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225 Cards in this Set

  • Front
  • Back
Van't Hoff Equation
Q10=(MR2/MR1)^(10/(T2-T1))
Q10
-the change in a biological rate (HR, metabolism, etc.) for a 10C change in temperature.
-usually about 2-3 for physiological processes.
Net Change in Heat Content
=metabolic heat production +/- conduction +/- radiation - evaportation
Endothermy/Ectothermy
defining animals based on where they get most of the heat in body.
Ectothermy
dominant source of heat comes from external environment
Endothermy
-dominant source of heat produced within the animal.
-3 to 8X great oxygen consumption (VO2)
-can raise temp. above evironmental temperature.
Homeothermy
body temperature remains at a constant temp throughout differing env. temps.
--maintain homeostasis across wide range of env. temps through physiological processes.
Poikilothermy
thermoconformer
--usually ectotherms, not always.
Homeothermy/Poikilothermy
defining animals based on the stability of their body temps
Heterothermy
-Regional : different strategies in different parts of the body
-Temporal : switching between endo/homeo and ecoto/poikilo based on time of day/temp of month
Characteristics of Ectotherms
-dont produce much heat and quickly lose heat that is produced (poor insulation keeps heat in and out)
-do not totally conform to external environment.
-low MR
-Plasticity: some species have acclimatized so body functions optimally.
-body functions adapt to the environment the organisms live in.
-preferred body temp is not random, has biochemical/physiological correlations
Heliothermy
-behavioral thermoregulation of basking in the sun
Thigmothermy
behavioral adaptation
-adjusting body temp by putting body against cool/warm substrate
How ectotherms gain heat
-posture (larger surface area=more heat gained)
-microclimate
-coloration
How ectotherms lose heat
-posture
-microclimate
-blood flow
-evaporative water loss
Why do high temps kill?
-denaturing of proteins: 3D structure of proteins can be altered so they cannot perform normal funtions; causes blood clotting; have heat-shock proteins as counteracting strategy.
-insufficient O2: MR can go faster than you are able to bring O2 to tissues; hemoglobin affinity goes down despite the need for more O2.
-Reduced activity of enzymes
-variable effects of temp on related reactions: imbalance.
-membrane fluidity altered: more fluid/leaky.
Heat-shock Proteins
-counteracting strategy to the denaturing of proteins due to high heat
-can be induced at high temps
-helps proteins maintain structures and function correctly
Freezing Point of Cells
-0.1 to -1.9C
--freezing point not zero because of the solutes in cells
-formation of ice crystals inside cells can cause poking of hold in cell membrane and blood vessels
How body temps below zero are achieved
-Supercooling
-Antifreeze
Supercooling
-lowering a liquid below its freezing point without it becoming a solid.
-no nucleating agents
-often combined with colligative antifreezing
Colligative Antifreeze
Affect the freezing point by increasing the total concentration of solutes in the body fluids.
-Use glycerol, sorbitol, etc.
-Don't use inorganic ions because the increase in concentration will mess up membrane potentials and change 3D structure of proteins
Noncolligative Antifreeze
-Glycoproteins
--prevent big crystals
-It takes a very low concentration to depress freezing.
-As ice crystals grow, antifreeze will insert themselves in crystal and prevent further grotwth
--end up with small, nonthreatening crystals
How animals actually survive freezing
-Have nucleating agents (ice crystal promoters) in blood plasma and interstitial fluid, causing them to freeze first (before cells)

--Ice crystal formation in int. fluid and floods plasma:
--Ice crystals first form in these locations
--They grow by attracting water molecules so all the salt that was dissolved gets left behind.
--Water moves out of the cells so the osmotic concentration within the cells increases, making their freezing point very low.
-Cells do shrink while all the water moves into int. fluid and blood plasma so organic solutes must be substituted in
--glycerol in insects, glucose in vertebrates
Countercurrent Heat Exchange
-minimizes heat loss
-Arteries and veins run parallel and in close contact to one another.
--blood moving twds periphery exchanges heat with artery/vein going back into body.
Rete mirabile
-a complex of arteries and veins lying very close to each other
--enables countercurrent heat exchange
Why regulate at high body temps? (endothermy)
-partially optimal conditions for enzymes (though adaptations can alter this)
-mostly because things work faster at higher temps
--Q10 effect
Negative effects of increasing body temp
Amount of protein needing replacement increases
Temperature Neutral Zone (TNZ)
Region of ambient temperatures in which an organism does not need to increase their MR
-as ambient temp increase or decreases away from TNZ, MR increases.
