2. On the basis of presence or absence of striations
Striated – skeletal and cardiac muscles
Non-striated – smooth muscle
Depending upon the control
Voluntary muscle – skeletal muscle –
controlled by somatic nerve
Involuntary muscle – cardiac and smooth
muscles – sympathetic and parasympathetic
division of autonomous NS
Classification of Muscle
3. Depending upon the situation
Skeletal muscle – attached to bone
Cardiac muscle – form the
musculature of heart
Smooth muscle – associated with
visceral organs.
11. PRODUCING BODY MOVEMENTS.
STABILIZING BODY POSITIONS.
STORING AND MOVING SUBSTANCES
WITHIN THE BODY.
GENERATING HEAT (THERMOGENESIS)
FUNCTIONS OF MUSCULAR TISSUE
30. Based on the contraction time
Red muscle
Long contraction time
Myoglobin content is more (red)
Sarcoplasmic reticulum is less extensive
Blood vessels are more extensive
Mitochondria are more in number
Long latent period
Contraction is less powerful
Fatigue occurs slowly
Contraction Time
31. White muscle
Shorter contraction time
Myoglobin content is less (pale)
Sarcoplasmic reticulum is more extensive
Blood vessels are less extensive
Mitochondria are less in number
Short latent period
Contraction is more powerful
Fatigue occurs quickly
32. Strength of stimuli
Number of Stimulus
Temperature
Load
Factors Affecting Force of
Contraction
33. Sub minimal or subliminal stimulus
Minimal stimulus or Threshold stimulus
or liminal stimulus
Submaximal stimulus
Maximal stimulus
Supramaximal stimulus
EFFECT ON STRENGTH OF
STIMULUS
34. Effect of two stimuli
1. Beneficial Effect
2. Superposition or superimposition
or incomplete summation
3. Summation
EFFECT ON NO OF STIMULUS
37. Physiological tetanus
When multiple stimuli are applied at a high
frequency, muscle remains in a contracted
state.
Relaxes only after stoppage of stimulus or
fatigued.
Pathological tetanus
Toxin of Clostridium tetani – affect NS lead to
paralysis of muscle
Upper jaw muscle – locking of jaws
If not timely treated lead to death.
TETANUS
40. The failure of relaxation of muscle after contraction in
death.
ATPs are not available and Ca++ cannot pumped back.
Develop fully up to 12 hrs and passed off when
decomposition starts after 48 hrs of death.
Medico legal importance
Determining the time of the death (rigor mortis takes
different time to set in different individuals)
Can predict, whether the death is after a long
Rigor Mortis
44. Resting membrane potential is the electrical potential
difference (voltage)across the cell membrane under
resting condition
It is also called membrane potential ,transmembrane
potential,transmembrane potential difference or
transmembrane potential gradient
There is negativity inside and positivity outside the
muscle fiber.
The condition of the muscle during resting membrane
potential is called polarized state
RMP of skeletal muscle: -90mv
Resting Membrane Potential
46. The ionic imbalance is produced mainly by 2
transport mechanisms in the cell membrane:
1.Sodium -potassium pump
Sodium and potassium ions are transported by
this pump,
It moves 3 Na ions out of the cell and 2
potassium ions inside the cell by using
energy from ATP
IONIC BASIS OF RMP
47.
48. 2.SELECTIVE PERMEABILITY OF CELL
MEMBRANE
1. Channels for major anions(negatively
charged substances )like proteins are
absent or closed.so these substances
remain inside the cell and maintain RMP
49. 1. LEAK CHANNELS
Cl- Channels are mostly closed in resting conditions
,Cl -ions are retained outside the cell.
In resting condition,all the k+ leak channels are
opened but most of the Na + leak channels are
opened.Because of this K+ which are transported
actively into the cell,can diffuse back out of cell in an
attempt to maintain the concentration equilibrium
That is,in resting condition ,the passive k+ efflux is
much greater the the passive Na+ influx
50. The sequential change of membrane potential after
application of a stimulus is known as AP.
After application of a stimulus
Magnitude of membrane potential changes
51. 2 phases
Depolarization
Initial phase of AP in which interior of the muscle
becomes positive and exterior becomes negative
Repolarization
It is the phase of AP when the potential inside the
muscle reverse back to the RMP
52. During onset of depolarization,there is slow influx of
Na+.when depolarization reaches 7- 10 Mv,the voltage
gated Na+ channels start opening at a faster rate and cause
overshoot
But the Na+ transport is short lived.So the channels
open and close quickly.
