St. Luke’s College of Medicine – William H.

Quasha Memorial
PHYSIOLOGY BLOCK 1

Lecture: 7 – Skeletal Muscles Date: August 7, 2015

Lecturer: Irving Tan, MD Trans Team: Saballo, Salenga, Santos, F., Santos, J.

Topic Outline
I. Striated and smooth muscles
II. Skeletal muscles
A. Structure of skeletal muscles
B. Structure of the sarcomere
III. Molecular characteristics of contractile filaments
IV. Mechanism of muscle contraction
A. General mechanism: The sliding filament theory
B. Molecular mechanism
V. Relaxation of Skeletal muscles
VI. Role of ATP and ATP production
VII. Slows and Fast Fibers
VIII. Characteristics of Muscle Contraction
A. Motor Units
B. Length-Tension Relationship
C. Muscle twitch, summation & tetanus

I. Striated and smooth muscles

Types of muscles:
Figure 3. Diagram of the Sarcomere
 Skeletal – voluntary control, striated, multinucleated
 Cardiac – involuntary control, striated, one nucleus
III. Molecular Characteristics of Contractile Filaments
 Smooth – involuntary control, not striated, one nucleus
 About 40% of the body is skeletal muscle, while another
10% is smooth and cardiac muscle 1. Thin filaments which are composed of:
 In all three muscle types, contraction is due to interaction  Double helix of actin molecules which have binding sites
between actin and myosin for myosin heads
 Troponin, which consists of 3 subunits:
II. Skeletal Muscles o Troponin C – binds to calcium ions
o Troponin T – strong affinity for actin
A. Structure of skeletal muscles o Troponin I – strong affinity for tropomyosin
 Tropomyosin – intertwined with the actin molecules;
covers the binding sites of actin

Figure 4. Components of the thin filaments

Figure 1. Basic structure of Skeletal Muscles 2. Thick filaments which are composed of:
 One pair of heavy chains, and two pairs of light chains of
 Skeletal muscle is composed of bundles or groups of
myosin molecules
muscle fibers called fascicles; fascicles are made up of
 Myosin heads – large globular structures protruding from
muscle fibers (i.e., muscle cells)
the heavy chains; acts as an ATPase; bind to actin
 Each muscle fiber is covered by a connective tissue, the
endomysium
 Individual fascicles are surrounded by the perimysium
 Epimysium surrounds the entire muscle

Figure 5. Myosin molecule: two heavy chains and four

light chains

IV. Mechanism of Muscle Contraction

A. General Mechanism: The Sliding Filament Theory
 Contraction is due to the shortening of the sarcomere, which
Figure 2. Myofibrils and the sarcomere results from the sliding of actin filaments over myosin
filaments.
 Muscle fibers are composed of several myofibrils, divided  Contracted state: actin filaments are pulled inward
into sarcomeres completely overlapping the myosin filaments
 Myofibrils are composed of the thick and thin filaments

B. Structure of the sarcomere

 Basic contractile unit in skeletal muscles
 Z-line – demarcates the sarcomere
 I-band – contains the thin filaments (actin)
 A-band – overlap of thick (myosin) and thin filaments
 H-band – contains the thick filaments only
 M-line – center of sarcomere
 Titin anchors myosin filaments to the Z-line
 Extends from Z-line to the center of sarcomere
Figure 6. Contraction of muscle fibers = shortening of sarcomere
 Very large elastic protein
 Important for organization and alignment of thick filaments

