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Unit 2 Study Guide for Exam 2

by: mak15k

Unit 2 Study Guide for Exam 2 PET3322

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This is the study guide for Exam 2. Lots of information and explanations for understanding the concepts of muscular and nervous systems.
Functional Anatomy and Physiology I
Arturo Figueroa-Galvez
Study Guide
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This 12 page Study Guide was uploaded by mak15k on Thursday October 13, 2016. The Study Guide belongs to PET3322 at Florida State University taught by Arturo Figueroa-Galvez in Summer 2016. Since its upload, it has received 126 views. For similar materials see Functional Anatomy and Physiology I in Anatomy and Physiology at Florida State University.


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Date Created: 10/13/16
Exam II Study Guide Functional Anatomy and Physiology All red font is Dr. Figueroa's outline, all black font is information from my notes and for studying purposes. Make sure that you study the processes (eg. how a nerve travels from the brain to the spine and back) very thoroughly...know what everything is called, the hierarchy of systems and components of the systems, as well as how they interact as a whole. Dr. Figueroa really stresses that we understand the concepts, not just memorize them; I would recommend using this guide as an outline, understanding the content, and mock-teach a friend or yourself in the mirror. (: Good luck!! Nervous System  Nervous system o Sensory input, Integration, Motor Output 1. Receiving sensory input. Monitor internal and external stimuli 2. Integrating information. Brain and spinal cord process sensory input and initiate responses 3. Controlling muscles and glands (skeletal muscles specifically) 1. Maintaining homeostasis. (Regulate and coordinate physiology) o Central and Peripheral CNS = brain and spinal cord PNS = cranial nerves (brain, 12) and spinal nerves (nerves that are connected to the spinal column, 31)  Peripheral Nervous System o Sensory & Motor  Somatic Fibers  Visceral Fibers Sensory (afferent): sensations/sensitive...pain, smell, vision, etc.; origin of these sensations are the receptors in our bodies; transmits action potentials from receptors to CNS  somatic fibers: impulses from skin, skeletal muscles, and joints to the brain  visceral fibers: impulses from visceral organs to the brain Motor (efferent): means motion; stimulate contraction of the skeletal muscle; transmit action potentials from CNS to effectors o Motor Division  Somatic Nervous System  Autonomic Nervous System o Neurons (Nerve Cells)  Structure  Cell body, axon, dendrites, axon hillock, axonal terminals o Functions  Neurotransmitter  Function of Neurons  Myelin Sheath  Structure and Function  Unmyelinated Axons  Neurons: functional unit of nervous system that receive stimuli and transmit action potentials; electrical excitability; more mass in soma, less mass in axons o cell body/soma: single nucleus with prominent nucleolus  nissl substance/chromatophilic substance/ rough ER- site of protein synthesis o dendrites: input  short, often highly branches  receptors  sendritic spines- little protuberance where axons synapse with dendrite o axons: output  can branch to form collaterals  initial segment- beginning of axon  trigger zone- site where action potentials are generated; axon hillock and part of an axon nearest cell body  synaptic vesicles  presynaptic terminals- what causes the muscle contraction (if neuromuscular)  axoplasm  axolema  The Action Potential o Resting Membrane Potential o 1.Depolarization o 2. Repolarization o 3.Hyperpolarization o Ionic Events  Action potentials: (1) sensory receptors- PNS via action potentials, (2) sensory neurons- PNS on dorsal spinal cord, (3) interneuron- axon terminals with vessicles with neurotransmitters at presynaptic neuron, (4) postsynaptic neuron- send signal to cortex/thalamus, (5) upper motor neuron- send signal to muscles in hand, (6) presynaptic central motor neuron- synapse in motor neurons beforehand motion, motor because movement, central because CNS in spine, (7) neurotransmitters will release and bind to receptors in post synaptic neuron, (8) stimulation causes motion across skeletal muscles (neuromuscular junction)  Resting membrane potentials (electrical charge): o Gated ion channels- for facilitated diffusion of sodium  charge inside resting cell is negative caused by the proteins in the cytoplasm  charge of membrane outside the cell is positive produced by a high concentration of sodium  resting membrane potentials for each cell varies o Voltage gated channels- for potassium o polarization- electrical charge becomes either positive or negative; usually caused by sodium...moving from high to low = facilitated diffusion by using gated-channel proteins after Ach (comes from axon terminal) opens the gate o depolarization- potential difference becomes smaller/less polar; more positive +  Depolarization- If extracellular concentration of K increases: less gradient between inside and outside. o hyperpolarization- potential difference becomes greater/more polar; more negative  Hyperpolarization- If extracellular ion concentration decreases: steeper gradient between inside and outside.  