physiology:-muscle system,function,types

-muscle is an excitable tissue
-types:-1)skeletal,cardiac,smooth
cardiac-:
wall of heart
involuntary muscle
branching shows intercalated disc
self excitability
refractive period longer,doest get fatigue

skeletal:-
attached to bone
voluntary
no braching.
fatigueness

smooth:-
wall of hollow organs ,GIT,urinary bladder.
involuntary.
no branching.
self excitatory
refractive period moderatly longer.

motor unit :-single motor neuron innervating skeletal muscle is known as motor unit.

neuro muscular junction:it is the junction between motor of neuron and muscle fiber ,it is also called as myoneural junction.

Structure of  NMJ:-
1)prejunctional membrane -axon terminal of motor neuron forms the pre junctional membrane,where it fix into the depressionin the sacrolemma called asterminal butter
-mylin is disappears at the junction
-contains vescles with neuro transmitter ACH
-contains mitochondria.
-synaptic cleft:-gap between pre and post junction membrane ,it is is about 20-30nm.,structuraly discontinues but functionaly it is continues.
acytyl choline esterase prensent in rim of junction fold


Events during transmission of impulse:-
-arrival of action potential at mitochondria at motor neuron.
-the prejunctional membrane becomes permeable to CA++
-Vesicles move toward prejunction membrane and they break and release neurotransmitter
-ACH travels to cleft and attaches to recepter in post junctional membrane.
-post junctional membrane permeable to sodium.
-there for sacrolemma depolarized action potential is developed
-spreads through sacrolemma through T-tubule cuases muscle contraction.
-end plate potential is developed.
-even at rest some amount of neurotransmitter are release and potential developed is called as miniature end plate potential(maintain rigidity of mucle)
-ACH cant remain at prolonged in cleft acetyl choline esterase enzyme breaks in to acetyl co-enzyme and choline
-acetylcoA+ choline----choline acetyl transferace



NMJ blockers;_
these are the substance which blocks the transmission of impulses from motor neuron to the skeletal muscle.
classification:-
1)prejunctional blockers:-inhibits release ACH eg:botulinum toxin
                                                                                 inhibit actin of ACH eg:tetanin toxin
2)post synaptic blockers :-competitive blockers eg:succinyl choline

Myasthemia gravis:-
NMJ disorder.
-auto immune disorder
-cuase-antibodies are produced against the recepter,it will destroy the recepter,
symptom :-
-depolirization will be weak cause weakness muscle
-fatigue
-extraoccular muscle is affected -drooping of eyelid
-masticatory deglutition muscles are affected.
-expression on face -facial muscles are affected.
-respiratory muscles affected
-enlargement of thymus due to production antibodies
treatment:-removal of thymus ,physostigmine/neostigmine-inhibit action of esterase.


muscle contraction:-(10 mark)
-muscle fibers -myo fibrils -myofilament-thick-myosin
                                                                  -thin-actin,troponin,tropomyosin
sacromere:-

-structural and functional unit of mucle fiber
-its interval between two z lines
it consist of full A band and half I band on either side.

contraction :-
Z lines come nearer
-h zone disappear -m line
-width of A remains same
-width of I reduce


muscle protein :-
1myosin:-

2)actin-
3)troponin-I-inhibits action between myosin head and actin
                 - C-ca+ binding
                  -T -
4)tropomyosin filament cover active site of actin molecule

sacrotubular system:-

function-
T tubule transmits the impulse
L tubule release calcium attach the troponin c and there fore initiate muscle contraction.

Excitation contraction coupling:-
-muscles get excited and gets contracted and it is coupled by calcium ion
-from the motor neuron through NMJ impulse is  conveyed in the the muscle ,which cause muscle is conveyed in the muscle ,which cause muscle contaction-which is a mechanical event
-maximum shortening of muscle-30%
6mm length muscle is contracted to 4mm

steps:-
1)arrival of action potential at NMJ.
2)release of ACH
3)action potential is conveyed to endplate to end plate and throughout the T tubule
4)release of  calcium from L tubule system and it attaches the troponin C
5)tropomyosin slips and exposes active site in actin molecules.
6)myosin and actin complex formed.
7)actin molecule pulled toward center cause shorteneing
8)muscle contraction

relaxation :-calcium puped back to cisternae of Ltubule
-cross bridge breaks between actin and myosin
-dissociation of actin -myosin complex
-muscle complex

Energy source :-
1)ATP
2)creatinine phosphate ----ADP---ATP------creatinine
3Stored glycogen undergoes beta oxidation

Molecular basis of muscle contraction:-
1)cross bridge formation
-orientation of myosin filament  head in one half of the thick filament fist opposite to other half
-there fore this filament can be pulled to the center from either side cuasing shortening of muscle .
-cross bridge between myosin head and actin molecules remains until one more molecule of atp fits in cleft of myosin head.
2)

Rigour mortis :-
stiffening of muscle (irreversible)after death.
-cuase exhaution of ATP therefore calcium cant come back to L tubule.
-the crossbridge between actin and myosin will  not be broken since calcium still attached to to trponin C.

significance:-
-after 2h of death rigormortis occurs after 24 hrs decompositiojn occurs 
-by looking at the condition we can determine the time of death.

types of muscle contraction:-
1)isotonic-tension remains same 
-muscle sortens 
eg:lifting of object.
2)isometric :-
tension increases
no lengthening or shortening of muscle 
length of muscle remain same 
-no work is done
eg:pushing the wall.
























credits:therapist@physiotherapycls.com