Upper-critical Temperature (UCT)
Upper temperature threshold where animal need to expend more energy
Lower-critical Temperature (LCT)
Lower temperature threshold where animal needs to expend more energy
Metabolically inexpensive ways for Endotherms to decrease heat loss
Behavior, vasomotor responses, insulation
Vasomotor Responses in Endotherms
-In the cold, need to reduce blood flow to the skin
--larger distance from surface of skin when vasoconstriction occurs
--blodd traveling more deep, conserving body heat.
-Under normal conditions, lots of heat lost by conductance across skin, as lots of blood is able to go close to surface
Insulation in Endotherms
-Use fur (piloerection) or feathers (tiloerection)
-feather/fur traps air by body
--air has low k value, so its a good insulator (16X better than fat)
--greatly increases distance between blood and external environment
-Animals that live in water need a different mode of insulation
--Blubber on the outer layer of an animal also acts as a way of keep heat in
--since blubbler is 1/16 as effective as air at insulating, animals need very thick layer of it.
Mechanisms for increasing heat production in Endotherms
-shivering thermogenesis
-nonshivering thermogenesis:
--brown adipose tissue
--liver/muscle (Na, K, Ca leaks)
--mitochondrial mutations
-Regional or temporal heterothermy
Shivering
-alternating the contractions of antagonistic muscle pairs in order to burn through ATP and contract heat.
Brown Adipose Tissue
(mammals)
-contains much more mitochondria than regular yellow fat
-located in regions between shoulder blades and near heart.
-receive rich supply of blood vessels
-Has electron transport chain without ATP synthesis (has thermogenin specialized for heat production) so heat is rapidly liberated
Na, K, Ca pumps in liver/muscle
-Na, K, Ca pumps use ATP and by making cells more leaky, pumps need to work harder in order to maintain a gradient, thus releasing more heat.
--The increase in ATP use increases amount of heat loss
Mitochondrial Mutation
-mutation decreases efficiency of mitochondrial membrane, making it have to work harder
--need to increase uptake of calories/have a high fat diet to help fuel this mutation.
-Mutation found in ppl in cooler climates (0% africa, 75% arctic, 14% europe/temperate)
Regional Heterothermy in Endotherms
-Maintaining warmer regions of the body relative to other parts
-Peripheral temps may approach ambient temp.
--vasoconstriction (down side: less O2/nutrient/waste product removal in those areas causing pain
-Countercurrent exchange saves energy without limiting transport of important nutrients etc
--allows you to continue blood flow but heat barely arrives at periphery.
-Maintain a constant core temperature (warmer)
-Don't allow body temp to go below freezing point of cells (dont want ice crystal formation).
Temporal Heterothermy in Endotherms
-Entire body alters its temperature
--happens at certain points during animals life
-Programmed lowering of set point (daily, annually, etc) or reactive lowering (depends on environment temp, etc)
-Reduction in the difference between ambient temp and body temp
-Need to heat back up though, so cost of reheating must be less than energy saved to make this process worthwhile
--Larger you are, the more energy it takes to warm back up
Continuum of controlled hypothermia
-mild (nocturnal) hypothermia
-torpor
-hibernation
-winter sleep (carnivore lethargy)
Mild (nocturnal) Hypothermia
-short period of time (12 hours or less)
-about a 7-10C drop in temp
Torpor
-combined with behavior of hiding
-small mammals and birds
-unresponsive while in this state
-profound drop in body temp (body temp can reach ambient temp if not too low)
-takes .5-1hr to warm back up
-happens daily
Hibernation
-medium (>100g) mammals; poorwill (bird)
-long-term torpor (days to months) associated with winter
-periodic arousal
Winter Sleep (carnivore lethargy)
-bears, badgers
-weeks to months
-decrease body temp only by about 5C
-around rapidly
-like extended mild hypothermia
Seasonal control of body temp in Endotherms
-animals may be able to withstand lower temps more efficiently depending on the season (i.e. winter)
--acclimatization
-Insulation increases/decreases depending on season (more fur in winter)
-migration (avoidance)
Adaptation in Endotherms to maintain body temp/MR
-SA/V
--Bergmann's rule
-Allen's rule
-insulation
-heat exchangers (heterothermy)
Bergmann's Rule
animals at high latitudes have typically larger body size compared to ones in lower latitudes
-size of animal increase as latitude increases
--larger animals have smaller SA/V so heat loss slower
Allen's Rule
animals at higher latitudes have shorter appendages
--larger appendages lose more heat
--smaller limb length with increased latitude
Metabolically Inexpensive ways to increase heat loss
microclimates, posture, decrease insulation, vasodilation
In response to heat, how to increase evaporative water loss
-sweating/cutaneous water loss
-panting
-gular flutter
-breathe via mouth
-saliva or urine
Defense of Brain Temp
-Brain can only tolerate temp up to 40.5C though body temp may exceed that
-Use countercurrent exchange to maintain temp
--carotid rete in mammals (keeps brain temp about 3-4C lower than core)
--opthalmic rete in birds (warm blood heading to brain is cooled at nasal passage before getting to brain)
--using evaporative cooling in nasal passage to indirectly cool brain.
