Skeletal, Smooth and Cardiac Muscle Flashcards
Muscles: function
Generate force and movement
3 types of muscle + voluntary/involuntary
- Skeletal - voluntary
- Smooth - involuntary (/voluntary)
- Cardiac - involuntary
Striated muscle examples
- Skeletal: anything you can contract voluntarly
- Cardiac (heart - doesn’t fatuige)
Where would smooth muscles be found
Blood vessels, vas deferens, airways, uterus, GI tract, bladder…
Explain skeletal muscle cells
(histology)
- AKA muscle fibres
- Multinucleated
- Inc in size during growth
- Muscles are mundles of fibres encased in CT sheaths (white film)
- Attached to bones by tendons
What happens if skeletal muscle is damaged
- Myoblasts do not replace damaged cells
- Some satellite cells differentaite to form new muscle fibres
- Other fibres undergo hypertrophy to compensate
- Muscle never completely recovers
How does skeletal muscle form in the womb
brief - link to nuclei
Lots of small muscle cells merge together and nuclei spread out - leads to tissue becoming multinucliated
Why do skeletal muscles need a blood supply
Need energy/O2
What can too musch hypertrophy lead to
decreased vasculature
Thin filament
actin
Thick filament
myosin
What are striations
muscle tissue that is marked by transverse dark and light bands, is made up of elongated usually multinucleated fibers (includes skeletal and cardiac muscle)
What are:
* I band
* A band
* Z line
(skeletal muscle)
- I band: light bit
- A band: dark bit
- Z line: divides adjacent sarcomeres
Sarcomere
Basic contractile unit of a myocyte (muscle fibre). Is composed of two main protein filaments (thin actin and thick myosin) which are the active structures responsible for muscular contraction.
How does skeletal muscle contraction work
Physically
A band remains same length, but I badn and H zone both reduced
see sheet
What does myosin contain lots of
Binding sites on each monomer for myosin cross-bridge head
When a skeletal muscle contracts, where is there also movement
Cross bridge movement
How does ATP affect the myosin cross-bridge (head)
skeletal muscle
Resets myosin head
Give the cross bridge cycle
skeletal muscle - brief
- Cross-bridge binds to actin ([Ca2+] rises)
- Cross-bridge moves (head releases ADP+Pi)
- ATP binds to myosin causing cross-bridge to detach
- Hydrolysis of ATP energizes cross-bridge
What molecule is essential for contraction
(not Ca2+)
ATP
Explain the role of tropomyosin/tropin in skeletal muscle contraction
- Tropomyosin partially covers myosin binding site
- Held in blocking position by troponin
- Co-operative block
- Ca2+ binds to troponin
- Troponin alters shape - pulls tropomyosin away
- Remove calcium - blcoks sites again
Role of lateral sacs
skeletal muscle
Store Ca2+
sarcoplasm
cytoplasm of striated muscle cells
What makes up a motor unit
skeletal muscle
motor neurons + muscle fibres
What do motor neurons (or mototr units) do
control/regulate contraction
Tension
force exerted by muscle
Load
force exerted on muscle
Isometric
(twitch)
Contraction with constant length
e.g. weightlifting
Isotonic (or concentric)
(twitch)
contraction of shortening length
e.g. running
Lengthening
contraction with increasing length
e.g. sitting down
what are twitch contractions
single AP –> muscle fibre –> TWITCH
Explain an isometric contraction
Latent period (time to trigger Ca2+), contraction time, muscle fatuigues
Latent period
skeletal muscle
Time before exitation contraction starts
Contraction time
Occurs between start of tension and time when we have peak tension
What does skeletal muscle contraction time demend on
[Ca2+] that can be released into cytoplasm
features of isometrci contraction
skeletal muscle
Shorter latent period, but longer contraction event: as load inc, contraction velocity and distance shortened dec
Explain tetanus
in skeletal muscles
- AP is 1-2ms long but twitch may last up to 100ms
- May get more AP during contraction
- These add up = summation
How does tetanus work
Tetanic tension greater than twitch tension since [Ca2+] never gets low enough to allow troponin/tropomyosin to re-block myosin binding sites - keep [Ca2+] high in cytoplasm —> sustains contraction until muscle fatuigues
Explain the length-tension relationship
skeletal muscle
- Less overlap of filaments = less tension
- Too musch overlap = filaments interfere with each other
- Muscle length for greatest isometric tension = optimal length
