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Dystrophin–Glycoprotein Complex

  1. Dystrophin–Glycoprotein Complex

The large dystrophin protein forms a rod that connects the thin actin filaments to the transmembrane protein – ß dystroglycan in the sarcolemma by smaller proteins in the cytoplasm, syntrophins



ß dystroglycan is connected to merosin (merosin are basically laminins) in the extracellular matrix by a dystroglycan. The dystroglycans are in turn associated with a complex of four transmembrane glycoproteins:  a, ß, ? and d sarcoglycan.


This Dystrophin–Glycoprotein complex adds strength to the muscle by providing a scaffolding for the fibrils and connecting them to the extracellular environment.

Extra Edge
  • Duchenne Muscular dystrophy : X linked, mutation of dystrophin gene.
  • Becker muscular dystrophy – dystrophin altered.


1. Motor Unit

  1. Definition: Each single spinal motor neuron along with the muscle fibres if innervates is called a motor unit A motor unit follows the all or none law
  2. Size principle : Slow motor units innervate slow muscle fibres, fast motor units innervate fast muscle fibres,

2. Henneman prlincipe  : In large muscles, the small, slow units are recruited first; then if required, the large units are recruited



a. Summation : 2 types

  1. Temporal = A single motor unit, stimulated many times by the same strength of stimulus
  2. Spatial = Many motor unit, stimulated at the sametime by increasing the strength of the stimulus

Muscle fibre types



Type I

Type II

Other names

Slow, red, Oxidative

Fast, White, glycolytic


For long, slow contractions

For fine, skilled movement


Fatigue late

Fatigue early

Myosin ATPase activity



Ca++ pumping capacity of sarcoplasmic reticulum






Glycolytic capacity



Oxidative capacity




Back muscles

Extra ocular muscles




High oxidative slow twitch

High oxidative fast twitch

Low oxidative fast twitch

Speed contraction




Myosin ATPase activity




Primary source of ATP production

Oxidative phosphorylation

Oxidative phosphorylation



Glycolytic enzymes




No. of mitochondria








Myoglobin content




Muscle color




Glycogen content




Fiber diameter




Rate of fatigue





Isometric and Isotonic contraction



Tension increases

Constant tension

Length remains same

Length decreases

No external work is done

External work is done

Heat released is less; more energy efficient

Heat released is more; less energy efficient



antigravity muscles maintaining e.g. legs moved in walking posture.

Length – Tension Relationship

  1. There is definite length – tension relationship in skeletal muscle. There is a particular length at which the active tension developed is maximum. This is called the optimum length.
  2. The tension developed depends upon the number of cross-bridges that can be formed between actin and myosin. On stretching no of cross-bridges increase thereby active tension is more with increase in length of muscle. On further stretching the no. of cross-bridges decrease so active tension developed is decreased. In heart this relation is called Frank Starling Law

2. Energy for muscle contraction

  1. ATP stores (last seconds)
  2. ATP from creatinine phosphate (min.)
  3. ATP from glycolysis (hrs)
  4. ATP from aerobic metabolism (days)


3. XI.  Fibrillation / Fasciculation

  1. Fibrillation : Potentials arising spontaneously in single denervated muscle fibres;
  2. Not visible grossly. fibrillation potential arise at the end plate where increases Ach   sensitivity involves the whole of the muscle end plate. seen in LMN lesion.
  3. Fasciculation: Involuntary contraction of a single motor unit; Visible grossly.

4. MUSCLE – Cardiac Muscle

  1. Functional histology
  • Muscle fibres branch and interdigitate
  • Intercalated disks are present at Z-lines Intercalated disc is the place of mechanical electrical coupling of muscle fibres
  • (Electrical coupling is by means of gap junctions)
  • The T-tubule system is at Z lines (In skeletal muscle it is at A-I band function
  1. Electrical activity

    This is different in the
  • Pacemaker cells And
  • Contractile cells                                                     


After depolarization or After potentials

  1. Introduction: It’s occurrence is abnormal. As the name suggests, these are basically potentials or depolarisations that develop after a conducted action potential.
  2. Classification: Depending on which phase of the ventricular action potential the after depolarisations occur, it can be classified as
    1. Early after depolarisations (EAD)
    2. Late after depolarisations (DAD)
  3. Significance Both EAD and DAD can set up tachycardia. They can do this either on their own or because they can trigger an activity in an already formed automatic tissue (secondary to ischaemia is an infarcted tissue etc.)
  4. EAD: Appears at the end of phase 2 or in phase 3 of the ventricular action potential. They are associated with prolonged Q-T interval i.e. it tends to occur at slower heart rates.  Thus, quinidine, which decreases the heart rate, can actually set up tachycardia (by causing EADs); this is called torsades de pointes. The exact cause of EAD is not known.
  5. DAD: Appears near the very end of phase 3 or beginning of phase 4 of ventricular action potential. They are exaggerated by tachycardia. The cause is due to increased intracellular calcium; this induces a transient diastolic inward current, possibly by promoting Na-Ca exchanger. The current causing the repetitive after depolarization is switched on by an increased intracellular calcium level. Therefore, the Ca++ antagonist verapamil and a low external Ca++ level both inhibit DAD. DADs are thought to be underlying the development of ventricular automaticity during digitalis poisoning.