---shunt when cold
What is a nervous system?
Made up of glial cells and neurons
-Protists and sponges don't have true nervous systems
Glial Cell
-Provide support and protection for neurons
-maintain extracellular environment
-Wrap their membranes around axon
--Oligodendrocytes
--Schwann Cells
Typical parts of a neuron
-dendrites
-soma
-axon
-axon terminal
Dendrites
Attached to the soma and recieve information from other cells or the environment
-where stimuli enters
Soma
The cell body
-has numerous projections: dendrites
Axon
-Received signal to the neuron travels down it from soma
-serves to propagate action potential
Axon terminal
Area where cell communicates with other neurons
-had presynaptic terminals where neuronal output occurs
Membrane Potential
differences in electrical charge across a membrane
-cells are inside negative
Voltage at rest of a Neuron/proporties
-20 to -100 mV (like all cells)
-many are excitable
--can carry and action potential
Action Potential
A momentary reversal of membrane potential followed by a restoration of original membrane potential
-rapid change in voltage of cell, propagated along it
-The action potential is triggered by any depolarization of the membrane that reaches a critical value of depolarization, the voltage threshold
Ions inside/outside of typical cell
-More K inside
-More Cl and Na outside
-Maintained by action Na/K pumps and passive distribution of ions like Cl
--Donnan Equilibrium
-Equilibrium potential of cells at rest is closer to the ion equilibrium of K since cell is more permeable to K
Goldman Equation
-The contribution of each ion is weighted by its ability to permeate the membrane, with the more-permeating ions having more of an effect. The value of the membrane potential (Vm) produced by the contributions of several permeating ion species is determined by this equation:

Vm=(RT/F)ln(ratio of ions in and out of cell)
--positive ions: outside goes ontop, inside on bottom
--negative ions: opposite
Depolarization
a decrease in the absolute value of the membrane potential towards zero (becoming less negative inside the cell)
Hyperpolarization
an increase in the absolute value of the membrane potential away from zero (becoming more negative inside the cell)
Graded Potential
a change in potential that is proportional to the stimulus applied
Anatomy of an Action Potential
-has slow increase/depolarization, crossing voltage threshold
-followed by rapid depolarization in the "Rising Phase"
-Can have an "Overshoot" if potential crosses over to +
-"falling phase" characterized by rapid membrane repolarization
-Some "undershoot", ducking below resting potential
-return to resting potential
Sequence of Na and K channels during an action potential
1. at rest, K is flowing in and out of cell; voltage gated Na and K channels are closed during resting membrane potential.
2. Rising phase: Some stimulus causes depolarization and the open of the voltage gated Na channel; since Na is very far from equilibrium potential, it flows rapidly into cell
3. Falling phase: inactivation gate for Na channel closes and voltage gated K channel opens, releasing K out of the cell
--Absolute refractory period
4. Reaches equilibrium potential for K and then voltage gated K channel closes
--Relative refractory period
Refractory Period
Period in time, once an action potential has been initiated, where it is difficult to cause a second action potential.
-absolute refractory: due to Na channel inactivation
--keeps action potential going one direction
-Once some inactivation removed, relative refractory
Mechanisms for increase speed of action potential
-increase diameter of neuron
--resistance to longitudinal spread decreases
--trade off: spatial constraints
-Myelination (vertebrates and some crustaceans)
-increase temp
Myelination
-Use glial cells to form myelin sheath around axon
-Oligodendrocytes in brain/spine
-Schwann cells on rest of nerves
-Increase transmembrane resistance and thickness and enhances current spread
--resistance that occurs from having + less impressive since they are now farther away
--also prevents + from leaking
-Action potential can spread faster and for longer but still decrement over time-->nodes of Ranvier.
Nodes of Ranvier
gaps between areas of myelination
Saltatory conduction
-Action potential jumping from node to node
-Areas wrapped with cells do not have voltage gated channels so the action potential can decrement
-as long as the action potential is enough to start another one at each node, the action potential can carry through the axon
How action potential can cross to next cell
-Electrical: used when you need rapid response and a whole bunch of cells acting in unison.
--use gap junctions called connexin
-Chemical:
--use neurotransmitters
Connexin
-the gap junctions through which electrical signals travel between cells.
-arranged to form a pore directly between cell 1 and cell 2.
-very quick communication
-usually positive charges moving through junctions-->excitatory
-signal is a graded potential, so it decrements over time
Why not only use electrical synapse?
