Term
| Congenital Central Hypoventilation Syndrome |
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Definition
| Disease the correlates with hypoventilations at night time. Your ability to breathe at rest, to provide your body with O2 overnight, is severely hindered. |
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Term
| Are the muscles for respiration voluntary or involuntary? |
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Definition
The muscles for respiration can be voluntary as well as involuntary.
Breathing rate will change as a function of the changes as |
|
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Term
| What do we require muscles for? |
|
Definition
To generate force, to generate heat and to generate movement around joints.
Pumping blood.
Maintenance of structures of organs. Alter shape/volume of organs/vessels. |
|
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Term
| What's the difference between cardiac muscle, smooth muscle and skeletal muscle? |
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Definition
Smooth muscle - lots of small, large nucleus cells.
Cardiac muscle - Branched cells connected by gap junctions.
Skeletal muscle - multinucleated. Has striated pattern, relatively about a few cm long. |
|
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Term
|
Definition
| Basal Matabolic Rate - the amount of energy expended daily under resting conditions, defined as being in a post-absorptive state (not digesting food) and in thermally neutral environment. |
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Term
| Which organ(s) contribute to the most oxygen consumption? |
|
Definition
Skeletal muscle and the heart.
Skeletal muscle makes up 49.8% of the body mass but uses 88% of the oxygen
Cardiac muscle makes up 0.4% of the body mass but uses 11% of the oxygen
**This is under resting conditions |
|
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Term
| BMR, Exercise, NEAT and the Thermic Effect of Food take up how much of the energy expenditure? |
|
Definition
BMR - 60%
Exercise/NEAT - 15-50%
Thermic effect of food: 10-15% |
|
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Term
|
Definition
Non-activity thermogenesis
(the generation of heat without activity)
Examples:
-Sitting, Standing, Chewing gum, Fidgeting, Climbing stairs, Shopping
**Climbing stairs marks the highest magnitude increase. |
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Term
| If you wanted to increase the average of your calorie expenditure, which perameter of your energy expenditure would it be most effective to increase? |
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Definition
| NEAT - non-activity thermogenesis. |
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Term
|
Definition
Muscle memory.
Predetermined sequences or patterns of action potentials that dictate movement. |
|
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Term
| What does motor control include? |
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Definition
• Planning of movements
• Selection of motor programs
• Execution
• Feedback (corrections/improvements/learning) |
|
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Term
| What is the final, common pathway for all motor programs? |
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Definition
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Term
| What is the pathway that efferent impulses take? |
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Definition
| Spinal cord --> ventral root --> Alpha-motor neuron --> Neuromuscular junction (endplate) --> skeletal muscle fiber (muscle cell) |
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Term
| Which portion of the spinal core (the ventral root) leads into the alpha-motor neurons? |
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Definition
| The ventral portion of the spinal core. |
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Term
| What are the functional properties of muscle? |
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Definition
• Contractility - ability to shorten and develop force
• Excitability - ability to respond to a stimulus
• Extensibility - ability of a muscle to stretch
• Elasticity - ability of a muscle to recoil to resting length
• Energy utilization and supply |
|
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Term
| What are muscle fescicles? |
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Definition
| Bundles of muscles (IE 3 muscles in a bundle = muscle fescicle) |
|
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Term
| What are skeletal muscles composed of? |
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Definition
Skeletal muscle (muscle fescicles --> muscle fibers (cells))
Blood vessels
Nerves
Connective tissue and tendons |
|
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Term
| Which components of skeletal muscles serve the function of mechanical support? |
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Definition
Connective tissue.
It has elasticity for contraction/relaxation cycle |
|
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Term
|
Definition
| One nerve + all muscle cells it innervates |
|
|
Term
| Describe the architecture of the skeletal muscle? |
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Definition
From outside to inside:
Epimysium (surrounding the bundles of vescicles), perimysium (Surrounding the vesicles), edomysium (surrounding the muscle themselves), artery/nerve/vein, capillaries, muscle fibers. |
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Term
| What are the two kinds of muscle fibers? |
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Definition
Slow-twitch muscle
Fast-twitch muscle
Different kinds:
Slow oxidative muscle cells
Fast glycolitic muscle cells |
|
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Term
| How does the number of muscle fibers vary with movement type? |
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Definition
By movement type we mean the precision of the work.
For delicate, precise work: <10
For less precise contractions: >100 |
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Term
| Describe alpha-motor neurons. |
|
Definition
Alpha motor neurons:
- Large, myelinated axon.
- Conduction Velocity: 15-120 m/sec
- Each axon branches to innervate several muscle fibres
- All muscle fibers respond simultaneously
- Number of muscle fibers and motor units vary depending on the preciseness of the work.
- It determines the contractility and metabolic properties of muscle cells |
|
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Term
| Where is the most mitochondria found within a neuron? |
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Definition
At the motor end plate.
Synthesizing neurotransmitter, packaging, release it, take it back, then release it again.
**Because of this, the synaptic terminals become impaired first if you become deprived of oxygen. |
|
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Term
| Explain how neurotransmitters are released into the synaptic clefts. What happens after that? |
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Definition
AP's cause voltage gated Ca+ channels to open and an inward current ensues. The calcium interacts with many enzymes and cause the synaptic vesicles to migrate to the surface, fuse with the membrane and release chemical messengers (acetylcholine) into the synaptic cleft.
