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41 Cards in this Set
- Front
- Back
4 types of locomotion |
1) Muscular contractions 2) Hydrostatic pressure/water vascular system 3) Cytoplasmic streaming 4) cilia and flagella |
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Draw the net cost of locomotion graph Label: x axis, x intercept, y axis, y intercept What happens/when does the line peak? Does the graph not start at zero? Why is the graph nonlinear? |
X axis = speed (km/hr) x intercept at peak = max aerobic speed y axis = O2 consumption (ml O2/hr) y intercept at peak= VO2 max Standard MR is not zero Organisms change their behavior with increased speed. |
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Impact of body size on net cost of locomotion 4 Large 5 small |
Large: 1) lower mass specific NCT 2) greater weight = less O2 consumption/distance 3) can store more elastic energy during movement due to gravity. 4) greater muscle size = more elastic tension = more power Small 1) more energetically expensive to move (steeper slope NCT) 2) need more economical fast-twitch fibers to move appendages faster 3) Water = increase SA to vol, small muscles cannot overcome drag 4) Terrestrial = decrease stride length = increase stride freq. 5) Smaller muscle = less elastic force= less powerful |
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Impact of environment on net cost of locomotion |
Land = more energetically expensive due to gravity Air = lift minimizes the effect of gravity Water = most efficient, buoyancy |
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Ecological cost of transport = ? What factors effect ETC? Mammals v reptiles |
DMD (km/day) x NCT (J/km) / DEE (J/day) Increased body mass = increase DMD largest DMD for carnivorous mammals high DEE mammals = lower ECT low DEE reptiles = high ECT |
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5 properties of skeletal muscles 3 functions |
Voluntary, extend, elastic, excitable, contract Produce heat, Movement, Posture/stability |
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Composition of skeletal muscles |
Fascicles : bundles of muscle fibers Myofibrils: individual fibers held together by connective tissues highly vascularized |
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5 components of muscle cells |
1) Sarcoplasm 2) Sarcolemma 3) T-Tubules: conduct electrical charge 4) Sarcoplasmic Reticulum: store/release Ca+ 5) Myofibrils: protein segments (sarcomeres alternating light and dark bands that give muscle its striated appearance) |
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Myofibrils |
1) Myosin: thick filament, contractile protein, motor molecule, binds to actin, head with ATPase which hydrolyzes ATP, energy release allows head to swivel and bind to actin. 2) Actin: thin filament, contractile protein, 2 strings of G-proteins, 5-7 active sites for myosin. 3) Troponin: regulatory protein, binds to CA+ and pulls tropomyosin away from binding sites on actin 4) Tropomyosin: regulatory protein, woven around actin, covers the binding sites |
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CNS PNS Motor/efferent (output) |
Brain and spinal cord sensory input from the body somatic NS (voluntary movement) |
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Neuromuscular Junction |
somatic motor neuron (Presynaptic) innervates a skeletal muscle cell (Postsynaptic) |
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sequence of excitation events btw a somatic motor neuron and a skeletal muscle fiber leading towards muscle contraction (9 steps) |
1) AP arrives at somatic motor neuron terminals 2) Voltage gated CA+ channels open, CA+ moves in via elecrochemical forces. Motor neuron depolarizes. 3) CA+ causes fusing and opening of vessicles, release of ACH, ACH diffuses into synapse 4) ACH binds to ligand gated receptors on motor end plate of a muscle cell 5) channels open, leading to influx Na+ 6) NA+ depolarizes muscle, release of CA+ from the sarcoplasmic reticulum, AP propagates down muscle fiber via increased T-tubule SA 7) Muscle contracts 8) ACH reuptake by motor neuron, diffused out of synapse, BD by enzyme acetylcholineasterase. 9) Ligand gates receptors close, muscle relaxes, no more depolarization |
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3 levels of how the CNS controls movement |
1) Spinal cord to brain stem (knee jerk) 2) brainstem, cerebellum to posture, hand/eye coordination 3) basal ganglia, cerebral cortex to voluntary movement (planning, initiation, execution, higher order processing) |
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Sliding filament model |
muscle shortens as actin and myosin slide past each other sliding filaments = crossbridge cycling = muscle contraction = increased shortening = increased contraction force |
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Cross bridge formation |