Resting potential exists because: 1. concentration of ions different inside & outside  extracellular fluid rich in Na and Cl +  cytosol full of K , organic phosphate & amino acids 2. membrane permeability differs for Na and K +  50-100 greater permeability for K+ + +  inward flow of Na can’t keep up with outward flow of K  Na /K pump removes Na+ as fast as it leaks in  The movement of the action potential is called propagation  Number of potentials produced per unit of time to a stimulus (simply memorize these...) o Threshold stimulus: causes a graded potential that is great enough to initiate an action potential. o Subthreshold stimulus: does not cause a graded potential that is great enough to initiate an action potential.  Myelinated sheaths increase the speed of some neurons. It is a phospholipid that allows for a faster propagation for the action potential.  Un-myelinated axons are just regularly transmitted propagations of action potentials o Peripheral = soma of that neuron is in the spinal cord (even this is in the CNS...spinal cord and brain...the soma are outside of the spinal cord, so it's still peripheral) o Neuromuscular junction = communication between muscles and the neurons  Rate of impulse propagation is determined by: o Axon diameter – the larger the diameter, the faster the impulse o Presence of a myelin sheath – myelination dramatically increases impulse speed  Axons of the Central Nervous System o Tracts  somatosensory cortex- most external area in the brain; "somato" = body  Know how to identify the origin and insertion of the spinal tracts  "spinothalamic tract" ---> from the spine to the thalamus in the CNS (know the identification of the meaning of the names (lateral corticospinal tract...cortex to spinal cord in CNS) not their function or any details like that)  Synapses o Presynaptic and Postsynaptic Neurons o Synaptic Cleft o Ca at axon terminal o Neurotransmitter binding to postsynaptic neuron o Removal of neurotransmitter  Types of cells in synapse: o presynaptic releases neurotransmitters o postsynaptic elicits the response  neurotransmitters produced in soma and stored in the presynaptic terminals to cause action potentials  ACh is really the only neurotransmitter needed for the test (norepinephrine will be on exam 3) o Enzymatic degradation:  ACh: acetylcholinesterase splits ACh into acetic acid and choline. Choline recycled within presynaptic neuron.  2 components: (1) acetate & (2) choline  together they stimulate the receptor  if they are separated, there would be no effect (see step 3)  if ACh is inactive, the response is also inactivated in the cell  ACh produced in the soma  Neurotransmitters are excitatory in some cells and inhibitory in others o a depolarizing postsynaptic potential is called an EPSP  it results from the opening of ligand-gated Na channels o an inhibitory postsynaptic potential is called an –PSP +  it results from the opening of ligand-gated Cl or K channels  it causes the postsynaptic cell to become more negative or hyperpolarized o the postsynaptic cell is less likely to reach threshold  Inhibitory Synapses o Its effect (K+, Cl-, and hyperpolarization as the only electrical event).  Is hyperpolarization the only electrical event in the cell?  No. This is part of the re-polarization which is part of the stimulation; when we re-polarize, we stimulate and activate the cell. Hyperpolarization is the consequence of trying to restore the negative charge to the cell, and is part of the process. o Hyperpolarization = more negative than the resting membrane potential  Neurotransmitters are excitatory in some cells and inhibitory in others o a depolarizing postsynaptic potential is called an EPSP  it results from the opening of ligand-gated Na channels o an inhibitory postsynaptic potential is called an IPSP  it results from the opening of ligand-gated Cl or K channels  it causes the postsynaptic cell to become more negative or hyperpolarized o the postsynaptic cell is less likely to reach threshold  In the heart muscle, ACh is inhibitory o When we excite the cell, the resting membrane becomes less negative/ more positive until an action potential is stimulated after the threshold is passed (depolarization --> repolarization (hyperpolarization) ) o in the heart, hyperpolarization occurs, but this is different!  