The acetylcholine binds to a channel (acetylcholine receptor on a ligand gated Na+ ion channel) which causes it to change its conformation and allow Na+ ions to flow into the cell.
The Na+ causes depolarization in the cell, triggering an action potential if the magnitude is great enough. |
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Term
| A muscle twitch is composed of what phases? |
|
Definition
Contraction phase
- Amount of tension/force development here
- Time of peak tension
Relaxation phase
- Rate of relaxation differs between cell types |
|
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Term
| Describe an action potential's action in a neuronal cell. |
|
Definition
1. Synaptic action potential
2. Depolarization synaptic membrane
3. Open voltage-gated calcium channels
4. Increase synapse Ca concentration
5. Movement + fusion of vesicles with synaptic membranes
6. Release acetylcholine
7. Bind acetylcholine receptors on sarcolemma
8. Depolarization of sarcolemma - action potential
9. Muscle activation |
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Term
|
Definition
| The triad is the regional junction between two sarcoplasmic reticulum cisterna and the transverse tubule. |
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Term
| A sarcomere is made up of what sections of a myofibril. (what band to what band) |
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Definition
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|
Term
| What structure binds all other structures in a sarcomere? |
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Definition
| The z-band. It's made up of a protein called alpha-actinin. |
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Term
| A muscle fiber is composed of what? |
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Definition
Thin and thick filaments.
Thin filaments = made of actin. Composed of a few different proteins within it: tropomyosin - the protein that leaves the myosin binding sites and goes along the entire length of the filament. Also made out of a group of proteins called the troponin complex (TnT, TnC, TnI) which have the ability to bind calcium.
Calcium binds to the troponin complex and initiates a conformational change.
Thick filament = made out of myosin.
- Long tail and "head" group. Most will form a dimer + has an orientation where the head will be facing up/towards the MBS
○ The head is the binding site for the actin filament.
§ Has two small proteins attached to it called "regulatory light chain" and "alkali light chain"
□ Alkali light chain - structural function. Holds the neck of the myosin.
□ Regulatory light chain - can effect that ability of the head group to interact with actin. |
|
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Term
|
Definition
| The bound version of myosin and actin. |
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Term
| What is the regulatory light chain and alkali light chain? |
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Definition
Small proteins attached to the myosin head group.
□ Alkali light chain - structural function. Holds the neck of the myosin.
□ Regulatory light chain - can effect that ability of the head group to interact with actin. |
|
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Term
| Which portion of the muscle fiber (Z, I, H, etc) does not shorten during muscle contraction? |
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Definition
|
|
Term
| Describe excitation-contraction coupling. |
|
Definition
Excitation-contraction coupling:
1. Action potential - alpha motor neuron
2. Acetylcholine (Ach) release - end plate
3. Binds to Ach receptor, sarcolemma (Na entry)
4. Depolarization sarcolemma
5. Action potential - sarcolemma
6. Bi-directional propagation - 6 m/sec
7. Also propagation down T-tubules
a. And then what? |
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Term
|
Definition
| DHP receptors - primary function in skeletal muscle is as a voltage sensor. Senses the change in voltage potential at level of T-tubules. |
|
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Term
| What are Ryanodine receptors? |
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Definition
| Proteins form a calcium release channel in the membrane of the sarcoplasmic reticulum. |
|
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Term
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Definition
| Binding protein that is found in the sarcoplasmic reticulum. Binds to calcium. |
|
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Term
| What is the name of the protein that binds calcium within the sarcoplasmic reticulum? |
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Definition
|
|
Term
| What ionic signal causes muscles to contract? |
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Definition
Ca+.
The release of calcium from the sarcoplasmic reticulum into the intracellular space of a muscle cell causes the depolarization of the muscle cell. (initiates AP) |
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Term
| What occurances happen during the relaxation phase of an action potential |
|
Definition
The removal of acetylcholine from the post-synaptic receptors
Removal of calcium back into the sarcoplasmic reticulum (performed by active transport pumps) |
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Term
| What if you had leaky ryanodine receptors? |
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Definition
You would experience muscle spasms, but it will improve lean body mass.
This channel is triggered by stress and so "leaks" occur more often with the higher levels of stress. |
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Term
| What initiates the release of the myosin head from the binding site? |
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Definition
| The binding of ATP causes the release of the myosin head from the filament. |
|
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Term
| Describe the cross-bridge cycle. |
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Definition
-To reset the cross bridge cycle, ATP binds to myosin head, which causes a dissociation of the actin-myosin complex.
-then ATP is hydrolyzed, causing myosin heads to return to their resting conformation.
-A phosphate is bound to the myosin head group, which puts it in the cocked state.
-a cross bridge forms and myosin head group binds to a new position on actin.
-phosphate is released, causing the myosin head group to change conformation, resulting in the power stroke. The filaments slide past each other.
-ADP is released, leaving the group in attached state. |
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Term
| What is rigor mortis caused by? |
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Definition
Rigor mortis is caused by the inability to create new ATP after death.
Therefore you cannot detach the myosin head group and muscles remain in the attached state.