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B. Molecular Mechanism
Generation and propagation of action potential along IV. Relaxation of skeletal muscles
sarcolemma of the muscle fiber
 As long as there is an AP and Ca2+ is present in the
1. Acetylcholine released into the NMJ from the axon sarcoplasm, muscle will not relax
terminal stimulates opening of Na+-channels on the post-  Ca2+ reuptake by the sarcoplasmic reticulum is needed for
synaptic membrane on the muscle fiber, which causes muscle relaxation
depolarization of the membrane and thus generating  Ca2+-pumps such as SERCA (sarcoplasmic endoplasmic
action potential (AP)
reticulum calcium ATPase) is responsible for the re-uptake
2. AP will be propagated bi-directionally away from the
of Ca2+ from the cytosol
center of the muscle fiber.
 SERCA has no “switch”, it is continuously pumping Ca 2+ into
3. AP travels along sarcolemma and to the T-tubules.
the SR
4. DHPR (dihydropyridine receptor) on the T-tubule
senses the voltage change and becomes activated. DHPR  If depolarization is stopped, continuous action of these Ca2+
is in contact with the RYR (ryanodine receptor ATPases will decrease the cytosolic Ca2+ concentration
channels) or the calcium release channels of the SR  Due to low Ca2+ concentration, tropomyosin again covers the
(sarcoplasmic reticulum). binding sites on the actin molecules and muscle contraction
5. SR is a specialized ER of the muscles that houses high stops
concentrations of calcium ions. Activation of DHPR
triggers opening of RYR, and thus allows release of V. Role of ATP and ATP production
calcium ions into sarcoplasm. Functions of ATP
 Hydrolysis of ATP energizes the cross bridges and
maintains membrane potential
 Binding of ATP to myosin dissociates cross bridges bound
to actin
 Hydrolysis of ATP by Ca-ATPase in the SR provides
energy for Ca2+ ion transport into the reticulum
ATP production
 ATP already present in the cytosol is not enough for
sustained muscle contraction
 Hydrolysis of creatine phosphate (or phosphocreatine) by
Figure 7. Release of calcium ions from the SR through the action creatine phosphokinase regenerates ATP by converting
of DHPR and RYR ADP to ATP (which still cannot support prolonged
contraction)
Role of Calcium Ions in Muscle Contraction  Glycolysis and oxidative phosphorylation generates ATP
from the metabolism of glycogen to glucose
1. Cross bridge formation o ATP yield is dependent on oxygen supply, this is why
 Troponin-tropomyosin complex inhibits the actin filament most muscles fibers have high myoglobin content
(i.e., physically covers or inhibits active sites on actin) o more than 95%of ATP used in sustained, long term
 Ca2+ binds to troponin C and causes conformational change contraction comes from oxidative phosphorylation,
of the tropomyosin. This causes the binding sites on the which utilizes carbohydrates, fats and proteins
actin filament to be exposed. Fenn effect
2. Power stroke  The greater the amount of work performed, the greater the
 Myosin head binds to the actin filament through the exposed amount of ATP cleaved
binding sites
 As myosin head bends, bound ADP and Pi are released VI. Slow and Fast fibers
3. ATP attaches to myosin head Slow Fibers
 A new ATP molecule needs to bind to the myosin head to  Type 1, red muscles
detach it from the binding site on actin  smaller than fast fibers, innervated with smaller nerve
4. ATP is cleaved into ADP and Pi (which remain bound to the fibers
myosin head)  have more extensive blood vessel system, greatly
 ATPase activity of the myosin head immediately cleaves increased number of mitochondria and a large amount of
ATP to ADP and inorganic phosphate (Pi), which cocks the myoglobin which gives its red appearance
myosin back to its perpendicular condition (with respect to Fast Fibers
the actin).  Type 2, white mucles
 are larger for greater muscle contraction
 Mg2+ is a co-factor needed for muscle contraction; it helps  have more extensive sarcoplasmic reticulum for rapid
the myosin head in splitting ATP releases of Ca2+
 The greater the number of cross bridges in contact with the  have a large amount of glycolytic enzyme for rapid release
actin, the greater the force of contraction of energy (glycolysis)
 have less extensive blood supply and fewer mitochondria
Video on cross bridge cycling: as oxidative phosphorylation is secondary
https://www.youtube.com/watch?v=Ct8AbZn_A8A]
 deficit of myoglobin responsible for its white appearance
Table 1. Skeletal muscle fiber types and their characteristics
Characteristics of the three types of skeletal muscle fibers
Slow-Oxidative Fibers Fast-Oxidative Fibers Fast-Glycolytic Fibers
Primary source of ATP Oxidative phosphorylation Oxidative phosphorylation Glycolysis
Mitochondria Many Many Few
Capillaries Many Many Few
Myoglobin content High (red muscle) High (red muscle) Low (white muscle)
Glycolytic enzyme activity Low Intermediate High
Glycogen content Low Intermediate High
Rate of fatigue Slow Intermediate Fast
Myosin-ATPase activity Low High High
Contraction velocity Slow Fast Fast
Fiber diameter Small Intermediate Large
Motor unit size Small Intermediate Large
Size of motor neuron
Small Intermediate Large
innervating fiber