this is the ONLY electrical event, causing inhibition of the this case the cell is the heart, and if the heart is inhibited, then it will contract with less force, the heart rate will decrease o potassium leaves, chlorine enters  In skeletal muscle, ACh is inhibitory, but the receptor is different o depends on the receptor Central Nervous System  Central Nervous System Components o Brain and Spinal Cord  brain stem- beginning of the spinal cord that contains the cranial nerves o three areas: mid-brain at top, pons in between, and medulla on the bottom  Cerebral Cortex o Motor Areas, Sensory Areas o Primary Motor Cortex  Voluntary Movement  Motor Homunculus  Understand Proportion Concept  Somatic Motor Pathway o Motor Tracts  Pyramids  Decussation of pyramids  There are areas in our body that are more sensitive than others; most sensitive areas are the hands (mainly fingers) and the lips because they have more receptors in the brain  your face has more control over contraction than the muscles of the legs because of the amount of neurons in the brain of the respective areas o the face has small motor units that allow for more precise movements  stimulation of motor neurons in CNS will bring action potentials to the spinal cord  80% of left brain refers to the right side of the body, and 20% remains referred to the left side (opposite is true of the right brain); the crossing over sections of the left and right axons is called decussation of pyramids in the brain stem, medulla oblongata  cervical spinal cord = muscles of the arm  lumbar area = muscles of the legs  Motor homunculus refers to the diagram of the cross-section of the brain that explains which parts of the somatosensory cortex are responsible for motor function in various parts of the body; more of the brain controls facial expression than leg movements  Skeletal muscles are innervated by lower motor neurons, located in either the spinal cord or the brainstem (somatic)  Axons of lower motor neurons travel via either spinal nerves or cranial nerves to reach the muscles they innervate (somatic) o Cranial reflexes are integrated in the brainstem o Spinal reflexes are integrated in the spinal cord o Somatic reflexes have responses involving skeletal muscles o Autonomic reflexes involve internal processes, and are usually not consciously perceived  Corticospinal Pathway o Function o Pathway  Peripheral Distribution of Spinal Nerves o How signals are sent and received to and from the spinal cord  Crossing Over o Axon in anterior corticospinal tract pathway  The Direct (Pyramidal) System  Direct motor pathways descend from the cerebral cortex to lower motor neurons o Lateral corticospinal tract o Anterior corticospinal tract- This pathway carries information for pain, temperature, itch, and tickle sensations  First-order neurons travel to the spinal cord and synapse in the posterior gray horn  Second-order neurons cross to the opposite side of the spinal cord, then ascend in the spinothalamic tract to the thalamus  Third-order neurons project from the thalamus to the cerebral cortex o Posterior Column Pathway- This pathway carries information from touch, vibration, and proprioceptors  First-order neurons travel via the posterior column of the spinal cord to the medulla oblongata  Second-order neurons cross to the opposite side of the medulla, then ascend via the medial lemniscus to the thalamus  Third-order neurons project from the thalamus to the cerebral cortex o Somatic Sensory Pathways- carry information from the body to the somatosensory cortex, and to the cerebellum o Sets of three neurons carry information along the pathways  First-order neurons carry signals as far as the spinal cord or brainstem  Second-order neurons carry signals on to the thalamus  Third-order neurons travel from the thalamus to the cerebral cortex o CNS regions where the three neurons synapse with each other are known as relay stations - these include the spinal cord, regions of the brainstem, and the thalamus o Corticobulbar tract o The pyramidal tracts include both the corticospinal and corticobulbar tracts. These are aggregations of upper motor neuron nerve fibers that travel from the cerebral cortex and terminate either in the brainstem (corticobulbar) or spinal cord (corticospinal) and are involved in control of motor functions of the body. o The corticobulbar tract conducts impulses from the brain to the cranial nerves. These nerves control the muscles of the face and neck and are involved in facial expression, mastication, swallowing, and other functions. o The corticospinal tract conducts impulses from the brain to the spinal cord. It is made up of a lateral and anterior tract. The corticospinal tract is involved in voluntary movement. The majority of fibers of the corticospinal tract cross over in the medulla, resulting in muscles being controlled by the opposite side of the brain. The corticospinal tract also contains Betz cells (the largest pyramidal cells), which are not found in any other region of the body. o The pyramidal tracts are named because they pass through the pyramids of the medulla. The corticospinal fibers when descending from the internal capsule to the brain stem, converge to a point from multiple directions giving the impression of inverted pyramid. Skeletal Muscle  Structure of Skeletal Muscle o Sarcolemma, sarcoplasm, tendon, epimysium, endomysium, perimysium, fascicle, muscle fiber, myofibril  Connective tissue membranes: (prefixes are the same as neurons...