Rigor mortis does not stop until the membranes and cellular structures break down. |
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Term
| What is the speed with which the muscle contracts dependent on? |
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Definition
| It is dependent on the speed with which the cross-bridge cycle occurs. |
|
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Term
| What are the main features of the cross bridge cycle? |
|
Definition
• cycle of attachment and detachment of myosin and actin
• Powerstroke
• Myosin pulls thin filament to move relative to the thick filament
• Switch: Calcium
• Energy cost: 1 ATP/cycle
• ATP required for detachment - rate limiting step. |
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|
Term
| What determines the maximum force a cell can develop? |
|
Definition
|
|
Term
| What determines the time course of force development of a muscle contraction? |
|
Definition
|
|
Term
| What determines the time course of relaxation of a muscle cell contraction? |
|
Definition
|
|
Term
| How many ATP are required to completely one cross-bridge cycle? |
|
Definition
| 1 ATP per cross-bridge cycle |
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|
Term
| Describe the different steps neuromuscular transmission. |
|
Definition
Activation
1) Calcium release - switch is on
2) Troponin moved from the binding sites
3) Cross bridge cycling can be propagated
Relaxation
1) Calcium reuptake into SR thru pumps
2) Calcium releases the troponin, prevents further cross bridging |
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|
Term
| What's the difference between the two types of twitch fibres? |
|
Definition
Slow twitch muscle - Type I - slow rate of development of force contraction. Has a long relaxation time. Last longer before they fatigue.
Release/reuptake of calcium limits speed.
Fast twitch muscle fiber -
Type II -use anaerobic metabolization. Better at generating short bursts of strength or speed than slow muscles.
Type Iia - Intermediate fast twitch - can use both aerobic / non-aerobic metabolism almost equally.
Type Iib - "classic" fast twitch fibers that excel at producing quick, powerful bursts of speed. |
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Term
| What are isometric contractions? |
|
Definition
Isometric contractions create force without moving a load.
- Elastic elements are in series
- Sarcomeres shorten while elastic elements stretch, resulting in little change in overall length. |
|
|
Term
| What are isotonic contractions? |
|
Definition
Isotonic contractions create force and move a load
- Concentric action is a shortening action
- Eccentric action is a lengthening action |
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Term
| What determines the amount of force a muscle will develop? |
|
Definition
| Total Force = force (pull) of an individual cross-bridge multiplied by the number of cross-bridges attached and pulling |
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|
Term
| What elements of muscle fibres contribute to the amount of force a muscle will develop? |
|
Definition
A) Cell cross-section
• Cell type / pattern of activity / sex
B) Initial muscle length (filament overlap)
C) Frequency of stimulation
D) Fatigue (decrease in expected or required power output)
-duration and intensity of activity/composition of the muscle cell |
|
|
Term
| What does a length-tense relationship express or describe? |
|
Definition
Length on bottom, increasing force on Y.
Shows passive and active forces.
Passive : Stretching elastic elements (rubber band effect)
Active: force development in response to nerve stimulation |
|
|
Term
| At what initial muscle length would you generate maximum muscle force? |
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Definition
| At roughly the resting length of the muscle there is maximum overlap of the development of crossbridges |
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|
Term
| Why is it that there is reduced possible output when your initial muscle length is shorter than resting or stretched? |
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Definition
Stretched - you pull the filaments apart. When you stretch to 2x it's length there is zero force.
Shortened - steric hindrance. They align with the wrong filaments, hitting the Z-band in the sarcomere. Deformation of the sarcoplasmic reticulum which makes it less efficient at EC coupling. |
|
|
Term
| How does the frequency of stimulation effect the force developed by a muscle cell? |
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Definition
| Temporal summation --> does not have enough time to relax after the initial stimulation. Without the time in between, the force summates and increases with each stimulation. |
|
|
Term
|
Definition
| It is when it builds up to a maximum tension and does not increase anymore. |
|
|
Term
|
Definition
Fused tetanus - maximum force that a muscle cell can develop when the stimulation occurs frequently, one right after the last.
**increasing the frequency of stimulation increases the force that a muscle cell will develop. |
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|
Term
| What is the force and duration of a muscle contraction a function of? |
|
Definition
Force/muscle cell:
- Muscle length
- Frequency of stimulation
- Cell diameter
- Fatigue
Number of muscle cells:
- Number of motor units recruited
- Number of muscle cells / motor unit |
|
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Term
| What is the order of recruitment for muscle cell types? |
|
Definition
| Start with smaller, fatigue resistant units until you move up until you hit ones that fatigue readily. |
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Term
| What does the velocity of shortening reflect load? |
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Definition
At no loads you have maximum velocity. Increasing the load decreases the velocity.
It reflects the number of cross bridges that are available to attach and pull across and ratchet the actin filament over a myosin filament.
Influenced by type of myosin and load. |
|
|
Term
| What is the energy molecule used by muscle cells? |
|
Definition
|
|
Term
| How is creatine phosphate used? |
|
Definition
Two ways.
One - as a temporal or time buffer to allow muscle contractions to proceed for a longer time by providing a source of energy substrate for the cross bridge cycle.