 Slow vs fast fibers:

 Glycolytic fibers are faster than oxidative fibers
 Glycolytic fibers fatigue faster; they are only for short
Figure 8. Cross-bridge cycling bursts

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 For long-term action, oxidative fibers are needed

VIDEO:
VII. Characteristics of Muscle Contraction  Cross bridge cycling:
A. Motor units https://www.youtube.com/watch?v=Ct8AbZn_A8A
 all muscle fibers innervated by a single nerve fiber
 Small motor units produce precise movements IX. QUIZ
 Large motor units produce gross movements 1. Differentiate actin filaments and myosin filaments.
 Recruitment – increase in the number of motor units Describe main function(s)
stimulated increases force and velocity of muscle 2. __________ is a thin membrane enclosing a skeletal
contraction muscle fiber.
3. What are I bands and A bands?
B. Length-Tension Relationship 4. Interaction between ___________ and __________
causes contraction
5. ________ acts as a template for initital formation of
portions of contractile filaments of the sarcomere
6. Function of mitochondria in the sarcoplasm
7. True or false: Action potential across the membrane is
brought about by the efflux of Na+ ions caused by the
opening of acetylcholine gated channels
8. Muscle contraction occurs by a _________
9. Differentiate the relaxed state and the contracted state
of a sarcomere
10. What ion is released upon generation of an action
potential and activates forces between actin and myosin
causing muscle contraction

Answers:
1. Actin Filaments: thin filaments; made up of G-actin that
forms F-actins resulting to a linear polarized filaments.
Myosin- thick filaments; utilize energy from ATP
hydrolysis to generate mechanical force
Figure 10. Illustration of length-tension relationship Functions: responsible for muscle contraction
2. Sarcolemma
 Determined by the amount of myosin-actin filament overlap 3. I bands: light bands composed on actin filaments;
 Maximum tension: when the actin filament has overlapped isotropic to polarized light
all cross-bridges of the myosin filament (Fig 10-C), but has A bands: contains myosin filaments as well as the ends
not reached the center of the myosin filament (Fig 10-A and of actin filaments where they overlap with the myosin
B) filaments
4. Cross-bridges; actin filaments
C. Muscle Twitch, Summation and Tetanus 5. Titin molecules
6. Supply myofibrils with ATP
7. True
8. Sliding filament mechanism
9. Relaxed state: barely overlapping ends of actin
filaments extending from two successive Z disks
Contracted state: actin filaments are pulled inward
among the myosin filaments, making their ends overlap
to their maximum extent
10. Calcium

Figure 11. Patterns of muscle twitch, summation, and

tetanus

Twitch “Education is not the filling of a pail, but the

 Demonstrated by electrically stimulating the nerve to a lighting of a fire”
muscle
 Gives rise to a single, sudden contraction lasting for a
fraction of a second

Summation
 Stimulus is delivered one after the other resulting in an
more elevated muscle response
 addition of individual twitches increases intensity of overall
muscle contraction
 Multiple fiber summation – depends on the number of
units contracting simultaneously (size principle)

Tetanus
 Frequency summation
 Stimulus is delivered continuously with increasing
frequency resulting in an successive contractions that
become so rapid that they fuse together
 Muscle contraction appears completely smooth and
continuous
 At a higher frequency, contraction strength will reach a
point where any increase in frequency has no further
effect in increasing contractile force

VIII. References
 Dr. Irving Tan’s lecture
 Guyton and Hall Textbook of Medical Physiology. 12 th ed.
 Berne and Levy Physiology. 6th ed.

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