-Advantages of chemical synapse:
--can have both excitatory and inhibitory cells
--more communication: more control, more functional plasticity
Synaptic Cleft
the gap between the two cells where action potential is passes chemically
How neurotransmitter is released/received chemically:
-Presynaptic action potential opens voltage-gated Ca channels
-increase in Ca concentration initiates exocytosis of vesicles containing neurotransmitter
-neurotransmitter diffuses across synaptic cleft
-neurotransmitter activated ligand-gated ion channels (fast) or second messengers, changing voltage
-neurotransmitter degraded and/or actively taken up
Spiking Neuron
-has long axon
-information carried by an action potential
-frequency of action potential related to amount of neurotransmitter released
Nonspiking neuron
-Shorter axon relative to spiking neuron
-information carried using a graded potential
-amount of neurotransmitter released is proportional to magnitude of depolarization
ionotropic receptors
-located on the post-synaptic cell
-what receptors bind to neurotransmitter they open to allow ion flow in
-fast response
metabotropic receptors
-located on the post-synaptic cell
-produce a metabolic change in the postsynaptic cell
--relatively slow, long-last modulatory effects
Excitatory Neurotransmitters
Ach and glutamate
-excitatory because they open Ca/Na channels, causing depolarization (normally more inside than out)
Inhibitory Neurotransmitters
GABA and glycine
-inhibitory because they open K/Cl channels, causing hyperpolarization (normally more in cell than out)
Magnitude of the effect of the AP depends on...
-the ion being released
-the concentration gradient
-how long the release occurs for (frequent AP can keep Ca channels open and create more release of neurotrans)
--usually need more than one AP to make a large enough GP
---axon terminals all over receiving neuron
Integration
-refers to processes (like summation) that produce coherency and result in harmonious function.
-refers to all the axon terminals found on the post-synaptic cell working together, each sending same/diff signals which result in different outcomes
Temporal Summation
occurs when a nerve is stimulated rapidly and all those stimuli are added together to make an excitatory post-synaptic potential
Spatial Summation
Occurs when different nerves contribute and add together to create a stimulating/inhibitory potential
Why have summation instead of a 1:1 relationship with stimulus and AP?
-allows control
-allows plasticity
What other cells do neurons communicate with (besides other neurons)?
-neuron-->effector cells (neuromuscular junction):causes some action
-sensor-->neuron
Labeled Line Principle
-Action potentials look the same no matter the stimulus
-the brain knows that an AP comes from a certain location on the body (certain nerve) and understands what is being signaled
--perceives stimulus based on where it comes from
Reflex Arc
A neural pathway that controls an action reflex
-can be single-cell connection, monosynaptic reflex arc, or polysynaptic reflex arc
Afferent Neurons
Carry signals from receptor/sense organ to the central nervous system
Efferent Neurons
Carry signals from the central nervous system to effectors
Advantage of polysynaptic reflex arc
have more control if more neurons are involved in relaying a message
Cephalization
the consolidation of the nervous system in the head
General organization of the Vertebrate Nervous System
-Central nervous system (brain/spinal cord): major sight of integration
-Peripheral nervous system (everything else): somatic and autonomic motor/sensory neurons
Somatic Nervous System
part of the peripheral nervous system that control skeletal muscles (striated)
-effects most observable behavior
Autonomic Nervous System
part of the peripheral nervous system that controls all neuron-controlled effectors other than skeletal muscle (cardiac muscle, smooth muscle, and glands)
-effects on visceral organs, mostly internal/unnoticable
-divided into two nervous systems:
--sympathetic
--parasympathetic
Sympathetic Nervous System
-division of the autonomic nervous system
-mostly inhibits functions related to autonomic system:
--inhibits digestion, gastrointestinal secretion/motility
--increases rate/force of heart
--constricts vessels to kidney, gut
--dilates vessels to skeletal muscle
--dilates lung passages
--increases blood pressure
--stimulates epi (fight or flight)
Parasympathetic Nervous System
-division of the autonomic nervous system
-mostly stimulates functions related to autonomic system:
--stimulates digestion, gastrointestinal secretion/motility
--slows heart
--dilates blood vessels
--decrease blood pressure
-constricts lung passages
Endocrine System
-Involves endocrine tissues, hormones, specific glands, neurohemal areas, and other organs of the body
-Secretions of the glands are released into the blood stream
Hormone
chemical messenger produced and released by nonneural endocrine cells or neurons, carried in blood to communicate with target cells