Two - as a spacial buffer by making the enzyme (creatine kinase) which tries to reserve energy specifically for the cross bridge cycle. |
|
|
Term
| Which level of the arterial system controls the blood flow to muscles? What stimuli does it respond to? |
|
Definition
Arterioles control the blood flow to muscles. They're really the valves that control the flow to the tissues.
1) Coming from the muscle itself - vasodilator stimuli. Adenosine
2) Sympathetic nervous system but is vasoconstrictive signal. Norepinphrine |
|
|
Term
| What are the muscle cell types? |
|
Definition
SO - slow oxidative. Type 1.
- Myosin actin ATPase low
- less extensive SR
- Speed and intensity of contraction low.
- Loaded with mitochondria depend on cellular resp. for ATP
- Low glycogen content
- Resistant to fatigue
- Dominant in muscles and responsible for posture.
FG - fast glycolitic. Type Iib (not in humans) / IIx (fastest muscle cell in humans)
- Myosin actin ATPase high
- Extensive SR network
- Fast speed of contraction/ high intensity of contraction
- Depends on glycolysis for ATP production
- High glycogen content
- Low in myoglobin
- Fatigue easily
- Dom. In muscles responsible for brief, forceful contractions. |
|
|
Term
| What are the different type of fatigues? |
|
Definition
Muscle fatigue and central fatigue.
Central fatigue = Central nervous system = causes psychological effects / protective reflexes
Peripheral fatigue = reduced neurotransmitter release, receptor activation. Cause change in membrane potential.
Sarcoplasmic reticulum situations --> reduced calcium release, reduced calcium-troponin interaction.
Depletion theories: PCr, ATP, glycogen
Accumulation theories:
H+, Pi, Lactate |
|
|
Term
| What is adaptation and what does it act on, to modify? |
|
Definition
Adaptation = changes in muscle capacity / ability upon usage.
Modify and improve motor programs:
- Central nervous system training
- Increase the rate and accuracy and motor skills |
|
|
Term
| What is angiogenesis and what increases its activity? |
|
Definition
Angiogenesis is the generation of new arterials and piping.
Aerobic exercise increases angiogenesis |
|
|
Term
| How does muscle hypertrophy occur? |
|
Definition
There is a basement membrane present on the surface of bundles of muscle fibers. Within this membrane you will find stem cells, called satellite cells in muscles.
Satellite cells can be triggered to reproduce due to damage of the muscle fibers. This will cause cytokins to be released, which releases the satellite cells and allows them to be influenced by growth factors which converts them into the required muscle cells.
Myostatin is a protein that is released from muscle and inhibits stem cell release and replication. |
|
|
Term
|
Definition
| Myostatin is a protein that is released from muscle and inhibits stem cell release and replication. |
|
|
Term
| Does the number of muscle fibers change? |
|
Definition
| The number of muscle cells does not change. Increase in muscle size during growth and exercise results from an increase in the diameter of existing muscle fiber. |
|
|
Term
| What factors influence the synthesis and degradation of proteins? |
|
Definition
Balance, influenced by:
Use (activity), feeding, aging, disease
Anabolic hormones:
Testosterone, GH (growth hormone) IGF1, insulin
Catabolic Hormones:
Glucocorticoids, myostatin (negative regulator of growth) |
|
|
Term
| How does muscle atrophy occur? |
|
Definition
1. Disuse:
Bedrest,
immobilization (casts),
denervation (spinal cord injury),
Unloading, (making it so a portion of body is no longer weight bearing...wheel barrow position),
loss of gravity (muscle has no work to do
2. Food deprivation
3. Aging (sarcopenia)
4. Disease (muscular dystrophy, cachexia {cancer induced}) |
|
|
Term
| How is the number of muscle cells, or the muscle cell itself, altered during hypertrophy? |
|
Definition
| Hypertrophy involves the increasing of the muscle cross section by increasing the number of muscle cells that are in parallel to one another. |
|
|
Term
| If the protein synthesis in a muscle exceeds protein degradation than how is the muscle affected? |
|
Definition
| The muscle will experience growth (hypertrophy) |
|
|
Term
| If protein degradation in a muscle exceed protein synthesis than how is the muscle affected? |
|
Definition
| The muscle experiences atrophy. |
|
|
Term
| How does the structure of heart muscles differ from skeletal muscles? |
|
Definition
Cardiac muscle:
- Cells are shorter and are branched / interconnected thru gap junctions.
- Possess pacemaker cells that initiate contraction -> autonomic nervous system modulate but does not initiate contraction.
Aerobic, a lot of mitochondria.
- Presence of intercalated disks (separates each cardiac cell)
- Action potential spreads rapidly from cell to cell. |
|
|
Term
|
Definition
Found in cardiac muscles. It is a form of synaptic cleft between cells that is for electrical transmission rather then chemical.
Gap junctions are regions of very low electrical resistance. |
|
|
Term
| What gives the heart its characteristic rhythm? |
|
Definition
| The influence of the Sinotal Node (SA node) in the heart. |
|
|
Term
| How do you modulate the force of contraction within the cardiac muscle? |
|
Definition
| You modulate the force of contraction by the amount of calcium that is released within the cell. |
|
|
Term
| In cardiac muscle, what ion serves as a signaling molecule? |
|
Definition
Ca+, same as in skeletal cells, is the on off switch.