-mysium = muscle) o epimysium- connective tissue that covers and surrounds the whole muscle o perimysium- denser; surrounds a group of muscle fibers (fasciculus) o endomysium- loose connective tissue with reticular fibers  myocytes = muscle cells...more usually called "muscle fiber"  sarcolemma: membrane of skeletal muscle  sarcoplasmic reticulum: a network of membranous sacs around the myofibrils; the SR stores calcium ions.  myofibril- muscles can be broken down to this level; it is made of myofilaments: o actin or thin filaments (smaller); 2 of them; attached to the z-disk; allows the muscle to contract and become stronger o myosin (bigger); 1 of them; located in the center of the sacomere when muscle is relaxed  Calcium in the stored in the skeletal muscle- sarcoplasmic reticulum (thin and porous and thicker at the ends) in the cisterna  transverse tubule: where the sarcomere enters into the membrane so that the action potential can propagate itself to release Ca from the SR to the sarcoplasm so it can bind to troponin-C, move tropomyosin, allowing myosin to bind to the active sites, producing a muscle contraction  Sarcomere o Structure  Z-disc, I band, A-band (what myofilaments are in the bands?)  How it changes during contraction  striated = banded; appearance of muscle (under microscope) due to light and dark banding; smooth muscle doesn't have striations  function of the sarcomere (between the z-disks that together make up striations of myofibrils) is to contract the muscle and become shorter (move actin to the center of the muscle, taking along with it the z-disk) and its length is shortened  the dark and light band colors are caused by density of proteins/ filaments o since myosin is bigger, it is more dense; in the region of the sarcomere where we have more myosin, it will look darker o the opposite is true- actin is smaller and therefore less dense, so it appears lighter; 1/2 of the light band belongs to one sarcomere, and the other half belong to the band adjacent to it o only focus on the A band for the exam- it looks dark because of the myosin density (more protein)- and the I band- it looks light because of the actin density (less protein)  Striated appearance o I bands: from Z disks to ends of thick filaments o A bands: length of thick filaments o H zone: region in A band where actin and myosin do not overlap  Length of the A-band is not changing because this is the myosin...the I-bond shortens because this is the actin moving over the myosin o Myofilaments  Actin  G-actin, tropomyosin, ,troponin, troponin regulatory subunits  Actin filaments: has three components... o most important is called G or F-actin (looks like blueberries on the slide) because it has active sites (yellow dots on slide) which are a kind of receptor for the heads of the myosin filaments o tropomyosin- another stranded protein that covers the active site of the G-actin during a relaxed state; to uncover the active sites and remove the tropomyosin we need troponin o troponin- only globular/ bulbous protein; has 3 subunits- one is attached to the G-actin, one is attached to the tropomyosin, and one free one on the top that is the receptor for Ca+  TnI: attached to the G-actin  TnC: receptor for Calcium  TnT: attached to tropomyosin  Myosin  Tails, Heads, ATPase enzyme  Myosin filaments o myosin heads are the most important because there is an enzyme (ATPase) that helps to release the energy from ATP that is important for muscle contraction during exercise  What is important in the myosin head? An enzyme called myosin-ATPase; the ATPase takes ATP (3 phosphates) and cuts the last phosphate, releasing the energy to complete the power stroke  Contraction of Skeletal Muscle o Sarcollema, Sarcoplasmic Reticulum, T-Tubules, terminal cisternae, triads, stimulation via motor neurons o Neuromuscular junction  Axon terminal, ACH, Synaptic Cleft, ACH receptors, Na+/K+ pump, acetylcholinesterase  ACh is the only neurotransmitter in the neuromuscular junction; in the sarcolemma there is an enzyme that will deactivate ACh...acetylcholinesterase o Steps: 1. Acetylcholine (ACh) is released from axon terminals into the synaptic cleft 2. ACh binds to ACh receptors in the sarcolemma 3. A muscle action potential is generated 4. ACh is broken down by acetylcholinesterase o if acetylcholinesterase doesn't work then the muscle is contracted for a longer time and cramps ensue...ACh will stay bound to receptors and the sodium channel will remain open and stimulated...this is why the enzyme is so important o most of the ACh is produced in the soma  the sarcolemma continues in the t-tube...the muscle fiber is made of myofibrils...action potentials propagate through the t-tubule and start polarizing myofibrils in the t-tubule, which