CHAPTER 57 — Smooth Muscle 427

contraction is produced with little energy expenditure.

• Penile erection and dysfunction—Sildenafil RMP of smooth muscle is unstable (less when muscle is ac-
inhibits enzyme phosphodiesterase (which tive and high when inactive. Slow sine wave potentials are
produced which are few mV in magnitude. Action poten-
normally decreases cGMP by converting it tial is fired when the slow potentials reach threshold value.
to 5’GMP). NO relaxes smooth muscle by In visceral smooth muscle of gut, spike potentials are seen.
increasing cGMP. So, sildenafil increases Spike potentials are superimposed over sine waves and is
accompanied by mechanical shortening of muscle.
cGMP and blood flow in smooth muscle of
penile corpus cavernosum, offsetting pe-
nile dysfunction. RECENTLY ASKED QUESTIONS
IN EXAMINATION

CHAPTER RECAPITULATION • Excitation contraction coupling in smooth muscle

• Action potential in smooth muscle
Morphologically, smooth muscle cells lack cross striations • Single unit and multiunit smooth muscle along with
and are of smaller size. Therefore, smooth muscle is also applied aspect
known as plain muscle. Contractile units consist of inter- • Latch bridge mechanism
digitating irregular shaped and randomly arranged thick
and thin filaments. Latch bridge mechanism —Actin and
myosin remain attached even after cytoplasmic Ca2+ falls.
This is important for smooth muscle because sustained Cardiac muscle—Refer to CVS

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 Topics of Special Interest 58
KNOWLEDGE GOALS
• Differences between skeletal muscle, • Electromyography
smooth muscle and cardiac muscle • Denervation hypersensitivity
• Ryanodine receptor • Important values
• Rigor mortis

• Mutation in RyR3—Alzheimer disease.

DIFFERENCES BETWEEN SKELETAL
• Mutation of RyR also in Myasthenia gravis.
MUSCLE, SMOOTH MUSCLE AND
CARDIAC MUSCLE (Table 58-1)
Applied aspect
RYANODINE RECEPTOR a. Malignant hyperthermia— Autosomal dom-
inant disease occurring due to mutation in
• Named after plant alkaloid—Ryanodine used RyR gene, characterised by rapid rise in
in its recovery. body temperature, rhabdomyolysis, rigidity.
• This is a ligand gated calcium ion channel (cal- Precipitated by—Stress, Muscle relaxant, an-
cium as its own natural ligand). aesthetics.
• Forms • Treatment—Dantrolene Na (mortality re-
• RyR1- Skeletal muscle duces from 80% to 5%).
• RyR2- Myocardium (most important) b. Central core disease (CCD)—Autosomal
• RyR3- Widely found (especially brain) dominant disease in infants (inborn mus-
• Mechanism cle disorder) occurs due to mutation in
• In cardiac muscle—Ca2+ with DHPR (Dihy- RyR gene and characterized by hypotonia,
dropyridine receptor) at wall of T tubule→ delay in development of child, facial mus-
activates RyR→ Ca2+ release from sarcoplas- cle weakness and skeletal malformations.
mic reticulum→ Ca2+ spark. Core is formed in muscle as is devoid of
• CICR (Calcium induced calcium release). mitochondria and some enzymes.
• In skeletal muscle—Physical coupling of
DHPR with RyR.
• Clinical significance
• Antagonists—Ryanodine, dantrolene, local RIGOR MORTIS
anaesthetics (procaine, tetracaine).
Permanent irreversible contraction of muscles af-
• Agonists—Heparin, cyclic ADP polyribose
ter death is called as rigor mortis. It occurs due
(physiological antagonist), xanthines.
to depletion of ATP leading to permanent link
• Mutation in RyR1—Malignant hyperthermia,
between actin and myosin that is actomyosin fails
CCD (central core disease).
to dissociate.
• Mutation in RyR2—Arrythmogenic right ven-
tricular dysplasia, stress-induced ventricular • Rigor mortis occurs 2–3 h after death and disap-
tachycardia. pears after 24–36 h due to release of lysosomal

429

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430 SECTION VII — NERVE MUSCLE PHYSIOLOGY

Table 58-1 Differentiating features of skeletal muscle, smooth muscle and cardiac muscle