It binds to troponin and allows the CB to work as it does it skeletal muscle. |
|
|
Term
| Contractions of the heart are subject to what form of regulation? |
|
Definition
They are subject to neuronal/hormonal regulation.
Neuronal = signals coming from the sympathetic nervous system.
Hormonal = norepinphrine / epinephrine
- epinephrine -> causes increased contractility (increases interaction between troponin/calcium)
- Norepineprine -> signals the heart to slow action potentials / heart rate. |
|
|
Term
| What are the key differences between the function of cardiac muscles and skeletal muscles? |
|
Definition
Main difference:
1) Spntaneous action potential from pacemakers
a. Presence of gap junctions
b. AP's in cardiac heart muscles do not summate. One AP = one contraction.
2) Hormonal regulation of contractility
3) Calcium induced caclium released as a way of releasing from the SR
4) Importance of getting calcium outside the cell with a sarcolemma calcium pump
5. Twitch duration is slower than skeletal muscle cells.
6. Length-tension curve is right-shifted. Muscle cells stretch which increases force of contraction. |
|
|
Term
| How do smooth muscle cells differ from skeletal muscle cells? |
|
Definition
Lower number of mitochondria
Non-striated muscle --> has "dense bodies", which are the equivalent to the Z-bands in skeletal muscle. This is where thick/thin filaments attach and is the mechanical coupling between cells.
Thick filament (smooth muscle) = made up of different types of myosin from skeletal or cardiac muscle
Thin filament = made up of actin and tropomyosin but no troponin. Therefore, calcium cannot bind to troponin to initiate the reaction.
Has gap junctions for electrical and chemical communications. |
|
|
Term
| What is the difference in the contractile properties of smooth muscle and skeletal muscle? |
|
Definition
smooth muscle can contract to 50% of its original size.
Skeletal muscle can contract to 30% of its original size. |
|
|
Term
| What causes smooth muscle to have a much slower contraction than skeletal muscle? |
|
Definition
| it is the cross bridge cycle that limits the speed at which SM contracts. |
|
|
Term
| Describe the control of smooth muscle functions: |
|
Definition
Neural control:
- Extrinsic innervation : from autonomic nervous system
- Intrinsic innervation : from pacemaker cells
○ From nerve plexus within the smooth muscle tissue
Hormonal control:
Local Control : mediators released from surrounding tissues
- Endothelial cells
- Skeletal muscle cells
○ Release nitric oxide (vasodilator) or adenosine |
|
|
Term
| What is the difference between multiunit and unitary smooth muscle? |
|
Definition
The cells in multiunit smooth muscle are electrically isolated, which allows for finer muscle control.
The cells in unitary smooth muscle are electrically connected by gap junctions so that when one smooth muscle contracts, they all do. |
|
|
Term
| Describe the excitation-coupling of smooth muscles. What are they regulated by? Where is the control of the contraction from? |
|
Definition
Instead of binding to troponin, calcium binds to Calmodulin to form a calcium-calmodulin complex.
The calcium-calmodulin complex then binds to the enzyme myosin light chain kinase. This is the signal for the muscle to contract.
Myosin light chain phosphatase is the enzyme that removes the phophates and allows a new contraction to occur. This step is very slow!
It is under thick filament control - IE the control of contraction is found on the thick filament.
CALCIUM IS THE ON-OFF SWITCH!
Regulated by:
Voltage gated calcium channels, receptor mediated calcium channels, receptor mediated calcium release from endoplasmic reticulum |
|
|
Term
| In smooth muscle cells, how is the force of contraction mediated? |
|
Definition
The degree of force depends on the degree of phosphorylation of the myosin in smooth muscle.
The amount of phosphorylation that occurs is proportional to the concentration of calcium that is in the cells. |
|
|
Term
| How many ATP does the cross-bridge cycle for smooth muscle require? Is it more energetically expensive than skeletal muscle? |
|
Definition
2 ATP
Even though it requires more ATP, it is less energetically expensive because of how long each contraction takes. For 1 ATP you get tension for a much longer period in smooth muscle cells. |
|
|
Term
| What is calcium dependent phosphorylation? What molecule is influenced by this and what does it o? |
|
Definition
Calcium dependent phosphorylation requires the binding of calcium to a molecule in order phosphorylate another molecule.
In smooth muscle, calcium binds to calmodulin to form Ca+-Cal complex. This complex them binds to the enzyme Myosin Light Chain kinase which phosphorylates the myosin and causes it to contract. |
|
|
Term
| Why do larger organisms require circulatory systems? |
|
Definition
| Because simple diffusion is not efficient enough to reach all of the tissues of a multicellular organism. |
|
|
Term
| What is most crucial when considering the efficiency of simple diffusion? |
|
Definition
| The length of the diffusion path. The longer it is the less efficient diffusion will be. |
|
|
Term
|
Definition
Bulk flow.