Therefore, there is an optimal window of overlap for max contractile strength
lever system
lever system amplifies muscle shortening velocity producing inc maneuvability
- muscles exert far more force than the load they support
What provides the energy for contraction
ATP
What does the hydrolysis of ATP do and how does this work
Energises X-bridges:
* ATP binds to myosin
* Dissociates bridges bound to actin
* New cycle may begin
What is a secondary thing that ATP can power
Ca2+ATPase in sarcoplasmic reticulum where Ca2+ is pumbed back into the SR and contraction ends
How does muscle fatigue arise in skeletal muscles
Factors causing fatigue
During high intensity, short duration exercise:
* conduction failure due to inc [K+] —> depolarisation
* inc [lactic acid] –> acidifies proteins
* inc [ADP] and [Pi] inhibity X-bridge cycle, delaing myosin detachment from actin filaments
* Thus, important to have rich blood supply to remove waste products
Long term, low intensity exercise:
* dec muscle gycogen
* dec blood glucose
* dehydration
Central command fatigue - cerebral cortex can’t excite motor neurons effiectively
What leads to fatigue and how does it happen
Repeated muscle stimulation —> muscle fibre overrides brain and contraction stops
What does mucle fatigue depend on
fibre type, length of contraction, fitness of individual
Why do skeletal muscles fatigue (purpose)
Prevent muscles using up vast amounds to ATP which would cause rigor (e.g. muscles not able to activate new X-bridge cycles)
2 ways to characterise muscle fibre types
- Fibres fast or slow-shortening
- oxidative or glycolytic ATP forming pathways are used
Difference between fast and slow muscle fibre types
- FAST - myosin has high ATPase activity
- SLOW - had low ATPase activity
Compare oxidative and glycolytic fibres
OXIDATIVE fibres:
* inc mitochondria leads to inc oxidative phosphorylation
* inc vascularisation to deliver more O2 and nutrients
* contain myoglobin so ince O2 delviery
* Fibres red with low diameters
GLYCOLYTIC fibres:
* few mitochondria
* inc glycolytic enzymes and glycogen
* lower blood supply (don’t need so much O2)
* white fibres with larger diameters
3 types of muscle fibre
- Slow oxidative (I) —> resist fatigue
- Fast oxidative (IIa) —> intermediate resistance to fatigue
- Fast glycolytic (IIb) —> fatigue quickly
Which fibres fo most muscle groups have
mix of each
How can we recruit muscle fibres
for more controlled force
- Inc load = inc need to activate more motor units
- inc number of active motor units = recruitment
- slow oxidative fibres activated first, the fast oxidative, with fast glycolytic last (start using up glycogen stores)
What does neural control of muscle tension depend on
- Frequency of AP to motor units
- Recruitment of motor units
What does destroyed nerve/NMJ lead to
Denervation atrophy
what does not using a muscle lead to
denervation atrophy
What do both denervation atrophy and disuse atrophy lead to/cause
decreased muscle mass
What does exercise cause
hypertrophys (inc muscle mass)
What does the type of exercise you do determine
Show this
The type of muscle fibres you have:
* aerobic exercise: inc mitochondria, inc vascularisation, inc fibre diameter (–> does o.phosphorylation better)
* anaerobic (strength) exercise: inc diameter, inc glycolysis
Properties of smooth muscle
- no striations
- Innervated by ANS (not somatic NS)
- not voluntarily controlled
- Has X-bridge cycle and uses Ca2+
- Filaments and excitation-contraction coupling are different
- Exists in hollow organs (e.g. GI tract, uterus, airways, ducts)
What would inc/dec [Ca2+] do for both smooth and skeletal muscle
- Inc [Ca2+] = inc contraction
- Dec [Ca2+] = dec contraction
Explain the filaments of smooth muscles
(e.g. sizes, arrangment, contractions)
- Thick myosin and thin actin filaments (like skeletal muscle)
- Filaments arranged diagonally across cells and are anchored to membranes and cell structures by dense bodies (like Z-lines)
- Filaments still slide together to contract cell
Give steps/process of smooth muscel X-bridge cycle activation
6 steps
- Inc [Ca2+]
- Ca2+ binds calmodulin (P which helps Ca2+)
- Ca2+ -calmodulin binds to myosin light chain kinase (phosphorylatory enzyme)
- Kinase phosphorylates myosin X-bridges with TAP
- Phosphorylated X-bridges bind to actin filaments
- Contraction + tension
How does smooth muscle relax
Action of myosin light chain phosphatase which dephosphorylates X-bridges