Features Skeletal Muscle Smooth Muscle Cardiac Muscle

Location Associated with bones Viscera Heart
Striations Present (as actin-myosin Absent Present
regularly arranged)
Shape Cylindrical and branched Spindle shaped and un- Ribbon like and branched
branched
Nucleus >1 (peripheral)a 1 1 (central)a
Length 1–4 cm 50–500 µm 80–100 µm
Diameter 50–500 µm 2–10 µm 15 µm
Myofibrils Present Absent Present
Sarcoplasmic reticulum Very well developed Well developed Well developed but less than
skeletal muscle
Sarotubular system Well developed, two triads/ Present, but not much de- Present, one triad/
sarcomere, T-tubule at A-I veloped sarcomere, T-tubule at
junction Z line
Mitochondria Less Less More
Troponin Present Absent Present
Stimulation Somatic nerves Autonomic (sympathetic- Autonomic (sympathetic-
inhibitory excitatory
Parasympathetic-excitatory), Parasympathetic-inhibitory)
hormones
Control Voluntary Involuntary Involuntary
Source of calcium Sarcoplasmic reticulum Extracellular Sarcoplasmic reticulum
RMP −90 mV −55mV −90mV
Excitability More Less Intermediate
Autorhythmicity Absent Present (single unit muscle) Present
Tetanised Can be Can be Can never be
Conductivity Rapid Slow Slow
Speed of excitation- Fast Very slow Very fast
contraction coupling
Rate of contraction and Rapid Slow Rapid
relaxation
All or none law Obeyed by single muscle Obeyed Obeyed
fibre
Fatigue Possible Possible Not possible
Summation Possible Not possible Not possible
To produce contraction Troponin Calmodulin Troponin
Calcium binds with
Oxygen consumption Moderate Less More

WAY TO REMEMBER: aAs heart muscle is central one, so nucleus is central. Skeletal muscle is present peripherally and is more in
number, so more than one nucleus is present.

enzymes from muscle which decompose and spontaneous activity in muscle. Muscle does not
disintegrate the muscle mass. produce potential during relaxed state, but pro-
• Muscle length is shortened with increase in duces on contraction (Fig. 58-1).
thickness and loss of muscle excitability and Motor unit consists of a motor neuron and skel-
muscle translucency etal muscle fibres innervated by its axon terminals
(Fig. 58-2). All motor units in a muscle forms
ELECTROMYOGRAPHY muscle pool. During contraction of single muscle,
group of motor units co-ordinate together.
Electromyogram—Recording of the electrical activ- During mild voluntary activity, few motor units
ity of muscle during its activity is electromyogram. discharge and with increase in activity more and
Electromyography (EMG)—Technique of re- more motor units discharge—Recruitment of
cording electromyogram. motor units.
Normally, at rest the muscle fibres do not con- Motor unit potential (MUP)—Potential pro-
tract individually, but there is a slow asynchro- duced as a result of excitation of a single motor
nous discharge from motor units resulting in unit (Fig. 58-3 and Table 58-2).

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 CHAPTER 58 — Topics of Special Interest 431

Figure 58-1 Electromyographic tracings from human

biceps and triceps muscles during alternate flexion
Figure 58-2 Motor unit.
and extension of the elbow. [Source: Barrett, Boitano,
Barman, Brooks. Ganong’s Review of Medical Physiology.
Twenty-Third Edition. McGraw Hill. Figure 5-14, Chapter 5,
Excitable Tissue: Muscle; Section II, Physiology of Nerve &
Muscle Cells; 105.]

Figure 58-3 Motor unit potential.

Table 58-2 Characteristics of MUP

Characteristics Features Normal Range Variations

Duration Measured from starting of MUP to return 5–15 ms Increase duration—Lower motor neuron
to baseline lesions (LMNL), neuropathy, reduced
muscle temperature
Small duration—Myopathy, myasthenia
gravis
Amplitude Measured from peak to peak 0.5–2 mV Increased amplitude—Reduced muscle
temperature
Phase and turns Peaks after crossing baseline—Phase Triphasic—Positive- Polyphasic potential and turns—
Peaks before crossing base line—Turn negative-positive Myopathy
Rise time Duration from initial positive to next 500 µs More rise time—Increased resistance of
negative peak, indicates distance intervening tissue
between needle and muscle fibre

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