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OBJECTIVES

• Explain the physiological characteristics of skeletal


muscle.
• Explain the excitation-contraction coupling.
• Explain the motor units, twitch contraction and
tetanus.
• Explain the motor units recruitment.
• Explain the isotonic and isometric contraction.
• Discuss the relationship between the length and tension
of skeletal muscle fibers.
• Discuss the skeletal muscle metabolism and their
importance in different types of exercise.
• Discuss muscle fatigue.
• Discuss the different types of skeletal muscle fibers and
their importance in different types of exercise.

INTRODUCTION CATEGORIZATION OF MUSCLE


• Muscle comprises the largest group of tissues in
the body.
• Skeletal muscle makes up 40 % of body wt in men
and 32 % in women.
• Contraction of muscle allows:
- purposeful movement of whole/parts of the body
- propulsion of contents through various hollow
organs
- emptying of contents of certain organs to the
external environment

MYOFIBRIL
SKELETAL MUSCLE
• Consists of alternating dark and light bands.
• Dark band = A band while, light band = I band.
• H zone = central region of A band, less dense.
• I band is bisected by Z line.
• Sarcomere = area between two Z lines (functional unit of skeletal muscle).

Whole
muscle → muscle fiber (single muscle)→ myofibril → thick and thin filaments →
myosin and actin

Electron myograph of a myofibril


#2 types of filaments forming myofibrils:
• Thick filaments:
- found in A band only.
- myosin.
• Thin filaments:
- from I band to A band but not in H zone.
- actin, tropomyosin and troponin.

• Myofibrils are surrounded by sarcoplasmic


reticulum
– rich in glycogen, ATP, Ca2+, creatine phosphate and
glycolytic enzymes.
• T (transverse) tubules : invaginations of sarcolemma
into the center of the cell
– propagate muscle action potentials down into the cell

Actin, TROPONIN AND


MYOSIN
TROPOMYOSIN

Functions:
• forms thick
filaments
• binds to ATPase
(for ATP
hydrolysis) • Actin: major component of thin filaments, binds to myosin.
• binds to actin (for • Tropomyosin: covers the binding site on actin molecules for
muscle attachment with myosin cross bridges.
• Troponins : T (binds to tropomyosin), I (binds to actin), C (binds to
contraction) Ca2+)

SKELETAL MUSCLE CONTRACTION


SLIDING FILAMENT MECHANISM
• Properties of skeletal muscle:
– Excitability
• Thin filaments slide inward over • can generate and propagate action potential
the stationary thick filaments – Contractility
during contraction. • can shorten and generate force
• Z lines are closer → sarcomere
shortens.
• All or none response: A muscle fiber that is exposed to
• H zone and I band become
threshold stimulus will contract with a complete twitch.
shorter but A band remains
unchanged.
• The length of thin & thick • Excitation-Contraction Coupling:
filaments do not change. – The series of events starting from muscle excitation by action
potential to muscle contraction that produces sarcomere
shortening.
EXCITATION-CONTRACTION
COUPLING

• Ca2+ bind to the


troponin
• Tropomyosin
 Nerve impulse reaches NMJ, synaptic vesicles release
moves aside to
acetylcholine (ACh). expose myosin
ACh bind to nicotinic receptors on sarcolemma.

binding sites on
 Action potential (AP) spreads across sarcolemma and down into T
tubules. actin filaments.
 AP in T tubules triggers Ca2+ release from sarcoplasmic reticulum
into cytosol.

• Fresh ATP binds to the myosin head


– Myosin-ATP complex has low affinity towards actin.
– Myosin dissociates from actin and assumes its
original conformation.
– Hydrolysis of the ATP by ATPase will energize the
• At rest, myosin head (cross-bridge) is energized by :
myosin head again.
ATPase
ATP ADP + Pi + energy
• Myosin-ADP-Pi complex contains high energy. • The contraction cycle will be repeated as long as
• Upon stimulation, the cross-bridge will bind to actin. there are ATP and Ca2+ available.
• The contact between myosin and actin produces power
stroke → bending of cross-bridge → thin filaments are
pulled inward → sarcomere shortening.
• Pi released during and ADP released after power stroke.

