein synthesis relative to protein degradation, bulkier muscle fibres and increased cross sectional area, increased force production

Cellular and circulatory adaptations

Increased capillary density
Increased myoglobin content
Increased enzyme activity
Increased mitochondrial density
These are late changes, occurring up to 12 weeks after the start of a sustained programme
Endurance exercise improves skeletal muscle mitochondrial activity and results in strength gains independent of muscle size