Neurosecretory Cells
part of the endocrine system instead of the nervous system because they synapse with blood vessels
Secretory cells
-often filled with vesicles containing hormone molecules
-mixed into other organs as well as endocrine tissue
Target cells
only respond to a hormone if they have the hormone receptor
-can have different ones on same cell
Exocrine Glands
releasing secretion of glands into ducts that dump secretions outside of the body
-like in the digestive tract (tube within a tube design)
Paracrine secretion
-different from endocrine secretion
-simple diffusion between cells close to each other
--secretion taken up by adjacent cells
autocrine secretions
-different from endocrine secretions
-signal messages to self
--e.g. inhibiting own functions
Roles of Endocrine System
Typically things occur over long period of time
-growth, development, reproduction
--slow, many tissues involved
Though things can happen over quicker time scale as well
-homeostasis (digestion, osmoregulation, etc)
Vertebrate Endocrine Glands
-each cell contacts a blood vessel
--has own blood supply
--closed circulatory system
Invertebrate Endocrine Glands
-bathed in hemolymph
-hormone diffuses to surface
--open circulatory system
3 General Classifications of Hormones
-Peptides (short chains of amino acids)
-Steroids (from cholesterol)
-Amine Hormones (from tryptophan or something made from that)
--composed of catecholamines, melatonin and thyroid hormones**
Where Peptide hormones are secreted from
most sites of hormone secretion besides adrenal cortex and medulla, thyroid gland, and pineal gland
Solubility of peptide hormone
water soluble
synthesis and storage of peptide hormone
-synthesized at rough ER, processed in golgi
-stored in vesicle
secretion of peptide hormone
exocytosis
transport of peptide hormone
dissolved in plasma or some bound to carrier proteins
half-life of peptide hormone
minutes
location of receptor for peptide hormone
surface of target cell membrane
action of peptide hormone at receptor cell
activates second-messenger system (alters membrane channels)
response of target cell to peptide hormone
changes activity of preexisting proteins
action duration of peptide hormone
seconds to hours
site of secretion of steroid hormone
adrenal cortex, gonads, placenta
solubility of steroid hormone
lipid-soluble
synthesis and storage of steroid hormone
synthesized on demand in intracellular compartments and is not stored
secretion of steroid hormone
simple diffusion through cell membrane
transport of steroid hormone
bound to carrier proteins
half life of steroid hormone
hours
location of receptor at target cell for steroid hormone
cytoplasm or nucleus (occasionally surface)
action of target cell in response to steroid hormone
alter gene expression
-activated genes initiate transcription/translation
response of target cell to steroid hormone
synthesize new proteins
--some may alter activity of preexisting proteins
action duration of steroid hormone
hours to days
site of secretion of amine hormones
adrenal medulla or pineal gland
solubility of amine hormones
water soluble
synthesis and storage of amine hormones
synthesized in the cytoplasm and stored in vesicles
secretion of amine hormones
exocytosis
transport of amine hormones
dissolved in plasma
half life of amine hormones
seconds to minutes
location of receptor molecule for amine hormones
surface of target cell
action at target cell that results from amine hormones
activate second-messenger systems
response of target cell to amine hormones
change activity of preexisting proteins
action duration of amine hormones
seconds to hours
site of secretion of thyroid hormones
thyroid gland
solubility of thyroid hormone
lipid-soluble
synthesis and storage of thyroid hormone
made prior to use and stored in a colloid island within gland
secretion of thyroid hormone
simple diffusion across membrane
transport of thyroid hormone
bound to carrier proteins
half life of thyroid hormone
days
location of receptor molecules for thyroid hormone
nucleus
action of target cell that results from thyroid hormone
alter gene expression
-activated genes initiate transcription and translation
response of target cell to thyroid hormone
synthesize new proteins
action duration of thyroid hormone
hours to days
What stimulates a cell to release hormone
-synaptic trigger
-other hormones
-environmental effect of membrane
--ex. release of ADH
For lipid soluble hormones:
-no vesicle used, diffuse out as made
For vesicle bound hormones:
-released by exocytosis
--AP, non-AP depolarization or intracellular signaling pathways raising Ca concentration
---ER or Ca channels
effect of hormone on target cells
For receptor proteins in cytoplasm/nucleus:
-lipid-soluble hormones interact with
-modulate gene expression (transcription/translation)
-long-term effects
For receptor proteins on plasma membrane:
-mostly-lipid insoluble hormones interact with
-effects membrane permeability, activity of existing proteins, etc.
