Alteration In Skeletal Muscle Function Flashcards
Replacement of muscle
Is a continual process
- contractile protein replaced every two weeks
ATROPHY
- destruction > replacement (muscle wastes away)
HYPERTROPHY
- replacement > destruction (muscle increases in cell size)
Skeletal muscle and exercise
- metabolic adaption
- sarcoplasmic reticulum swells
- increased volume of mitochondria
- increased Z band width
- increased ATPase
- increased density of T tubules systems
- increased number of contractile proteins
- little evidence of hyperplasia
Function
- movement
- posture
- joint stability
- heat generation
Exercise
High Resistance e.g. weightlifting
- stimulates contractile protein synthesis (actin and myosin) leads to fatter muscle fibres and larger muscles
- increases muscle mass and strength - may lead to hypertrophy of myosatellite cells
Endurance e.g. jogging
- increased endurance without hypertrophy
- stimulates synthesis of mitochondrial proteins, vascular changes allow for greater oxygen utilisation
- shift to oxidative metabolism (e.g. of lipids)
Atrophy
Disuse atrophy
- due to bed rest, limb mobilisation, sedentary behaviour, etc.
- loss of protein –> reduced fibre diameter –> loss of power
Atrophy with age
- +30 years muscle mass begins to decrease
- by 80 years 50% of muscle mass lost - sarcopenia
- can lead to hypothermia due to inadequate temperature regulation
Denervation (neurogenic muscular) atrophy
- signs of lower motor neutron lesions, weakness, flaccidity, muscle atrophy
- re-innervation within 3 months of recovery (after this time there is an increased risk of paralysis)
Adjustment of muscle length
- increases by sustained stretching
- addition of sarcomeres, changes in neurology and viscoelastic properties
- reduced length of muscle if immobilised (e.g. limb in plaster)
Neuromuscular junction disorders
- autoimmune destruction of the end-plate of ACh receptors
- loss of junctional folds of end-plate
- widening of synaptic cleft
Less acetyl CoA receptors, less surface area and a larger diffusion distance over the synaptic cleft
Myasthenia Gravis
SYMPTOMS
Fatiguability and sudden falling
- due to reduced ACh release
Primary signs
- ptosis (dropping upper eyelid), double vision because eyes don’t move in synchronisation
Effected by General state of health, fatigue and emotion, symptoms fluctuate
TREATMENT
- acetylcholinesterase inhibitors - keeps ACh in the synaptic cleft got longer to sustain muscle contraction for longer
- immune suppressants
- plasmapheresis - washes the blood
- thymectomy
Muscular Dystrophies
- genetic disorders that lead to progressive muscle weakness and wasting
Duchenne-Type and Becker-Type are the most severe
Muscle fibre damage in Duchenne Muscular Dystrophy
DMD
Consequence of protein abnormality
- muscle fibres tear themselves apart on contraction
- creatine phosphokinase is liberated into the serum
- calcium enters the cell causing cell death (necrosis)
- pseudohypertrophy (swelling) before fat and connective tissue replaces muscle fibres
Early onset
Gower’s sign (arms used to push and extend legs)
Contractures - imbalance between agonist and antagonist muscles
- steroid therapy (prednisolone)
Genetic research - gene therapy, stem cells, etc.
Skeletal muscle disorders
MYOPATHIES (primary muscle disease) - muscular dystrophies - inflammatory myopathies - myopathies secondary to systemic disease DENERVATION - neurological causes
Inflammatory e.g. Influenza
Electrolyte imbalance e.g. Hypokalaemia - low potassium
Thyrotoxicosis e.g. increased BMR
Hypothyroidism e.g. Hypocalcaemia causing tetany (muscle spasms)
Channelopathies e.g. Malignant hyperthermia - high temperature can be fatal
Origins of skeletal muscle problems
- neurological
- metabolic
- immunological
- neuromuscular junction
- muscle tissue