are made of sarcomeres  we store calcium in the cisternae  the sarcomere had two filaments, actin and myosin; actin has 3 components: G-actin, troponin, and tropomyosin...troponin has 3 subunits, the top is proponent C...the muscle is relaxed when the Ca+ levels in the sarcoplasm is low...high Ca+ levels in the sarcoplasm bind to troponin-C and the muscles relax, the cisternae Ca+ is stimulated to move from high to low concentration by facilitated diffusion (because it needs a channel) o Excitation-Contraction Coupling  Propagation of signal through muscle fiber, Ca release, Troponin and tropomyosin interaction, myosin cross bridge, Hydrolysis of ATP, Removal of Ca , Blocking of binding site on actin 1. Myosin cross bridge 2. Working Stroke 3. ATP detaches cross-bridge 4. ATP Split to cock head  Generating an action potential: 1. An action potential (orange arrow) arrives at the presynaptic terminal and causes voltage- gated Ca channels in the presynaptic membrane to open. 2. Calcium ions enter the presynaptic terminal and initiate the release of the neurotransmitter acetylcholine (ACh) from synaptic vesicles. 3. ACh is released into the synaptic cleft by exocytosis. 4. ACh diffuses across the synaptic cleft and binds to ligand-gated Na channels on the postsynaptic membrane. 5. Ligand-gated Na channels open and Na enters the postsynaptic cell, causing the postsynaptic membrane to depolarize. If depolarization passes threshold, an action potential is generated along the postsynaptic membrane. 6. ACh unbinds from the ligand-gated Na channels, which then close. 7. The enzyme acetylcholinesterase, which is attached to the postsynaptic membrane, removes acetylcholine from the synaptic cl+ft by breaking it down into acetic acid and choline. 8. Choline is symported with Na into the presynaptic terminal, where it can be recycled to make ACh. Acetic acid diffuses away from the synaptic cleft. 9. ACh is reformed within the presynaptic terminal using acetic acid generated from metabolism and from choline recycled from the synaptic cleft. Ach is then taken up by synaptic vesicles.  Action potentials and muscle contraction: 1. An action potential that was produced at the neuromuscular junction is propagated along the sarcolemma of the skeletal muscle. The depolarization also spreads along the membrane of the T tubules. 2. The depolarization of the T tubule causes gated Ca channels in the sarcoplasmic reticulum to 2+ open, resulting in an increase in the permeability of the sarcoplasmic reticulum to Ca , especially in the terminal cisternae. Calcium ions then diffuse from the sarcoplasmic reticulum into the sarcoplasm. 3. Calcium ions released from the sarcoplasmic reticulum bind to troponin molecules. The troponin molecules bound to G actin molecules are released, causing tropomyosin to move, and to expose the active sites on G actin. 4. Once active sites on G actin molecules are exposed, the heads of the myosin myofilaments bind to them to form cross-bridges.  Cross Bridge Movement 2+ 1. Exposure of active sites. Before cross-bridges cycle, Ca bind to the troponins and the tropomyosins move, exposing active sites on actin myofilaments. 2. Cross-bridge formation. The myosin heads bind to the exposed active sites on the actin myofilaments to form cross-bridges, and phosphates are released from the myosin heads. 3. Power stroke. Energy stored in the myosin heads is used to move the myosin heads causing the actin myofilaments to slide past the myosin myofilaments, and ADP molecules are released from the myosin heads. 4. Cross-bridge release. An ATP molecule binds to each of the myosin heads, causing them to detach from the actin. 5. Hydrolysis of ATP. The myosin ATPase portion of the myosin heads split ATP into ADP and phosphate (P), which remain attached to the myosin heads. 6. Recovery stroke. The heads of the myosin molecules return to their resting position, and energy is stored in the heads of the myosin molecules. If Ca is still attached to troponin, cross- bridge formation and movement are repeated (return to step 2). This cycle occurs many times during a muscle contraction. Not all cross-bridges form and release simultaneously.  Excitation contraction coupling- where does the excitation come from? The nerve in the axon terminal excited by the neurotransmitter (ACh) o first step of contraction is the binding of ACh to the receptor where sodium binds to the gate o then we produce the action potential and it propagates into the t-tubule o the Ca+ moves from the cisternae into the sarcoplasm o contraction starts at step 4 (picture on next page) o relaxation starts with the binding of ACh to the receptor, depolarization, and inactivate ACh via acetylcholinesterase, then Ca+ diffuses to the sarcoplasm and binds to troponin-C so we need to remove Ca+ and send it back to cisternae of sarcoplasmic reticulum to relax...but we always have more Ca+ in the sarcoplasmic reticulum, so to move from low to high concentration