At the same time,the K+ channels start opening ,this
leads to efflux of K+ out of the cell causing repolarization
IONIC BASIS OF AP
54. GP is a mild local change in the membrane potential
that develops in receptors ,synapse,or neuromuscular
junction when stimulated.
It is also called graded membrane potential or graded
depolarization.
GRADED POTENTIAL
55. ACTION POTENTIAL GRADED POTENTIAL
PROPAGATIVE
LONG DISTANCE SIGNAL
BOTH DEPOLARIZATION AND
REPOLARIZATION
OBEYS ALL OR NONE LAW
SUMMATION IS NOT POSSIBLE
HAS REFRACTORY PERIOD
NON PROPAGATIVE
SHORT DISTANCE SIGNAL
ONLY DEPOLARIZATION OR
HYPERPOLARIZATION
DOESNOT OBEY ALL OR NONE LAW
SUMMATION IS POSSIBLE
NO REFRACTORY PERIOD
56. Change in length of muscle fibers
Change in the tension
2.PHYSICAL CHANGES
57. Stages
1. Excitation contraction coupling
2. Role of troponin and Tropomyosin
3. Sliding Mechanism
Molecular basis of muscular
contraction
58. Meaning
Process that occurs in between the
excitation and contraction of the
muscle
Excitation Contraction Coupling
59. Impulse reaches the neuromuscular junction causing
release of Acetylcholine(Ach) from motor endplate
Ach causes opening of ligand gated Na channels
Development of endplate potential causing
generation of action potential in muscle fiber.
Action potential spreads over sarcolemma and also
into muscle fiber through T-tubules .
Excitation Contraction Coupling
60. Causing rapid spread of action potential into the muscle
fibers
When action potential reaches the cisternae of L- tubules
,the cisternae are excited
Ca ions stored in the cisternae are released into sarcoplasm
The Ca ions from the sarcoplasm moves towards the actin
filamnet to produce the contraction
61. Explains how the actin filaments slide over myosin
filaments and form actomyosin complex during
muscular contraction
It is also called ratchet or walk along theory
SLIDING MECHANISM
(SLIDING THEORY)
64. The length of all sarcomeres decreased as the ‘z’
lines come close to each other.
The length of the ‘I’ band decreases since the actin
filament from opposite side overlap.
The ‘H’zone either decreases or disappears.
The length of ‘A’ band remains the same.
Changes occuring in the sarcomere
65. Pumping of ca ions into L-tubules
Release of Ca ions from troponin C
Detachment of myosin head from F actin
Muscular Relaxtion
Relaxation of the muscle
66. ATP is needed mainly for,
1. Spread of action potential into muscle
2. Liberation of Ca ions from cisternae of L-tubules
inton sarcoplasm
3. Movements of mysosin head
4. Sliding mechanism
Chemical Changes
67. Muscle fibers have 3 ways to produce ATPs
1. From creatine phosphate
2. By anaerobic cellular respiration
3. By aerobic respiration
68. In resting condition –Alkaline
During onset of contraction-Acidic
During later part of contraction-Alkaline
At the end of contraction - acidic
Changes in pH during muscular
contration
69. Resting heat
Initial heat
1. Heat of activation
2. Heat of shortening
3. Heat of relaxation
Recovery heat
Thermal changes
70. Stimulation of muscle fiber by impulse
Generation of action potential in muscle
Spreading of action potential through sarcolemma and T
tubules.
Arrival of action potential at cisternae of L-Tubules
Release of calcium ions from cisternae into sarcoplasm
EVENTS OF MUSCULAR
CONTRACTION
71. Binding of calcium ions to troponin C and change in
position of troponin C
Exposure of active sites of F actin
Binding of myosin head with F-actin and power stroke
in myosin head
Sliding of actin filaments over myosin filaments
Muscular contraction
76. Skeletal muscle fibers are innervated by motor
nerve fibers.
Terminal branch of nerve fiber is called axon
terminal.
The portion of axis cylinder expanded like a bulb
which is called motor endplate.
