Lecture 8 - Skeletal Muscle Flashcards
Loss of muscle function
- polio
- tubocurarine
- musclular dystrophy
- motor neuron disease
- polio: infection of motorneurons
- tubocurarine: blocks neuromuscular junction
- muscular dystrophy: congenital disease of cytoskeleton
Myotonia
Failure to relax at the end of a voluntary ocntraction
- caused by CTG or CCTG repears
- abnormal Na or Cl channels cause membrane hyperexcitability
Malignant hyperthermia
- rare familial disease
- triggered by anaesthesia: SR Ca release channels are opened by halothane
- simultaneous release of Ca in all muscles causes contracture and raise of temp
- Caused by mutations in the SR Ca release channel
- untreated: death through respiratory failure
- TREATMENT
dantrolene: blocks SR Ca release
The cross bridge cycle
1- calcium binds troponin
2- Troponin displaces myosin from actin’s myosin binding site
3- in an ATP dependent manner, thin filaments are physically displaced towards one another
Muscle consume ATP for
1- cross bridging cycle: 1ATP
2- SR Ca pump: 1ATP per 2 Ca2+ pumped
3- Na/K pump: 1 ATP
Sources of ATP
- ATP
- phosphocreatine
- glycogen -> lactic acid
- Glycogen + 02 -> Co2 and H2O in mitochondria
McArdles disease
- lack myophosphorylase
- an go through oxidative phosphorylation and function at normal strength
- rapid, painful fatigue
- gentle exercise is okay
Mitochondrial myopathies
- very poor exercise tolerance
- severe metabolic acidosis
- damaged mitochondria
Rigor mortis
Skeletal muscle is quite resistant to ischemia
- not active at rest
- but if ischemia is long enough, ATP is slowly consumed, and myosin cant detach from actin -> rigor
Atrophy
Muscles become smaller and thinner with disuse
- no of cells constant
- less contractile proteins
Hypertrophy
Triggered by small number of maximal contractions
- 10 repetitions daily
Endurance
Large number of low force contraction per day
- fast fivers conver to thinner slow fibres, more aerobic and fatigue resistant