we need primary active transport via ATP as energy (similar to sodium-potassium pump)...if there is no ATP left (out of energy) then Ca+ will stay in the sarcoplasm and we will suffer a cramp o Sliding Filament Model of Contraction o Motor Units  Large and small  Sliding Filament Model/Theory- myosin moves the actins because the z-disk is attached and the length of the sacomere decreases as does the length of the muscle fiber & the whole muscle o actin slides over the myosin to create movement  In a relaxed muscle, the actin and myosin myofilaments overlap slightly, and the H zone is visible. The sarcomere length is at its normal resting length. As a muscle contraction is initiated, actin myofilaments slide past the myosin myofilaments, the z disks are brought closer together, and the sarcomere begins to shorten.  In a contracted muscle, the A bands, which are equal to the length of the myosin myofilaments, do not narrow because the length of the myosin myofilaments does not change, nor does the length of the actin myofilaments. In addition, the ends of the actin myofilaments are pulled to and overlap in the center of the sarcomere, shortening it and the H zone disappears.  Skeletal Muscle Twitch o tension  Muscle Twitch- muscle contraction in response to a stimulus that causes action potential in one or more muscle fibers; some tension in the muscle will increase o stimulus applied (electrical in the lab, action potential in the body) take time to start increasing the tension (not immediate because we need time to stimulate the receptor, open the gate, etc.) o the lag phase is this time (not important for the exam) o as the tension starts to increase and peak, it is called the contraction phase o as the tension relaxes, it is called the relaxation phase o the whole thing is called a twitch...there is more control on a muscle contraction o this is important because of the different types of muscle fibers (T1, T2)  Skeletal Muscle Contractions o Isometric Contraction o Isotonic Contractions  Concentric and eccentric  isometric- no change in length but tension increases (postural muscles of body)  isotonic- change in length but constant tension; includes concentric and eccentric motions; tension will increase for all types of contractions...the tension changes a little bit but is the same during the contraction; dynamic contractions involve movement and the length of the sarcomere and muscle is going to change o Energy for Contraction  ATP, creatine phosphate, anaerobic glycolysis, aerobic glycolysis  Sources of ATP  Sources of ATP in muscles: 1. Creatine Phosphate : Creatine Phosphate --> Creatine, yields 1 ATP per creatine phosphate energy = creatine phosphate oxygen not required duration of energy ≤10 seconds moderate and extreme exercise supported 2. Anaerobic Respiration- Glycolysis: Glucose --> 2 pyruvic acid (yields 2 ATP per glucose molecule)--> 2 lactic acid energy = glucose no oxygen required duration of energy ≤ 3 minutes extreme exercise supported 3. Aerobic Respiration- Glycolysis: Glucose --> 2 pyruvic acid (yields 2 ATP) --> citric acid cycle and electron transport chain (yields 34 ATP) energy = glucose, fatty acids, and amino acids 36 ATP produced supports hours of energy, resting and all exercise  Muscle Fiber Types o Type 1, Type 2b o Speed of Contraction o Oxidative and Glycolytic Fibers o Be able to differentiate them by their characteristics  We have to analyze time and tension when looking at different types of muscle fibers: o Slow-twitch oxidative  Contract more slowly, smaller in diameter, better blood supply, more mitochondria, more fatigue-resistant than fast-twitch, large amount of myoglobin.  Postural muscles, more in lower than upper limbs. Dark meat of chicken.  slow increase in tension and long time to respond/ maintain tension  weaker contraction, but don't fatigue easily  marathon runners and other long distances o Fast-twitch  Respond rapidly to nervous stimulation, contain myosin that can break down ATP more rapidly than that in Type I, less blood supply, fewer and smaller mitochondria than slow-twitch  Lower limbs in sprinter, upper limbs of most people. White meat in chicken.  Comes in oxidative and glycolytic forms  large and fast increase in tension and short time to respond/ maintain tension  stronger contraction, but fatigue easily  sprinters  hypertrophy- increase in muscle size/ mass o 2 mechanisms to increase muscle mass, and only one in humans: we don't produce more muscle fibers, we just make them grow in size  atrophy- reduction in the size of muscle cells  oxidative- ATP production in the cytoplasm, and in the sarcoplasm in the muscle via aerobic glycolysis  yielding acetyl CoA to make 36 ATPs using oxygen from the blood (oxidative)- this happens in the mitochondria...oxidative metabolism; anaerobic glycolysis is a net production of 2 ATPs that yields lactic acid from glucose in the cytoplasm


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