Skeletal Muscle Flashcards
Muscle types
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
Skeletal muscle structure
Muscles are composed of many cell types
- Muscle fibres (cells)
- Vascular cells
- Fibroblasts
- Satellite cells
skeletal muscle energy metabolism
The nonoverlapped
areas represent
specificity of
metabolic function
among the body’s
three energy
systems; the three
overlapped portions
represent
generality.
Skeletal muscle energy metabolism
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
Skeletal muscle energy metabolism and fibre
type
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
Neuromuscular junction
- Motor neuron’s action potential arrives at
the axon terminal
↓
Depolarizes plasma membrane - Opening Ca2+ channels
↓
Ca2+ions diffuse into axon terminal
↓
Ca2+binds to proteins - Synaptic vesicles release Ach
- 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) - local depolarization of the motor
end plate - Muscle fibre action potential
initiated - Propagation (end plate potential)
Events at neuromuscular junction: excitation-
contraction coupling
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
Excitation-contraction Coupling
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+)
Excitation-contraction Coupling
- 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
Calcium and Skeletal muscle contraction
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
Sliding filament mechanism
Shortening of the muscle is the result of certain parts of the actin
and myosin filament interacting with each other.
Sliding filament mechanism
Note: Typically, muscle
shortening involves one end
of the muscle remaining at a
fixed position while the other
end shortens toward it.
Cross-bridge cycle: 4 stages
- Energized myosin cross bridges on the thick
filaments bind to actin - Cross bridge binding triggers release of ATP
hydrolysis products from myosin, producing
angular movement - ATP bound to myosin, breaking link between
actin and myosin → cross bridge dissociate - 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
Tension vs load
- 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.
Types of muscular contractions
- 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
single fibre contractions
- 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.
shortening
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
Load-velocity relationship
- 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)
Frequency-tension relationship
When successive stimulations result in a sustained contraction, the contraction is
called TETANUS
Muscle-fibre type and force
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
Muscle-fibre type, force and fatigue
- 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
Muscle-fibre type, force and fatigue
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
Mechanisms involved in Muscle Fatigue
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
Techniques to determine fibre type?
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
Muscles and exercise: How do we get
stronger?
title
Neural vs. structural adaptations to strength
training
Increased strength
Increase in motor unit recruitment and firing frequency
+
Increase in muscle mass
Hypertrophy
- 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
Resistance training components
1- Time-under-tension
2- Intensity
3- Sets
4- Repetitions
6- Velocity
7- Exercise order
8- Recovery between sets
9- Frequency
10- Exercise type
Hypertrophy vs. hyperplasia
- 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
Increase in muscle mass: Increase in the
number of fibres?
- 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
Number of muscle fibres is not related to
muscle CSA nor strength
- 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
Whole-muscle and muscle-fibre
changes to resistance training
heading
Where can we find changes in muscle following
training?
CSA = area perpendicular to a muscle’s longitudinal axis
PCSA = muscle mass X cosine of the pennation angle fibre length X muscle density
Whole-muscle adaptation to resistance
training
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
Uneven distribution of whole-muscle
hypertrophy
- 6 m training 3 times/week
- Training: 8 x 6 unilateral
leg extensions 80% of RM - Femur length from
femoral head to lateral
condyle
Hypertrophy differences between muscle
groups
- 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
Muscle hypertrophy: Influence of gender
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
Time-course changes in muscle morphology
- 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
Increase in muscle size without an increase in
muscle strength
- 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)
Muscle-fibre type proportions and shifting
➢ 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
Specific muscle-fibre hypertrophic potential
- 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
summary
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
