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Prelim 2 Study Guide

by: Paige Seavey

Prelim 2 Study Guide PPE 497

Paige Seavey

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This is a review of the textbook of what seemed necessary and applicable to our notes in class. Good luck Studying!
Physiology of exercise
Study Guide
PPE 497, Exercise Physiology, Exercise Phys, Ex Phys
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This 17 page Study Guide was uploaded by Paige Seavey on Sunday November 8, 2015. The Study Guide belongs to PPE 497 at Syracuse University taught by Brutsaert in Fall 2015. Since its upload, it has received 68 views. For similar materials see Physiology of exercise in Physical Education at Syracuse University.

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Date Created: 11/08/15
Chapter 5: Cell Signaling and Hormonal Responses to exercise  Neuroendocrinology- a branch of physiology dedicated to the systematic study of control systems o Homeostatic involvement controls and regulates functions through nerves and the endocrine system (hormones) o The two systems work together to maintain homeostasis but operate in different ways  Endocrine glands release hormones (chemical messengers) into the blood stream, where it is carried to the target tissue to cause an effect  Hormones can be divided into several classes based on their chemical structure: amino acid derivatives, peptides/protein, and steroids  The nervous system releases neurotransmitters and relay action potentials from one nerve to the next until it reaches the target tissue. o Blood Hormone Concentration  the effect of hormone on a tissue is directly related to the concentration of the hormone in the plasma and the number of active receptors on the tissue.  Hormones in the plasma are dependent on:  The rate of secretion of a hormone from the endocrine gland  The rate of metabolism or excretion of the hormone  the quantity of transport protein (for some hormones)  changes in the plasma volume  Control of Hormone Secretion:  The rate at which a hormone is secreted from an endocrine gland is dependent on the magnitude of the input and whether it is stimulatory or inhibitory  the input can be chemical (eg. Ca ), or a substrate (eg. Glucose) in the plasma, or neurotransmitter (eg. Acetylcholine or norepinephrine)  most glands are under direct influence from multiple inputs o insulin: produced and released by the pancreas; only released in response to a change in plasma glucose levels, amino acids, norepinephrine from sympathetic neurons, and circulating epinephrine from parasympathetic neurons o elevated levels of glucose and amino acids increases insulin secretion o increase sympathetic nervous system activity (epinephrine, norepinephrine) decreases insulin activity.  Inhibitory versus excitatory input determines if there will be an increase of decrease secretion of a hormone  Metabolism and excretion of Hormones:  the concentration of a hormone in the plasma is influenced by the rate at which it is metabolized/inactivated or excreted  inactivation takes place near the receptor or in the liver o liver is a major site of hormone degradation o the kidneys also metabolize and excrete hormones  during exercise blood flow to kidney and liver decreases therefore hormone degradation decreases  elevation of plasma hormone levels  Transport Proteins:  The concentration of some hormones is influenced by the quantity of transport proteins in the liver o Steroid hormones and thyroxin’s are transported bound to plasma proteins because they are immiscible in water  For a hormone to interact with a receptor it must be free of its transport protein  The quantity of free hormones is dependent on the quality of transport protein and the capacity/affinity of the protein to bind the hormone molecules o Capacity= maximal quantity of hormone that can be bound to transport proteins o Affinity= tendency of the transport protein to bind to the hormone  An increase in quantity, capacity or affinity of transport proteins would reduce the amount of free hormones and its effect on tissues  Plasma Volume:  Changes in the plasma volume will change the hormone concentration (separate form the rate of secretion or inactivation of the hormone) o Higher plasma volume- more hormones o Hormone-Receptor Interaction:  Hormones (carried through