CA+ binds ti troponin, causing tropomyosin to move away from myosin binding sites on actin formation of cross bridge = muscle contraction |
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4 steps that allow muscle to contract |
1) cross bridge formation 2) powerstroke (head swivel of myosin) 3) cross bridge detachment 4) reactivation of myosin head |
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Calcium's relationship with Force? |
Force (%max) y axis Myoplasmic CA+ concentration, x axis Sigmoidal |
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6 steps occurring at the level of Actin and Myosin during a muscle contraction |
1) CA+ binds to troponin 1a) ATP binds to myosin head, detaches from actin 2) Tropomyosin moves from active site 3) ATP Hydrolyzes, energy release causes the head of myosin to swivel 4) ADP and phosphate released, actin and myosin slide toward each other 5) Rigor: myosin remains bound 6) ATP rebinds, myosin detaches |
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5 steps occurring at the level of Acting and Myosin during muscle relaxation |
1) ACH removed from synapse 2) Ca2+ removed actively via Calcium-ATPase pumps 3) Active sites on actin covered 4) No crossbridge interaction 5) Passive recoil of sarcomere to resting length (generate max. contractile force during subsequent contractions) |
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Invertebrate muscles |
Asynchronous nerve signals (1 signal can produce multiple contractions) oblique striation, thin and thick filaments connected to dense bodies Stretch activation: myofibril is selective to ca2+ when muscles are relaxed. Once a contraction occurs, it becomes calcium insensitive. Intercellular calcium remains high. |
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Nervous system |
control an communication of body systems fast and short-term movement of ions create electrical currents that are sent to specific target cells or release chemicals that interact with other cells |
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Types of nerves present in the PNS and CNS |
PNS = sensory and motor neurons CNS = brain and spinal cord, sensory, motor, and interneurons Sensory = carries/compiles info to CNS Motor = info away from CNS, cause response Interneuron = connection btw neurons Pathway = sensory cell to sensory neuron to interneuron to motor neuron to effector cell |
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Neuron Function Structure |
functional unit of the NS, excitable, respond to and produce electrical signals via ion concentrations. Dendrites: receive info/ AP Cell body Axon hillock: AP generated, highest density of voltage gated sodium channels, lowest threshold Axon: nerve fiber that conducts an electrical signal, AP jumps from node to node (saltatory conduction) myelin keeps ions in. |
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Resting membrane potential created by? GHK equation |
- 70mv created by potassium leak channels (more than sodium accounts for negativity). always open, ion specific, ions driven by electrochemical gradients K+ moves towards low concen. inside cell, excess negative charge. depends on concentration gradient and permeability of ions 61 log PNa[Na+]o+PK[K+]o / PNa[Na+]i+PK[K+]i |
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Nerst equation |
equilibrium potential: membrane potential necessary to balance the concentration gradient of a given ion. (concentration gradient = electrical gradient) Eion = 61/z log [concen]ionOutside/ [concen]ionInside |
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RMP mediated by |
Sodium-Potassium Pump Active transport (use of ATP) to move 2 K+ in and 3 Na+ out against their concentration gradients |
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Action potential |
uniform and propagated change in electrical/membrane potential across the cell membrane (result of permeability change) easier to excite when a RMP moves towards its threshold |
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Stages of an action potential |
1) RMP 2) Threshold: (-40mv) voltage gated sodium and potassium channels triggered. Voltage gated Na+ channels open 3) Depolarize: influx of Na+ (increased permeabiltiy of sodium) 4) Peak: timed closing of voltage gated sodium channels, voltage gated potassium channels open 5) Repolarize: efflux of K+ out of neuron, increase premeability of potassium 6) Hyperpolarize: below RMP VG K+ still active along with leak potassium and sodium-potassium pumps 7) Depolarize to RMP: VG K+ channels closed |
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Voltage gated Sodium channels |
At rest: Inactivation gate open, activation gate closed Depolarize: threshold stimulus opens both gates, influx sodium down electrochemical gradient +30mv (timed) Inactivation gated closes, decrease sodium permeability Repolarization (increased potassium) resets the gates to initial positions, no sodium movement, allows another action potential to be fired. |
