Skeletal Muscle Flashcards

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1
Q

Muscle types

A

Skeletal Muscle-Skeletal muscles are attached to bones by tendons, and they produce all the movements of body parts in relation to each other. Skeletal muscles are under voluntary control

Cardiac Muscle-only exists in the heart keeping blood pumping around the body. involuntary striated muscle.

Smooth Muscle-contracts without any voluntary control. It is made up of spindle-shaped, unstriated cells with only one nucleus. contracts slowly

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2
Q

Skeletal muscle structure

A

Muscles are composed of many cell types
- Muscle fibres (cells)
- Vascular cells
- Fibroblasts
- Satellite cells

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3
Q

skeletal muscle energy metabolism

A

The nonoverlapped
areas represent
specificity of
metabolic function
among the body’s
three energy
systems; the three
overlapped portions
represent
generality.

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4
Q

Skeletal muscle energy metabolism

A

1.CreatinePhosphate (CP)
* Provides energy very fast to
form ATP from ADP but lasts
only 1-2 seconds
2.Glycolysis
* Energy from glucose in the
absence of oxygen (anaerobic
metabolism)
3.Oxidative phosphorylation
* Energy from glucose or fat in the
presence of oxygen (aerobic
metabolism)
Replenishing muscle stores of glycogen and CP, and removing lactic acid requires energy.
To achieve this the muscle uses more oxygen to produce the energy needed after the exercise has finished. This is
referred to as the OXYGEN DEBT

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5
Q

Skeletal muscle energy metabolism and fibre
type

A

Two main types of fibres that differ in three characteristics:
* Primary mechanisms used to produce ATP
* Type of motor neuron innervation
* Type of myosin heavy chain expressed
Type:
* IIx: Fast-twitch, fast-glycolytic fibres
* IIa: Intermediate fibres, fast-oxidative glycolytic fibres
* I: Slow-twitch, slow-oxidative fibres

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6
Q

Neuromuscular junction

A
  1. Motor neuron’s action potential arrives at
    the axon terminal

    Depolarizes plasma membrane
  2. Opening Ca2+ channels

    Ca2+ions diffuse into axon terminal

    Ca2+binds to proteins
  3. Synaptic vesicles release Ach
  4. Ach diffuses from axon terminal to motor
    end plate, binding to nicotinic receptors
    5.Binding of Ach opens an ion channel

    Na+ and K+ can pass through these
    channels (electrochemical gradient across
    plasma membrane means more Na+ moves
    in than K+ out)
  5. local depolarization of the motor
    end plate
  6. Muscle fibre action potential
    initiated
  7. Propagation (end plate potential)
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7
Q

Events at neuromuscular junction: excitation-
contraction coupling

A

Note: Every action potential in a motor neuron normally
produces an action potential in each muscle fibre in its
motor unit.
This is different from synaptic junctions between neurons, where multiple excitatory
postsynaptic potentials must occur for threshold to be reached and an action potential
elicited in the postsynaptic membrane

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8
Q

Excitation-contraction Coupling

A

The sequence of events by which an action potential in the plasma membrane
activate the force-generating mechanisms

  • An action potential in a skeletal
    muscle fibre lasts 1 to 2 ms and
    is over before signs of
    mechanical activity begin
  • Mechanical activity following an
    action potential may last 100 ms
    or more (depending on
    availability of intracellular Ca2+)
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9
Q

Excitation-contraction Coupling

A
  • Relaxed Muscle
    Low Ca2+
    Cross-bridge cannot bind with Actin
    because Tropomyosin is covering the
    binding site (Troponin holds tropomyosin
    over binding site)
  • Active Muscle
    High Ca2+
    Ca2+ binds to troponin → tropomyosin
    moves away from cross-bridge binding
    site → Actin binds to cross-bridge
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10
Q

Calcium and Skeletal muscle contraction

A

Two proteins are responsible
for linking the membrane
action potential with calcium
release in the cell
– Dihydropyridine(DHP) receptor
(Membrane)
– Ryanodine receptor
(sarcoplasmic reticulum)
* Removal of Ca2+ from the
cytosol requires energy

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11
Q

Sliding filament mechanism

A

Shortening of the muscle is the result of certain parts of the actin
and myosin filament interacting with each other.

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12
Q

Sliding filament mechanism

A

Note: Typically, muscle
shortening involves one end
of the muscle remaining at a
fixed position while the other
end shortens toward it.