3 sources of cytosolic Ca2+
smooth muscle
- Sarcoplasmic Reticulum (SR): less SR in smooth muscle than in skeletal, no T-tubules + randomly arranged
- Exreacellular Ca2+: voltage-activated Ca2+ channels (VACC’s)
- Ca2+ removed from sytosol by pumbing back into SR and out of cell by Ca2+ATPases (slower than in skeletal muscle)
Compare skeletal and smooth muscle in terms of effect of AP
- Skeletal: 1 AP releases enough Ca2+ to saturate all troponin sites
- Smooth: only some sites activated, can grade contraction depending on number of AP that reach cells
What does smooth muscle have
TONE: basal level of Ca2+ in cells causes a constant level of tension
What factors affect contractile activity of smooth muscle
(all in dynamic balance)
- Spontaneous electrical activity in muscle membranes = pacemaker activity
- Autonomic neurotransmitters from varicosities
- Hormones (e.g. oxytocin)
- Local factors (paracrine agents, pH, O2, osmolaruty, ion, NO)
- Stretch
What 2 types of smooth muscle can you have
explain each and give examples
Single unit:
* many cells linked by gap junctions
* signals travel between cells
* contract cynchronously
* may contain pacemaker cells
* stretch evokes contraction
* GIT, uterus, small blood vessels
Multiunit:
* few or no gap junction
* richly innervated by ANS
* don’t respond to stretch
* airways, large arteries, hairs
What is smooth muscle in most organs composed of and what does this allow
Micture of single and multiunit populations of cells: means organ can have mixture of properties in different areas
Explain smooth muscles and persistent stimulation (and inc [Ca2+])
- Phosphorylated X-bridges may be dephosphorylated when still bound to actin
- Dec rate of ATP splitting
- Slows X-bridge cycle
- Means you can maintain tension for long time with low ATP consumption
(useful in blood vessel walls that have to stay open for long periods)
Explain the process of exicitation-contraction coupling
- depolarization of the plasma membrane and its membrane invaginations (the t-tubular system) by an action potential
- transduction of the depolarization signal to the sarcoplasmic reticulum (SR) membrane
- activation of Ca2+ release from the SR
Mechanics of skeletal muscle contraction
brief - see X-bridge cycle for more
driven by cross-bridges which extend from the myosin filaments and cyclically interact with the actin filaments as ATP is hydrolysed
sliding-filament theory of muscle contraction
a muscle fiber contracts when myosin filaments pull actin filaments closer together and thus shorten sarcomeres within a fiber –> max tension when length has inc
how do differences in elastic properties of muscles contribute to force production
By influencing the speed of contractile elements, elastic structures can effect muscle force/ower In very rapid movements, elastic mechanisms can amplify muscle power by storing the work of muscle contraction slowly and releasing it rapidly.
Because of force–velocity properties, slower contractions produce higher forces and do more work (given the same strain). The release of** elastic energy** in such systems can produce power outputs that exceed the capacity of the muscle for power production; thus, this process is often called ‘power amplification’.
not in PP but in course spec - maybe worth researching???
excitatory and inhibitory junction potentials (EJP and IJP)
Postsynaptic response in muscle?
intercalated discs
complex structures that connect adjacent cardiac muscle cells
autorhythmicity
The quality of being autorhythmic, or generating its own rhythm, as for example the cells of the cardiac muscle do
cardiac action potential
a measurement of the membrane potential waveform of the cardiac myocytes signifying the electrical activity of the cell during the contraction and relaxation of the heart
functional and relative refractory period
RRP; the interval of time during which a second action potential can be initiated, but initiation will require a greater stimulus than before.
FRP; the shortest interval between two consecutively conducted impulses out of a cardiac tissue resulting from any two consecutive input impulses into that tissue
pacemaker potentials
The voltage created by impulses from an artificial electronic pacemaker or the SA node which drives the rhythmic firing of the heart. The pacemaker potential brings the membrane potential to the threshold potential and initiates an action potentia