-short-term effects
islets of Langerhans
the endocrine tissue regions of the pancreas
-made up of two cell types:
--30-40% alpha-cells
--the rest: beta-cells
Pancreas
endocrine and exocrine glands
-mostly exocrine
-have islets of Langerhans
-produces/synthesizes glucagon and insulin
Glucagon
-produced/synthesized in pancreas
-secreted by alpha-cells
-released in response to low blood sugar (hypoglycemia)
Insulin
-produced/synthesized in pancreas
-secreted by beta-cells
-released in response to high blood sugar (hyperglycemia)
Type I Diabetes
-loss of beta-cells (cells producing insulin)
-autoimmune
Type II Diabetes
-loss of insulin receptor/signaling
--producing insulin by its not effective (will see glucose in urine)
-often associated with obesity because of observations about resistin
--resistin is released by fat cells and antagonize insulin receptors
Types of Animal Muscle
-smooth
-striated
--cardiac and skeletal
Cardiac Muscle
-type of striated muscle
-each cell has 1 nucleus
-interact with adjacent cardiac cells at gap junctions
--electrical signaling ensures the muscles contract in unison
Skeletal Muscle
-type of striated muscle
-made up of multiple nuclei
--developed by the fusion of many cells
-cells don't interact at gap junctions like cardiac cells
-controlled voluntarily while cardiac/smooth muscles are not.
What skeletal muscle is made up of
Sarcomeres make up a single muscle fiber(cell) and a bundle of fibers make a fascicle and muscle is made up of a bunch of fascicles wrapped together
Fascicle
a bunch of muscle fibers (cells)
Tendon
connects bone to muscle
-convergence of connective tissue
Sarcomere
-basic unit of a muscle
-overlapping filaments of actin and myosin
Myofibrils
-tubes that make up muscle fibers (cells)
-composed of repeating sections of sarcomeres
Anatomy of Sarcomere
Made up of:
-Z disc
-H zone
-A band
-M Line
-I band
M Line
-part of sarcomere
-helps anchor myosin
-inside H zone
I Band
-surrounds z disc
-distance from one myosin to next
--only made up of action and z disc
A Band
-occupied by all the myosin
-also contains the actin not in the I band
-MAde up of H zone and region where actin/myosin overlap
H Zone
-only myosin
-within the A band
Z Disc
-on both ends of sarcomere
Sliding-Filament Theory
-Discovered by Huxley and Huxley independently
-The theory that the thin filaments (actin) slide alone the thick filaments (myosin).
-Z discs move towards each other.
-I band and H zone shorten while there is no change in the thickness of A band
--shows that actin and myosin themselves dont shorten though the distance between them does
Thin Filament
Made up of:
-Actin (primary component)
--2 helical strings of beads (actin proteins)
-Tropomyosin
--filaments in the grooves of the helix that are involved in regulating muscle contractions
-Troponin Complex
--attached to tropomyosin and can move tropomyosin off of actin binding sites
Thick Filament
Made up of:
-Myosin (primary component)
--2 myosin chains with globular heads come in contact with tons of other chains, tails each anchored together my M line
--aggregate into thick filament
--have to biding sites (one for actin, one for ATP)
How do filaments slide?
By forming cross-bridges
-formed by myosin head binding to actin
Concept behind how cross-bridges form/detach
-at rest (in cocked position), ADP-P (ADP and inorganic phosphate--hydrolyzed ATP) is bound to myosin (though its binding to actin may not occur if tropomyosin is blocking the binding site)
-if tropomyosin is moved away, actin binding triggers release of the P causing a tighter bind between actin and myosin and then a power stroke
-the myosin head swivels in the power stroke, causing it to pull the attached actin towards the middle of the myosin filament.
-ADP is released at the end of the power stroke, though myosin is still tightly bound to actin
-ATP binding to myosin causes it to detach from actin
-Myosin hydrolyzes ATP to ADP-P, causing the angle of the head to change into cocked position and the whole process can begin again.
Role of ATP in formation/detachment of cross-bridges
-physical binding of ATP to myosin changes its conformation, causing it to detach from actin binding site
-Provides energy to cock the myosin head
How Ca regulates muscle contractions
-Discovered by Ringer & Buxton
-Troponin and tropomyosin block the myosin binding sites from actin while Ca is not present
-Ca can bind to troponin complex, dragging tropomyosin away from binding sites.
--Myosin rapidly binds since it is already cocked
Motor Neuron
efferent neuron from spinal chord (CNS) to muscle
Neuromuscular Junction
-motor endplate
-where motor neuron synapses muscle.
Motor Unit
(1) motor neuron and all the fibers it innervates
--only 1 in vertebrates
Sarcolemma
The cell membrane of a muscle fiber (cell)
Sarcoplasmic Reticulum
endoplasmic reticulum of a muscle fiber (cell)
-specialized in Ca storage
The Excitation at the Neuromuscular Junction
-AP travels downs the motor neuron and presynaptic AP triggers exocytosis of Ach.
-Ach opens ligand-gated cation channels on the muscle membrane, depolarizing sarcolemma
--race with Acetylocholinesterase (breaks down Ach) in extracellular matrix of synaptic cleft.