the whole circulatory system) only affect their target tissues (specific receptors)  the number of receptors depends on down regulation (diminishing due to high levels of hormone concentration)  however chronic exposure to low levels of hormones will increase receptors  occasionally, due to a limited number of receptors  all can be taken up by a hormone causing saturation  Mechanisms of Hormone Activity:  Alteration of membrane transport mechanisms  Alternating activity of DNA in the nucleus to initiate or suppress the synthesis of a specific protein  Activation of special proteins in the cells by “second messengers”  Membrane Transport:  Binding to a receptor  effect of hormone on/near membrane  increase movement of substrates/ions into the cell  Altering Activity of DNA in the Nucleus:  Hormones= lipid like characteristics= diffuse through plasma membrane and bind to a receptor inside the cell  The receptor then translocates into the nucleus= binds to specific protein linked to DNA which contains the instruction codes for protein synthesis  Second Messengers:  Hormones that bind to receptors on the cell membrane surface and activate g-protein= located inside the cell  The G-protein links the hormone receptor on the surface of the membrane to the events inside the cell  The G-protein can = open an ion channel to allow Ca 2+into the cell to can activate enzymes in the membrane o Adenylate cyclas (cyclic AMP)= formed from ATP, when increased it alters cellular activity (eg. Break down of glycogen to glucose) o cAMP is deactivated by phosphodiesterase 2+  if a G-protein activates a Ca channel, then calcium enters the cell and binds/activates calmodulin ( influences cellular activity like cAMP)  g-protein may activate phospholipase C= a phospholipid in the membrane is hydrolyzed into two i2+racellular molecules o inositol triphosphate= Ca release from intracellular stores o diaglycerol= activates protein Kinase C which activates proteins in the cell  second messengers= cyclic AMP, Ca , inositol triphosphate, and diaglycerol  Tyrosine Kinase:  Insulin doesn’t use second messengers- it uses tyrosine kinase  Insulin binds to the alpha subunits which are outside the cell  Binding causes the beta subunits (inside the cell) to phosphorylate – this leads to the movement of glucose transporters to the membrane so glucose can enter and activates the enzyme glycogen synthase  Hormones: regulation and Action: o Endocrine glands: hormones and how they are secreted/regulated o Hypothalamus and the Pituitary Gland:  Pituitary gland: located at the base of the brain attached to hypothalamus  2 lobes o anterior (true endocrine gland)= hormone release is controlled by chemicals which is eight stimulated or inhibited o posterior (neural tissue extending from the hypothalamus)= receives hormones from hypothalamus and move them to the blood stream  both lobes are under direct control of the hypothalamus  Anterior Pituitary Gland:  ACTH, FSH, LH, MSH, TSH, GH, and prolactin  Growth Hormone:  Secreted by anterior pituitary  Controlled by releasing hormones secreted by hypothalamus  Posterior Pituitary Gland:  Provides storage for two hormones o Oxytocin= stimulates smooth muscle o Antidiuretic hormone (ADH)  Antidiuretic Hormone (ADH):  Reabsorbs water from the renal tubules  2 stimuli o high plasma osmolality – low water concentration – that can be caused by excessive sweating without water replacement o a low plasma volume, which can be due either to the loss of blood or to inadequate fluid replacement o Thyroid Gland:  Thyroid gland is stimulated by TSH to synthesize iodine-contain hormones  They are central to establishing the overall metabolic rate  Calcitonin:  (small role) Regulates plasma calcium (Ca )2+  Regulates normal muscle and nerve function  Controlled by a negative feedback mechanism  Parathyroid Hormone: o Primary hormone involved in plasma Ca 2+ concentration o Release parathyroid hormone when low calcium concentration  bone releases calcium into the plasma and renal reabsorption of calcium  Adrenal Gland: o Adrenal Medulla:  Sympathetic nervous system  Most of secretions are epinephrine which affect the cardiovascular and respiratory systems, gastrointestinal tract, liver, muscles and adipose tissue.  