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Voltage gated potassium channels |
Threshold triggers delayed opening of gate until peak potential Once peak occurs, the channel is open until hyperpolarization Without this channel, the cell could repolarize due to leak channels, but 1) no hyperpolarization without the continued opening of VG K+ chennels 2) peak is higher (no counterbalance between Na+ and K+) 3) extended AP 4) Slower NS because fewer AP are sent over a given time |
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Phases of AP are regenerated down the axon by |
local changes in the membrane potential propagated down the axon sodium influx = depolarizes adjacent portions of the membrane, causing the neighboring areas to reach threshold |
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Refractory period (Absolute v relative) |
No backwards signalling because once an area experiences an AP it briefly enters an insensitive period, that lasts until the gates of the Voltage gated sodium channels are reset. Absolute: cannot fire again until reset Relative: cell is responsive and can fire again but requires a super stimulus. |
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Size of action potential relative to stimulus How do neurons send different messages |
all - or - none independent of the strength of the stimulus, as long as the threshold is met the cell fires the same every time. Vary frequency and number of action potentials occurring. |
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Conduction velocity |
speed an AP propagates down an axon, depends on: 1) Diameter of the axon: increase diameter = increase conduction velocity. because there is more room for ions to move, less likely to impact cell membrane and less likely to leak out (largest diameter in sensory neurons, speed important for quick response) 2) Myelination: insulation of the axon. extended cell membrane and cytoplasm. CNS= oligodendrocytes PNS= schwann cells Increases conduction velocity, allows Saltatory Conduction, prevents the movement of ions. maintains the depolarization. |
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Saltatory conduction |
jumping of an AP from node of ranvier to node. (number of nodes depends on the length of the axon). |
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Synaptic transmission |
electrical signal/AP is converted to a chemical signal (neurotransmitters) that interacts with neighboring cells Presynaptic: axon terminals before a synapse, releases the neurotransmitter. Postsynaptic: receives message (effector cells) |
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7 steps of synaptic transmission |
1) AP arrives at terminal, depolarizes presynaptic cell 2) VG CA2+ channels open 3) Influx Calcium down electrochemical gradient 4) Ca2+ influx causes vessicles to dock and release neurotransmitter into synapse 5) Neurotransmitter binds with ligand gated receptors on the post synaptic cell. causing ion/protein channels to open and ions move in or out 6) Movement of ions causes Excitatory Postsynaptic potential or an Inhibitory PSP 7) Receptors/ligand gated channels close, Neurotransmitter is diffused out of the synapse, BD by enzymes, or is reuptaken by the presynaptic cell |
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GRADED POTENTIALS Excitatory PSP Inhibitory PSP |
Depolarization of the cell membrane, brings the cell closer to threshold, more likely to fire Hyperpolarization, brings cell closer to RMP, less likely to fire |
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Graded potentials (how they differ from action potentials) |
1) small change in membrane potential
2) Occur at dendrites and cell body (less frequently near axon terminal) 3) Mechanically, chemically or VG channels 4) Movement of sodium, chloride, calcium 5) Na+ depolarizes, Cl- hyperpolarizes 6) Strength of signal depends on initial stimulus, can be summed! (rather than all or none) 7) Signal initiated by entry of ions through gated channels 8) No min. threshold required, no refractory period - maintain threshold = continued firing |
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Decremental |
charge of ions becomes weaker, having less effect in other areas of the postsynaptic cell, as it moves. Due to: Dispersal, resistance, ions leaked out EPSPs may be strong enough to cause a wave of depolarization to hit the axon hillock at threshold and cause an AP |
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Neural integration 3 factors that effect potential for firing |
occurs at the axon hillock, determines whether a postsynaptic cell fires 1) Location of incoming messages: closer to hillock=more likely to change action potential. (less decremental effect) 2) Spatial summation: currents from nearly simultaneous graded potentials combine 3) Temporal summation: graded potentials occur close together in time |