Table show cardiac ion channels

Table Cardiaction

Table Cardiacion Channels and Currents





Fast Na+ (INa)

Slow Na+ (IF)











Inward rectifier (IK1)




Transient outward(I10)


Delayed rectifier(Ikr)




Acetylcholine activated(Ik,ACH)



Voltage & Receptor
























Phase 0 of myocytes

Contributes to phase 4 pacemaker

Current in SA ans AV nodal cells


Slow inward, long – lasring current

Phase 2 of myocytes and phases 4

And of SA and AV nodal Cells


Transient current: contributes to phase 4 pacemaker current in SA and AV nodal



Maintains negative potential in phase 4 : closes with depolarization : its decay contributes to pacemaker currents


Contributes to phase 1 in myocytes


Phase 3 repolarization

Inhibited by ATP ; opens when ATP



Activated by acetylcholine; Gi-protein coupled

Mechanism of contraction

This is similar to skeletal muscle.

The T tubules are wide and filled with mucopoly-saccharide

There is also the phenomenon of calcium triggered calcium release (or calcium-induced calcium release). This means that

Ca++ entry from ECF into the cardiac muscle cell triggers the release of more Ca++ from the sarcoplasmic reticulum


1. Relaxation

S.R = Sarcoplasmic reticulum

Relaxation is by decreasing the cytosolic Ca++ level by

a. Ca++ pump in sarcoplasmic reticulum

b. Ca++ Na+ antiport

c. Na+- K+ ATPase (Phospholamban inhibits the Ca++ pump in S.R. This activity of phospholamban is inhibited by its phosphorylation)


2. Relationship between electrical and mechanical events

The action potential in ventricular muscle fibres is prolonged one and therefore the refractory period is also relatively prolonged. This is the reason as to why cardiac muscle cannot be tetanised


3. Length – tension relationship

Within physiologic limits, force of contraction (as reflected by stroke volume) is directly proportional to the initial length of the muscle fibre (as determined by the end-diastolic volume). This is known as theFrank- starling’s law


4. Muscle – Smooth Muscle

a. Nerve supply

The nerve shows varicosities; the nerve establishes functional contact at several points on the muscle as it courses alongside it; this is called synapse en passant. There can be excitatory or inhibitory functional potentials.

Functional anatomy

No troponin or tropomyosin

No Z – lines (The anchorage for the actin filaments is provided by structures called dense bodies)

No T-tubule

No (or rudimentary) sarcoplasmic reticulum.


1. Visceral (single – unit)

This is the type of smooth muscle present in hollow
viscera. There are gap junctions between muscle fibres.

2. Multi – unit

Eg. Intraocular muscle of the eye (ciliaris, iris) It behaves like skeletal muscle in the sense that its response can be graded.


a. Electrical activity

  • There is no steady resting membrane potential in smooth muscle
  • There is presence of slow-waves (pacemaker potentials). These are generated in multiple foci that shift from place to place
  • Action potentials (spike potentials) are formed ? superimposed on the slow-waves

b. Excitation / inhibition in smooth muscle

  • Multi – unit Can be excited only by nerves
  • Single unit

The response can be

  • Spontaneous
  • From adjacent cells (through gap junctions)
  • Nerves (i.e. by neurotransmitters)
  • Hormones
  • Stretch
  • Cold

c. Mechanism of contraction

(Excitation contraction coupling in visceral smooth muscle is a very slow process)

  • First Ca++ entry into the cell
  • Ca++ binds to calmodulin
  • The Ca++ calmodulin complex activates myosin light chain kinase (MLCK)
  • Activation of MLCK causes phosphorylation of myosin which causes increased myosin ATPase activity and binding of myosin to actin
  • This initiates the cross-bridge cycling & contraction
  • Relaxation is by dephosphorylation of myosin by myosin phosphatase.

d. Some unique features of smooth muscle contraction

  • The process is slow
  • It is a low-energy mechanism
  • It shows the presence of latching or latch state. This is the state in smooth muscle where, even after dephosphorylation of myosin, the cross-bridges continue to ‘cling on’ for sometime. The advantage is that it allows sustained contraction with minimum energy expenditure.
  • There is a higher percentage of shortening
  • There is no fixed length-tension relationship in smooth muscle. It shows the property of plasticity. Eg urinary bladder- cytometrogram.

Smooth muscle can generate as much or even more tension than skeletal muscle/ cardiac muscle.
Force of contraction of smooth muscles : 4-6 kg / cm2
                                 Skeletal muscles : 3-4 kg / cm2

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