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13
Q

Cross-bridge cycle: 4 stages

A
  1. Energized myosin cross bridges on the thick
    filaments bind to actin
  2. Cross bridge binding triggers release of ATP
    hydrolysis products from myosin, producing
    angular movement
  3. ATP bound to myosin, breaking link between
    actin and myosin → cross bridge dissociate
  4. ATP bound to myosin, is split, energizing the
    myosin cross bridge

ATPase: an enzyme which
determines the speed of ATP
hydrolysis and resulting
sarcomere shortening velocity

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14
Q

Tension vs load

A
  • Tension: The force that a muscle exerts
    on the joint when it is contracting is
    called the tension of the muscle.
  • Load: The force that is exerted on a
    muscle by an object is called the load of
    the muscle.

Muscle tension must exceed the load in order for the muscle fibres to shorten, and therefore move the object that is responsible for the load.
If muscle tension does not exceed the load then the muscle will either remain at the same length, or it will lengthen.

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15
Q

Types of muscular contractions

A
  • SHORTENING CONTRACTION (concentric contraction)
    ➢Constant load, muscle shortens
    ➢Tension > load
  • ISOMETRIC CONTRACTION
    ➢Constant muscle length
  • Free object: load = tension
  • Fixed object: load => tension
  • LENGTHENING CONTRACTION (eccentric contraction)
    ➢Muscle length increases
    ➢load > tension
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16
Q

single fibre contractions

A
  • The mechanical response of a
    muscle fibre to a single action
    potential is known as a twitch.
  • After the action potential, there is a
    latent period(few milliseconds)
    before the tension in the muscle
    fibre begins to increase.
  • The time interval from the beginning
    of tension development (at the end
    of the latent period) to the peak
    tension is the contraction time.
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17
Q

shortening

A

In a shortening contraction, an increasing load causes:
* The latent period to increase
* The velocity of shortening to slow down
* The total duration of the twitch to become shorter
* The distance shortened to become less

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18
Q

Load-velocity relationship

A
  • In the absence of a load, a shortening contraction
    reaches its maximum shortening velocity
  • When the load increases to the point where the
    muscle is not able to move it, then the contraction
    becomes isometric
  • When the load increases beyond the peak tension
    that a muscle can produce, the contraction becomes
    lengthening (eccentric)
19
Q

Frequency-tension relationship

A

When successive stimulations result in a sustained contraction, the contraction is
called TETANUS

20
Q

Muscle-fibre type and force

A

Skeletal muscle contains two main types of fibres that differ in
three characteristics:
* Primary mechanisms used to produce ATP
* Type of motor neuron innervation
* Type of myosin heavy chain expressed

Type:
* IIx: Fast-twitch, fast-glycolytic fibres

  • IIa: Intermediate fibres, fast-oxidative glycolytic fibres
  • I: Slow-twitch, slow-oxidative fibres
21
Q

Muscle-fibre type, force and fatigue

A
  • Most muscles have a mixed composition
  • Different fibres with different properties
  • Referred to as ‘fast’ (II) and ‘slow’ (I) twitch
  • Fast twitch equally sub-divided (IIa, IIx)
  • On average 45 –55% type I fibres in arm and
    leg muscles
  • No gender differences in fibre distribution
  • Large intra-individual variation
  • Trend in distribution consistent across
    muscle groups
22
Q

Muscle-fibre type, force and fatigue

A

Muscle fibres are categorised
based on how fast they
contract and the metabolic
pathways that they utilise to
produce ATP.

Slow oxidative fibres
Low ATPase activity, highly oxidative

Fast oxidative fibres
High ATPase activity, highly
oxidative/moderately glycolytic

Fast glycolytic fibres
High ATPase activity, highly
glycolytic

23
Q

Mechanisms involved in Muscle Fatigue

A

Fatigue is not associated with ATP depletion (Preventing rigor?)
1.CONDUCTION FAILURE Caused by potassium accumulation in
the T-tubules Fast recovery
2.LACTIC ACID BUILDUP Acidic environment in muscle affects the
physiological functioning of proteins and the mechanisms
involved in calcium release and re-uptake
3.INHIBITION OF CROSS-BRIDGE CYCLING Accumulation of ADP
and Pi in muscle fibres slows down the cross-bridge cycling by
preventing the release of cross-bridges from actin molecules
4.FUEL SUBSTRATES Muscle glycogen, blood glucose, dehydration.
5.CENTRAL COMMAND FATIGUE Failure to propagate signals from
the brain to the motor neurons

24
Q

Techniques to determine fibre type?

A

Colour of fibre (~1900)
* EMG identification of motor units (~1950)
* Fibre speed and oxidative capacity (~1970)
* Myosin heavy chain isoform (~1990)
* Genomic nomenclature (~2000)
Gene expression e.g. slow / fast contractile speed families,
mitochondrial gene families

25
Q

Muscles and exercise: How do we get
stronger?