Oxygen and glucose are brought close to cells by a process of bulk flow (perfusion) of internal medium (blood). |
|
|
Term
| Which has the longer diffusion step-length. A gas molecule in gas, or a gas molecule in fluid? |
|
Definition
| A gas molecule in gas will be able to travel further without bumping into another molecule. Therefore, gas in gas has longer diffusion step-lengths |
|
|
Term
| Describe the pathway blood takes through the heart. |
|
Definition
| Right atrium to right ventricle. Right ventricle to pulmonary arch. Lungs to left atrium. Left atrium to left ventricle. Left ventricle into aorta. Aorta into systemic circulation. Systemic circulation (superior/inferior vena cava) into right atrium once more |
|
|
Term
| If the heart muscle is stretched so that it contains more blood volume than normal, how does this affect cardiac output? |
|
Definition
It will increase the volume of cardiac output by signalling for a harder contraction.
This avoids volume loading in other portions of the circulation. |
|
|
Term
| At rest, what is the average volume flow for someone? |
|
Definition
|
|
Term
| Which organ systems have more than one capillary bed in series? |
|
Definition
| The kidneys. One for filtering and one for absorption. |
|
|
Term
| Which organ systems have more than one capillary bed in parallel? |
|
Definition
|
|
Term
| What is the speed of blood flow in the capillaries relative to the rest of the circulation system? Why? |
|
Definition
Blood flow is at a much lower velocity in the capillaries than in any other part of the CS.
It is much lower because of the drastic increase in cross-sectional area of capillaries due to so many capillaries running in parallel to one another. |
|
|
Term
| Blood velocity changes with a change in what? |
|
Definition
| Change in cross sectional area (higher cross-sectional area = lower blood velocity) |
|
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Term
| Which portion, the arteriole or venous, side of the circulatory system serves as the "blood store" |
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Definition
| The venous side of the circulation serves as the blood store. |
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Term
| Is the resistance to blood flow in the pulmonary system higher or lower than the resistance to blood flow in the systemic circulation? |
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Definition
| Resistance to blood flow in the pulmonary circuit is much less than resistance to blood flow in systemic surface. |
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Term
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Definition
| Change in volume to a change in pressure. Larger change means a higher compliance. |
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Term
| How much compliance would you have with a leaky vessel? |
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Definition
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Term
| How do collagen fibers influence artery compliance? |
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Definition
| Collagen fibers are stiff, so they decrease artery compliance. |
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Term
| How do elastin fibers influence artery compliance? |
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Definition
| Elastin fibers are distensible so they increase artery compliance. |
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Term
| What occurs to our central arteries as we age? |
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Definition
| They become less compliant (stiffer) which means that a lower volume will cause a higher transmural pressure on the walls of the arteries. This can lead to an aortic aneurism. |
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Term
| What are the names of the pacemakers found in the heart? What are the functions of both? |
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Definition
The SA node and the atrio-ventricular (AV) node.
SA node is found at right atrium and the AV node is found between the atrium and the ventricle.
SA node - sets the cardiac rhythm
AV node - slows down the electrical impulse before it reaches the ventricles. This is required so that the ventricles have an opportunity to fill between atrial and ventricular contraction. |
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Term
| Describe the conduction pathways through the heart. |
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Definition
1) SA node (at right atrium) sets cardiac rhythm
2) Bachmans bundle --> found between right and left atrium. Ensures that some of the message reaches the left atrium. **therefore, there is contraction and conductance of the electrical message DOWNWARDS in the heart.
3) AV node - atrial-ventricular node --> job is to slow down electrical message before it reaches the ventricles so the ventricles have a chance to fill.
4) Purkinje fibers --> resp. for sending AP's very rapidly. Composed of left/right bundle branches which are found on either side (running alongside) of the interventricular septum. They then run outside and branch upwards. **These depolarize the ventricle. |
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Term
| What is the SA node? How is it regulated? |
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Definition
SA node consists of small, modified muscle cells which generate the electrical signal which controls the heart.
Regulated by sympathetic/parasympathetic nervous system.
Norepinephrine - increases heart rate (tachycardia)
Acetylcholine - decreases heart rate (bradycardia) |
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Term
| What gives an SA nodes depolarization look much smoother? |
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Definition
| The leakyness of the SA node means that once an action potential has been fired off from the node and the node is repolarized, a slow depolarization is already reoccuring due to the leakyness of the node itself. |
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Term
| What determines the heart rate that the SA node sets? |
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Definition
| Heart rate is controlled by the rate of depolarization at the SA node pacemaker. This rate is, in turn, controlled by the sympathetic/parasympathetic nerves. |
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Term
| If you cut all nervous system input to the pacemakers, what would happen to heart rate? |
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Definition
| It would increase. This is because the parasympathetic input is usually more powerful than the sympathetic input (which tends to speed up the heart). |
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Term
| How does acetylcholine influence heart rate? |
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Definition
Acetylcholine is a parasympathetic neurotransmitter.
It tends to slow down heart rate.
It does this by decreasing the threshold for activation and by increase the polarization (hyperpolarizing) s that it is more difficult to reach the electrical potential. |
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Term
| Describe the sections of a normal ECG report for a heart beat. What does each segment relate to? |
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Definition
Composed of : P wave, QRS wave and T wave.