-Na rushes into the cell while much less K rushes out of cell
-1:1 transmission in twitch fibers
Excitation of Muscle after motor neuron
-Net inward movement of Na due to the binding of Ach to receptors on the muscle membrane initiates and action potential.
-AP propagates over the cell membrane and depolarizes t-tubules.
-Depolarization of t-tubules reaches DHPR (dihydropyridine receptors), causing it to change formation and open RyR (ryanodine receptor) calcium channel on the sarcoplasmic reticulum.
-Ca ions diffuse out of SR into cytoplasm and bind to troponin causing tropomyosin to move, exposing myosin-binding sites.
-When the wave of depol. ceases, DHPR returns and RyR is closed.
-ATP-dependent Ca pumps are continuously active, bringing Ca back into SR (2Ca per ATP).
DHPR
Dihydropyridine receptors
-when depolarization comes down t-tubules, causes DHPR to change conformation and detach from RyR
-On sarcolemma, connects to RyR on SR
RyR Calcium Channel
Ryanodine receptor calcium Channel
-after depolarization, DHPR changes conformation and disconnects from RyR, allowing Ca to flow out freely from SR
T-Tubules
Brings depolarization down to site of Ca pores
-depolarization alters configuration of DHPR, causing it to move away from RyR
What Requires ATP in Muscle Contractions
-Myosin
-Ca pumps
Sources of ATP for Muscle Contractions
-ATP "stores"
-Creatine phosphate
-Anaerobic glycolysis
-Aerobic catabolism
ATP stores as means of producing ATP for muscle contraction
-Have small amount of reserved ATP in cytoplasm at rest
--can be used for a few seconds of muscle contraction
Creatine Phosphate as means of producing ATP for muscle contraction
-Creatine is a phosphogen which stores high energy phosphate bonds.
-High energy phosphate of creatine can be donated to ADP to produce ATP
-We typically have enough for a couple seconds of muscle contraction
-Does not require O2 or create a waste product and donates P very rapidly
Anaerobic Glycolysis as means of producing ATP for muscle contraction
-ATP made quicker than in aerobic metabolism
-produces lactic acid
--negative effects of lactic acid:
---causing pain
---interfering with muscle contractions
---self-limiting: stops break down of glucose
---interferes with myosin/actin binding
Aerobic Metabolism as means of producing ATP for muscle contraction
-Produces a lot of ATP but slower than anaerobic glycolysis
-requires O2
Increase twitch size by...
increasing the amplitude of the stimulus, thus incorporating more motor units involved in twitch.
Why does it take time to reach peak tension?
-Have series elastic components (tendons, Z-discs)
-Have parallel elastic components (parallel cells, connective tissue)
--Need the force applied to muscle to deform elastic components before the force can be applied to a load.
Isometric Contraction
A contraction where the load does not move when you apply a force
Isotonic Contraction
A contraction where you maintain a constant tension
Length-Tension Relationship for muscles
-maximal tension is achieved when muscles are at their normal lengths in organisms
-The set length of the muscle fibers affects the length of the sarcomeres within it and thus the degree of overlap of the thick and thin filaments within the sarcomeres.
--the lengths that yield max tension were those in which the overlap of thick and thin filaments permits optimal cross-bridge binding with actin.
(less overlap when muscles are fully stretched out, so less binding sites to myosin. At shorter lengths, thin filaments overlap H zone where there are no myosin cross-bridges or go to far overall.
How to physiologically control the strength of muscle contractions
-size of active motor units
-recruitment (motor units, muscles)
-length-tension relationship
-temporal summation (tetanus)
-Muscle size
Motor Unit
a motor neuron and all the muscle fibers it innervates
Recruitment for controlling muscle contraction strength
Increasing the number of motor units being stimulated will increase the amount of muscle fibers twitching-->strengthens the twitch
Temporal Summation for controlling muscle contraction strength
-When a muscle is stimulated more than once within a brief period, the successive twitches produced add to each other, so the overall response is greater than the twitch response to a single stimulus.
-amplitude of the summed contractions depends on the interval of time between stimuli.
-Low frequencies of stimuli with relatively long intervals between each produce contractions that sum but are not fused.
Tetanus
-The smoothly fused muscle contraction produced as a result of a high frequency stimulation.
-Usually about 3-4X the amplitude of a twitch in mammals
How Ca enables summation/tetanus
-each AP triggers the release of a sufficient number of Ca ions, ultimately allowing cross bridges to form
-The contractile apparatus requires time to pull on the elastic components of muscle
-Ca is usually pumped back into the SR before the cross-bridges can fully stretch out the elastic elements
-HOWEVER, successive AP open the RyR channels with sufficient freq. that the cytoplasmic concentration of Ca keeps the actin-binding sites exposed, allowing cross-bridges to cycle repeatedly until the elastic elements are stretched taut and the full contractile potential of the muscle fiber is realized.