A

title

26
Q

Neural vs. structural adaptations to strength
training

A

Increased strength
Increase in motor unit recruitment and firing frequency
+
Increase in muscle mass

27
Q

Hypertrophy

A
  • Increase in muscle fibre size
  • Due to the addition of contractile
    proteins in the muscle cell
  • Protein synthesis > protein
    breakdown
    Depends on:
  • Initial strength
  • Duration of the training program
  • Training technique
28
Q

Resistance training components

A

1- Time-under-tension
2- Intensity
3- Sets
4- Repetitions
6- Velocity
7- Exercise order
8- Recovery between sets
9- Frequency
10- Exercise type

29
Q

Hypertrophy vs. hyperplasia

A
  • Increase in the number of
    muscle fibres
  • There is evidence of
    hyperplasia in animals
  • However, there is not
    enough evidence to
    support hyperplasia in
    humans
30
Q

Increase in muscle mass: Increase in the
number of fibres?

A
  • 12-wk elbow flexor
    resistance training 3
    times/wk
  • 3 sets of 4 elbow flexor
    exercises at 10RM
    ➢ Significant increase in
    muscle fibre CSA but not
    in number of fibres
31
Q

Number of muscle fibres is not related to
muscle CSA nor strength

A
  • Muscle fibre number was
    estimated in:
    ➢5 elite body-builders
    ➢7 intermediate body-builders
    ➢13 age-matched controls
  • Strong correlation between
    fibre CSA, muscle CSA and
    strength
  • No correlation between the
    number of fibres, muscle CSA
    and strength
32
Q

Whole-muscle and muscle-fibre
changes to resistance training

A

heading

33
Q

Where can we find changes in muscle following
training?

A

CSA = area perpendicular to a muscle’s longitudinal axis

PCSA = muscle mass X cosine of the pennation angle fibre length X muscle density

34
Q

Whole-muscle adaptation to resistance
training

A

14-wk lower-limb resistance
training (38 sessions)
* 4-5 sets of hack squats
* Incline leg press
* Knee extension
* Hamstring curls
* Calf raises
* 3-10 RM

10%increase

35
Q

Uneven distribution of whole-muscle
hypertrophy

A
  • 6 m training 3 times/week
  • Training: 8 x 6 unilateral
    leg extensions 80% of RM
  • Femur length from
    femoral head to lateral
    condyle
36
Q

Hypertrophy differences between muscle
groups

A
  • Upper body muscles
    appear to elicit greater
    hypertrophy with
    resistance training
    This could be due to:
  • Habitual loading of the
    lower extremities
  • Fibre-type composition
37
Q

Muscle hypertrophy: Influence of gender

A

Women have ~60-80%
strength, fibre and
muscle CSA of men
* Absolute changes in
strength and muscle
mass with resistance
training is greater for
men
* Relative change in
strength/mass is similar
between genders

38
Q

Time-course changes in muscle morphology

A
  • 6w training 3 x per/wk
  • Unilateral knee
    extensions 75% of RM
  • Trained leg (T): increased
    strength, fibre length and
    muscle mass
  • Untrained (UT) leg did not
    change its morphology
  • Morphological changes
    seen from the 3rd week
39
Q

Increase in muscle size without an increase in
muscle strength

A
  • 21 straight days of training
    Testing arm
  • 1RM test and maximal
    voluntary isometric
    contraction (MVC) for
    unilateral elbow flexion
    exercise
    Training arm
  • 1RM test and MVC + 3 sets
    of exercise (70% 1RM)
40
Q

Muscle-fibre type proportions and shifting

A

➢ Muscle-fibre type proportion
varies across sports
➢ Type II fibres have greater
potential for hypertrophy
➢ Type I fibres have greater
aerobic capacity
➢ Research has shown changes
from IIa to IIx and vice-versa
➢ Changes from type I to type II
fibres and vice-versa is less
clear

41
Q

Specific muscle-fibre hypertrophic potential

A
  • Low-load exercises
    can activate type II
    fibres only if
    performed until
    volitional fatigue
  • This could increase
    muscle fibre size due
    to the higher
    potential of type II
    fibres to hypertrophy
42
Q

summary

A

Muscular and neural factors responsible for gains in strength
* Mechanisms of hypertrophy
* Molecular mechanisms responsible for gains in muscle mass
* Whole-muscle and fibre-type adaptations to resistance
(strength) training

43
Q
A