P wave = contraction of atrium
QRS = represents the depolarization of the ventricular muscle
T wave = repolarization of the ventricular muscle |
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Term
| When, in an ECG, do you find the "isoelectric" period? |
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Definition
| Between the QRS and T wave. |
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Term
| What is the significance of the "isoelectric period"? Where do you find this period? What would cause it to deviate? |
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Definition
You find the isoelectric period between the QRS segment and T-wave on an ECG.
This segment is found in all normal people, so deviations in the isoelectric period are signs of issues in the heart.
This deviation represents partial or potential ischemia that usually shows up during exercise rather than at rest. |
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Term
| Why does the T-wave on an ECG show an upward inflection if it is due to repolarization? (and depolarization also shows as upward inflection) |
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Definition
Because the ECG marks equal and opposite flows of ions as the same inflection.
Depolarization in the heart occurs from apex to base.
The duration of an AP in the heart is longer at apex than at base.
Therefore, the apex depolarizes first but repolarizes last.
So, the direction of repolarization is opposite to that of depolarization and an upward inflection is seen for both.
If you see a downward deflection, than that means there is an issue with the order in which the heart depolarizes/repolarizes which could be caused by ischemia. |
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Term
| What are ectopic pacemakers? |
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Definition
| Ectopic pacemakers - muscle cells which take over the role or function of pacemaker cells |
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Term
| What is re-entrant excitation? |
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Definition
Caused by a block in the purkinje fibers (in the branches) of the heart.
When the impulse is blocked from traveling down one side of the fibers, the action potential will still branch but only on one side and therefore will nt cancenl out. That AP then crosses to the other side and conducts down, but upwards towards the blockage as well (reverse direction from normal flow). This causes part of the ventricle to depolarize at its own speed and to lose coordination of ventricular contraction. |
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Term
| What is first-degree block? |
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Definition
Occurs when there is damage to the AV pacemaker due to lack of oxygen.
It causes the P-R interval to be lengthened and is caused by the slow conduction at the AV node. |
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Term
| What is second-degree block? |
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Definition
Occurs when some of the P-waves are not followed by the QRS interval. A first degree block (longer P-R) can set you up to this.
**there is atrial contraction but you miss a ventricular beat.
Occurs more often then other issues… 1/50 students present this when running laps |
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Term
| What are third-degree blocks? |
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Definition
| When electrical signals no longer pass through the AV node. There becomes a dissociation between the depolarization rhythm in the atria and the repolarization in the ventricles. |
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Term
| How do bundle branch blocks present themselves on ECG's? |
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Definition
Right-bundle branch block: wide QRS segment, with dramatic downward deflection of R portion.
Left bundle branch block: Wide QRS segment but little differentiation between R and S portions in segment. (almost plateau) |
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Term
| What are the names of the valves in the heart and where are they located? |
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Definition
Tricuspid valve --> found on right side of the heart between atrium and ventricle
Pulmonary valve --> found on right side of the heart, between right ventricle and pulmonary artery
Mitral valve --> found between left atrium and left ventricle
Aortic valve --> found on left side of the heart between left ventricle / aorta |
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Term
| What is the pressure in the aorta during ventricular ejection? |
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Definition
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Term
| With regards to the heart, what is ventricular filling, isovolumetric contraction, ventricular ejection, isovolumetric relaxation refer to? |
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Definition
It is the cycle that the heart goes through with each pump.
Ventricular filling = diastole. Ventricles are still filling during this period.
Isovolumetric contraction = period where pressure begins increasing due to the increasing tension against the lump of blood (stretching heart walls increases tension)
Ventricular ejection = ventricles contract and blood goes into the pulmonary arteries or aortic arch
Isovolumetric relaxation = during repolarization of the heart.
Ventricular filling = diastole once more |
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Term
| How can you calculate blood flow? |
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Definition
| Stroke volume x heart rate = flow |
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Term
| What is the dicrotic notch? |
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Definition
| It is the period where the aortic outflow valve closes and the pressures start separation from each other. |
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Term
| What are the pressures in the ventricles during systole and diastole? |
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Definition
Systole/diastole
Right ventricle: 25/4 mmHg
Left ventricle: 120/10 mmHg
Aorta: 120/80 (80 due to elastic properties) |
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Term
| During diastole the ventricle still experiences filling. What s responsible for this? |
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Definition
| Back-pressure from the venous (pulmonary) side of circulation and later by atrium contraction. |
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Term
| Describe the pressure-volume loop of the left ventricle. |
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Definition
mitral valve opens (between atrium/ventricle) and ventricle gets filled by the back-pressure on the pulmonary side of circulation, then later by contraction of atrium. (volume increase without change in pressure, 50mL).
The mitral valve then closes and an increase in pressure occurs (to 80mmHg) with no change in volume.
This pressurizes the left ventricle until the pressure rises above that of the aorta, which makes the aortic valve open. This initiates the period of ejection.
As volume is ejected, pressure begins to drop until the pressure of the ventricles falls below that of the aorta once more and the aortic valve closes.
You then enter into the period of isometric relaxation where there is no change in volume but you are depressurizing the ventricles (relaxing myocardial elastic elements) |
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Term
| You multiply pressure by what to get "work"? |
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Definition
| If you multiple pressure by volume you will get work? |
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Term
| How can we calculate "work" with regards to the human heart? How can we increase the work that the heart does than? |
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Definition
By multiplying volume by pressure.