The motor endplate invaginates inside the muscle
fiber and forms a depression which is know as
synaptic trough or synaptic gutter
STRUCTURE
77. The membrane of the nerve ending is called the
presynaptic membrane.
The membrane of the muscle fiber is called postsynaptic
membrane which contain receptors called nicotinic
acetylcholine receptors.
The space between these two is called synaptic cleft.
Synaptic Cleft
78. The axon terminal contains mitochondria ,which is the
source of energy for synthesis of acetylcholine and
synaptic vesicles which contain acetylcholine,which is
responsible for neurotransmission
The postsynaptic membrane thrown into numerous
folds called subneural clefts
79. Definition
NMT is defined as the transfer of information from
motor nerve ending to the muscle fiber through neuro
muscular junction
It is the mechanism by which the motor nerve
impulses initiate muscle contraction
NEUROMUSCULAR TRANSMISSION
80. MOTOR NERVE FIBERS
• ACTION POTENTIAL
AXON TERMINAL
• OPENING OF VOLTAGE GATED CALCIUM CHANNELS
• ENERY OF CALCIUM IONS FROM EXTRA CELLULAR
FLUIDS
• OPENING OF VESICLES AND RELEASE OF Ach
Synaptic cleft
Passage of Ach
NEUROMUSCULAR TRANSMISSION
81. Postsynaptic membrane
• BINDING OF Ach WITH RECEPTOR AND
FORMATION OF Ach -RECEPTOR COMPLEX
• OPENING OF LIGAND GATED SODIUM
CHANNELS
• ENTRY OF SODIUM IONS FROM ECF
• DEVELOPMENT OF ENDPALTE POTENTIAL
MUSCLE FIBER
• GENERATION OF ACTION POTENTIAL
• EXCITATION CONTRACTION
COUPLING
• MUSCULAR CONTRACTION
82. Neuromuscular blockers are the
drugs ,which can prevent the
transmission of impulses from nerve
fiber to the muscle fiber through the
neuromuscular junctions
NEUROMUSCULAR BLOCKERS
83. Curare
1. Prevents transmission by combining with
acetylcholine receptors.So the Ach cannot combine
with the receptors
Bungarotoxin
1. It is a toxin from the venom of deadly snakes
2. It affects transmission by blocking the Ach receptors
IMPORTANT NEUROMUSCULAR
BLOCKERS
84. Succinylcholine and Carbamylcholine
1. These drugs block transmission by acting like
Ach and keeping the muscle in a depolarized
state.
2. These drugs are not destroyed by cholinesterase
causing muscle to remain in a depolarized state.
Botulinum Toxin
1. Dervied from the baccteria clostridium
botulinum
2. It prevents release of Ach from axon terminal
into NMJ
85. These drugs inactivate the enzyme,acetylcholinesterase
Examples
1. Neostigmine
2. Physostigmine
3. Disopropyl fluorophosphate
DRUGS STIMULATING NMJ
86. The single motor neuron,its axon
terminals,and the muscle fibers
innervated by it are together called
motor unit.
MOTOR UNIT
87. Muscular Dystrophy
1. Duchenne Muscular dystrophy
2. Becker’s muscular Dystrophy
Disease involving muscle tone
1. Hypertonicity hypertonia
2. Hypotonia
3. Myotonia
Becker type myotonia(generalised myotonia)
Thomsen type myotonia
Disorders of skeletal
Muscles(myopathy)
89. Muscular Dystrophy
1. Duchenne Muscular dystrophy
It is a sex – linked recessive disorder.
It is due to the absence of a gene product called
dystrophin in the X chromosome.
It is characterized by degeneration and necrosis of
muscle fiber
90. 2..Becker’s muscular Dystrophy
It is a sex- linked disorder
It occurs due to reduction in quantity or alteration of
dystrophin
Common features are slow progressive weakness of
legs and pelvis,pseudohypertrophy of calf muscles,fatigue
and mental retardation.
91. Slow and weak muscular contraction because of
defective neuromuscular activity
Inability to maintain the prolonged contraction of
skeletal muscular contractions
Weakness and fatigability of arms and legs
Double vision and droopy eyelids due to the weakness
of ocular muscles
Difficulty in swallowing due to weakness of throat
muscles
Difficulty in speech due to weakness of muscles of
speech
symptoms