RELAXATION
RIGOR MORTIS
• No AP in T tubules to trigger Ca2+ release.
• Ongoing activity of calcium-ATPase pump • A state of muscular rigidity that begins
returns Ca2+ back into sarcoplasmic 3-4 hours and lasts about 48-60 hours
reticulum. after death (“stiffness of death”).
• Ca2+ no longer bound to troponin.
• Tropomyosin slips back to its blocking • After death
position. – Ca2+ leaks out of sarcoplasmic reticulum →
• Actin and myosin can no longer bind. ↑ cytosolic Ca2+ → ↑ interactions between
myosin and actin
• Thin filaments return to their resting
– No fresh ATP → myosin head cannot
position. detach from actin → rigidity
VIDEO SUMMARY OF EXCITATION-
CONTRACTION COUPLING

https://www.youtube.com/watch?v=ousflr
OzQHc

FACTORS AFFECTING THE FORCE OF


SKELETAL MUSCLE CONTRACTION

• Length of muscle fiber prior to 1. LENGTH OF MUSCLE FIBER


contraction PRIOR TO CONTRACTION
• Frequency of stimulus
• Number of motor units activated
• Size of motor units activated

• Length-tension relationship: shows • AT OPTIMAL LENGTH (l0)


– Optimal zone of overlap between
how the tension/force of muscle thick & thin filaments
– Maximum tension
contraction depends on the length of
• AT LENGTH > l0
the muscle fiber before the onset of – Thin filaments are pulled out from
between the thick filaments
contraction. – Fewer actin sites available for
cross-bridge binding.
– Less muscle tension

• The tension a muscle fiber can • AT LENGTH < l0


– Thin filaments from the opposite
generate is directly proportional to the sides of the sarcomere overlapped
→ limits interactions between
number of cross-bridges formed myosin heads and actin
– Thick filaments forced against Z
between thin and thick filaments. lines → further shortening is
impeded.
– Less muscle tension
TWITCH CONTRACTION

• Twitch: mechanical response


(contraction-relaxation) of a
single muscle fiber to a single
AP.
2. FREQUENCY OF STIMULUS
• Latent period: short delay
between the muscle AP and the
beginning of muscle tension
development. Represents time
required for excitation-
contraction coupling to take
place.

AP is over/almost over before


the muscle twitch starts

TWITCH SUMMATION & TETANUS

3. Number of motor units activated


4. Size of motor units activated

MOTOR UNIT • Force increases as the number of motor units activated


increases.
• Motor unit recruitment = the process of increasing the
• Motor unit: one somatic number of active motor units for stronger muscle contraction.
motor neuron & all the • Effects of size: larger motor units generate more force than
skeletal muscle fibers it smaller motor units.
innervates • Precise movements require smaller contractions:
– Small motor units (fewer fibers)
• One nerve cell supplies
– Eg. external eye muscles, hand muscles
on average 150 muscle
• Powerful movements require larger contractions:
fibers that all contract in – Large motor units (many fibers)
unison. – Eg. leg muscles
• All muscle fibers in one
single motor unit are the
same fiber type.
TYPES OF CONTRACTION 2) Isotonic contraction
- Muscle tension remains
1) Isometric contraction constant but muscle
length changes
- Muscle tension increases - Important for body movement and for
but length of muscle moving object

remains the same a) Concentric isotonic


- E.g.: holding a book contraction
steady using an • Muscle shortens
outstretched arm • E.g.: Lifting up a book
- Important for maintaining b) Eccentric isotonic
posture and supporting contraction
objects in fixed position. • Muscle lengthens
• E.g.: Lowering a book to
the ground

SKELETAL MUSCLE METABOLISM MUSCLE FATIGUE


3 major sources of ATP: • Inability of a muscle to contract forcefully after prolonged
• Dephosphorylation of Creatine activity.
phosphate
- Creatine phosphate + ADP → Creatine + ATP • Contributing factors:
- supply lasts only about 15 sec! (very
quick but short-lived, good for a 100 m 1. Lack of ATP
sprint)
2. Accumulation of ADP and Pi → interfere with cross-bridge
• Glycolysis
- generates 2 ATPs for each molecule of
cycling and calcium release/uptake by SR
glucose metabolizedform pyruvate 3. Build-up of lactic acid
- runs in the absence of O2 (anaerobic
metabolism) 4. Accumulation of extracellular K+ → local reduction in
- For anaerobic/high-intensity exercise membrane potential → ↓ calcium release from SR
• Oxidative phosphorylation 5. Depletion of creatine phosphate
- generates 36 ATPs for each molecule
of glucose metabolized 6. Depletion of glycogen stores
- requires O2 (aerobic metabolism) 7. Central fatigue (psychological fatigue): subjective feelings
- slow, long lasting source of ATP of tiredness and desire to cease activity.
- for aerobic/endurance-type exercise

TYPES OF SKELETAL MUSCLE FIBRES


• Slow oxidative (type 1)
– Generates ATP mainly by aerobic respiration
– Slow contraction velocity
– Fatigue-resistant
– For aerobic exercise with low-level force
(jogging ,long distant swimming, marathon)
• Fast oxidative (type 11a)
– Can generate ATP via aerobic and anaerobic
respiration
– Fast contraction velocity
– Moderately resistant to fatigue
– For long-term anaerobic with high force
output (eg: 400 m run)
• Fast glycolytic (type 11b)
– Generates ATP mainly by glycolysis
– Contracts strongly and quickly but fatigue
easily
– For intense anaerobic exercise of short
duration (weight lifting, jumping, throwing a
ball)

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