By increasing either blood pressure or stroke volume the magnitude of work will increase (and the damage to your heart) |
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Term
By multiplying volume by pressure.
By increasing either blood pressure or stroke volume the magnitude of work will increase (and the damage to your heart) |
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Definition
Preload --> if you fill the heart more, it will eject more. Caused by increase in the diastolic volume. Preload = pressure in diastole.
Afterload --> caused by an increase in pressure when aortic outflow valve is open.
Inotropy --> a measure of the inherant contractility of fibers. If they have less contractility they will eject less. Increased contractility means ejecting more. |
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Term
| What factors influence pre-loading? (Ie the pressure the ventricles experience during diastole) |
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Definition
Increases:
- Increase in atrium contractility. will cause it to contribute more to filling and therefore increase preloading
- Ventricular failure. will decrease the ejection fraction and, at the start of the enxt cardiac cycle, there will be more blood retained in the ventricle causing preloading
- Increase in ventricular compliance
- Decrease in heart rate
- Increase in venous volume
Decreases:
- Increase in heart rate
- Outflow resistance/afterload (pushing/holding back blood in ventricles)
- Increase in inflow resistance |
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Term
| What is the frank-starling mechanism? |
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Definition
| It refers to the fact that increased venous return and ventricular preload causes increased stroke volume at a given inotropy and afterload |
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Term
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Definition
| A measure of the inherent contractility of fibers. If they have less contractility they will contract less (have lower inotropy) increased contractility means ejecting more |
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Term
| If you increase the afterload, what happens to a pressure-loop diagram? |
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Definition
The max pressure (vertical dimension) will increase.
This vertical increase is compensated for by a decrease in the horizontal dimension. |
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Term
| If you increase contractiliity, what happens to a pressure loop diagram? |
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Definition
| Loop widens towards the left. Vertical parameter increases somewhat. |
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Term
| How does a pressure loop diagram change with the increasing of preload? |
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Definition
| The loops widens to the right and the vertical parameter increases somewat. |
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Term
| What is dilated cardiomyopathy? What is it caused by? What poses the patient the most danger? |
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Definition
Characterized by a marked enlarging of the ventricle. However, musculature of the heart does not change. So, the walls of the ventricle become thin and weakened.
It is a sign that the heart has been overworked and is caused by the weakening of the ventricular muscles.
As you increase the radius of the ventricle, you increase the tension in order to generate the same arterial pressure --> this is demonstrated by LePlace's law. Can lead to the heart shredding itself.
P = T/R
P = pressure
T = tension
R = radius |
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Term
| What is hypertrophic cardiomyopathy? |
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Definition
Hypertrophic cardiomyopathy is a condition characterized by hypertrophy of the heart muscles. It will make it so that there are large pressures in the heart, with problems getting normal volume into the ventricles during diastole.
This reduces stroke volume. |
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Term
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Definition
P = T/R
P = pressure
T = tension
R = radius |
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Term
| What is the equation for pulse pressure? |
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Definition
| Pulse Pressure = P(systolic) - P(diastolic) |
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Term
| If a tube is rigid, would we expect a constant flow or a pulsatile flow? |
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Definition
| You would see a pulsatile flow. |
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Term
| What is the vinn keissel effect? |
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Definition
The vinn kessel effect is where there is a volume that can be retained in the tube (due to the expansion of the tube) that maintains flow over time rather than pulsatile.
Seen in the aorta. The central aorta will expand in volume during ventricular systole and bear down on the blood volume during diastole. This is why you get significant flow even during the period when the ventricle is cut off from the circulation. |
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Term
| What does aortic compliance do? |
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Definition
| Aortic compliance reduces the mechanical work load of the left ventricle. |
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Term
| What is the equation for work with regards to the circulation system? |
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Definition
| Work = pressure * flow rate |
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Term
| What happens to your veins/aorta/arterioles as you age? |
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Definition
They become more stiff, lose distensability.
For your aorta, this means that the compliance will be reduced. Therefore, you will not be able to store as much blood within the aorta to pressurize the system during diastole. Aging, therefore, results in the reduction in the diameter of the aorta.
This causes high blood pressure. |
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Term
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Definition
| The greater the preload, the greater the output. |
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Term
| What is the mean circulatory filling pressure? |
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Definition
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Term
| If you increase the cardiac output, than what happens to the venous pressure ? |
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Definition
| The right atrial/venous pressure will fall if there's an increase in cardiac output. |
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Term
| What occurs to a vascular function curve after a blood transfusion? |
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Definition
| You raise the vascular function curve because there's more blood (pressure) on the venous side of the system. |
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Term
| What happens to cardiac output and pressure during heart failure? |
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Definition
| During cardiac heart failure there is reduced cardiac output which is partially compensated but at the expense of an INCREASE in pressure on the venous side. This is because there is an increase in the volume on the venous side |
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Term
| Describe fick's principle and the equation that describes it. |
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Definition
| O2 consumption in tissues: cardiac output multiplied by the arterial venous oxygen content difference in the blood. (IE the concentration of oxygen in the arterioles and the concentration of oxygen in the veins) |
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