--length of twitch (time) is much longer than an AP so its relatively easy to catch a twitch before relaxation with a new AP
Trepe
partial tetanus
Effects of Muscle Size on muscle contractions
-slower time domain than the other influences
-force of contraction is proportional to the cross sectional area of a muscle
-resistance exercise changes size of muscles
-hyperplasia
Hyperplasia
-increasing the number of cells
-studies have shown that animals are able to increase the number of actual muscle cells that they have after extreme resistance training
-no firm evidence that humans can do this.
Hypertrophy
-increasing the actual size of a cell
Transient Hypertrophy
-edema: initial increase in muscle size due to fluid leaking out of blood vessels immediately after working out.
Chronic Hypertrophy
-each muscle fiber increases in cross-sectional area due to an increase in actin and myosin
Traditional Classifications for Vertebrate Twitch Muscle Fibers
-Slow oxidative (type I)
-Fast glycolytic (type IIB)
-Fast oxidative (type IIA)
Slow Oxidative Muscle Fiber
-Type I, MHCi (myosin heavy chain 1)
-slow contractions using aerobic metabolism
-high concentrations of mitochondria, capillaries and myoglobin
-will not fatigue rapidly because no lactic acid produced
-used for postural muscles
-red muscles
-active for long periods of time without fatigue
-small diameter since they have less room for actin/myosin with all the mitochondria
-slow myosin ATPase
-long twitches
-slow Ca uptake by SR
Fast Glycolytic Muscle Fiber
-Type IIB, MHCiib (non human) and MHCiix (mammals/humans)
-primarily anaerobic
-produce lactic acid, so fatigue easily
-less myoglobin
-used in strenuous exercise
-white muscle
-fast myosin ATPase activity
-short duration of twitch
-high rate of Ca uptake by SR
-few mitochondria
-large diameter
-many glycolysis enzymes
Fast Oxidative Muscle Fiber
-type IIA, MHCiia
-primarily aerobic
-fast myosin ATPase activity
-short twitches
-high rate of Ca update my SR
-medium resistance to fatigue
-many mitchondria
-high myoglobin content
-red
-medium diameter
-many capillaries
Composition of Fiber types in vertebrate skeletal muscle
-given motor unit innervates same type of muscle fiber
-most muscles are about 50/50 fast glycolytic: fast oxidative/slow oxidative
-Muscles involved in posture mostly composed of slow oxidative
-There is some plasticity in terms of types of muscle fibers found in muscles: mostly is genetic, but training can convert fast oxidative and fast glycolytic to one or the other.
Twitch Fibers
-generate action potentials that give rise to a twitch
-all or nothing-->full contraction
Tonic Fibers
-found in postural muscles of amphibians, reptiles, and birds and found in eye muscles of mammals.
-Cannot produce an AP
-contract very slowly
-long-lasting contractions with low energetic costs
--Ca pumps dont work as hard
-graded release of Ca from SR=graded force
-1 neuron still innervates the muscle fiber but can synapse multiple times
--temporal summation
Striated muscles of arthropods (invertebrates)
-same basic structure as in vertebrates (sarcomeres, t-tubules, SR, extracellular Ca, troponin, tropomyosin)
-Behaves like tonic muscle fibers
-Have 1-10 motor neurons per muscle
--no AP
--integration at muscle cell (instead of at presynaptic neuron in vertebrates)
-can have excitatory and inhibitory stimuli
Traditional Classifications for Vertebrate Twitch Muscle Fibers
-Slow oxidative (type I)
-Fast glycolytic (type IIB)
-Fast oxidative (type IIA)
Synchronous Flight Muscles
-used in flight
-each muscle contraction is synchronized with the action potential that initiated it, like in vertebrate skeletal muscle.
--1AP=1 muscle contraction
-Muscles are arranged vertically to the long axis of the animal.
-contraction up to 200Hz (200 contractions/s) compared to vertebrates that can do about 90 Hz
Asynchronous Flight Muscles
-used in flight
-each muscle is capable of contracting at much faster frequencies than synchronous flight muscles.
--1000Hz
-Individual contractions not synchronized with individual nerve AP
--many oscillating contractions per AP
-Muscles not attached directly to wings
-have opposing pairs of muscles
--alternate stretching an relaxation to signal contraction and relaxation
-Ca pumps in SR work very slowly relative to other animals (less ATP used and more Ca left in cytoplasm)
--Tropomyosin is moved by both Ca binding to troponin and moved by muscle contractions themselves (both need to occur to move actin/myosin).
--Just need AP at high enough frequencies to ensure enough Ca is present.