Epinephrine and norepinephrine both bind to adrenergic receptors (alpha and beta) in target tissues o Adrenal Cortex:  Secretes variety of steroid hormones  3 category of hormones  minera+ocortic+ids: (aldosterone) involved in the maintenance of the Na and K concentrations in plasma  glucocorticoids: (cortisol) involved in plasma glucose regulation  sex steroids: (androgens and estrogens) support pubescent growth with androgens being associated with post-pubescent sex drive in women o Aldosterone:  Mineralocorticoid  Regulator of sodium reabsorption and potassium secretion in the kindeys  Directly involved in water/sodium balance – therefore involved in plasma volume and blood pressure o Cortisol:  Contributes to maintenance of plasma glucose  Mechanisms for maintaining plasma glucose  Promote the breakdown of tissue protein to form amino acids – used by liver to form new glucose  Stimulate the mobilization of free fatty acids from adipose tissue  Stimulate liver enzymes involved in metabolic pathway leading to glucose synthesis  Block entry of glucose to tissues, forcing the tissues to use more free fatty acids as fuel o Pancreas:  Exocrine and endocrine gland  Glucagon and somatostatin  Insulin o Testes and Ovaries:  Testosterone – controlled by LH and is secreted by the interstitial cells of testes  Estrogen and progesterone – LH secreted controls female sex characteristics  Hormonal Control Of Substrate Mobilization During Exercise o Muscle-Glycogen Utilization:  Muscle glycogen is the primary carb fuel for muscular work  The intensity of exercise determines the rate at which muscle glycogen is used as fuel  Blood Glucose Homeostasis during exercise: o Plasma glucose concentration is maintained by 4 processes:  Mobilize glucose from liver glycogen stores  Mobilize plasma FFA from adipose tissue to spare plasma glucose  Synthesize new glucose in the liver from amino acids, lactate, and glycerol  Block glucose entry into cells to force the substitution of FFA as fuel  Cortisol: stimulates FFA mobilization from adipose tissue, mobilizes tissue protein to yield amino acids for glucose synthesis in the liver, and decreases the rate of glucose utilization by cells  Growth hormone: decreases glucose uptake by tissue, increases FFA mobilization, enhances gluconeogenesis in the liver  Epinephrine and norepinephrine: mobilization of glucose from liver, mobilization of FFA from adipose tissue, Interference with the uptake of glucose by tissues Chapter 7: The Nervous System: Structure and Control of Movement  General Nervous System Functions: o Central Nervous System (CNS): receptors capable of sensing touch, pain, temperature, and chemical stimuli are sent here and respond o Contained by the brain and spinal cord o The four major functions:  Control of the internal environment (in conjunction with endocrine system)  Voluntary control of movement  Programming spinal reflexes  Assimilation of experiences necessary for memory and learning  Organizing the Nervous System: o Peripheral Nervous System (PNS): consists of nerve cells other than the brain or spinal cord  Sensory: responsible for transmission of neuron impulses from sense organs (receptors) to the CNS  Afferent fibers: conduct information toward the CNS  Motor:  Somatic Motor System: innervates skeletal muscle  voluntary  Autonomic Motor System: innervates involuntary effector organs like smooth muscle, cardiac muscle and glands  involuntary  Efferent fibers: motor neurons that carry impulses away from the spinal cord o Structure of the Neuron:  Neuron: functional unit  Cell body: center of operation in neuron, also known as soma; contains the nucleus  Dendrites: serve as the receptive area that can conduct electrical impulses toward the cell body  Axon: aka the nerve fiber, carries electrical impulses away form the cell body toward another neuron or effector organ o Vary in length, only one per neuron but can be subdivided into several collateral branches that terminate at other neurons/muscle cells/glands o Synapses: contact points between the end of an axon and the dendrite of another neuron  Schwann cells: insulating layer on large nerve fibers o Membranes contain a large amount of lipid protein substance called myelin which forms a discontinuous sheath that covers the outside of the axon o The gaps between the myelin sheath are called nodes of Ranvier  The larger the diameter of the axon  the faster the neural transmission o Electrical activity in Neurons:  Neurons= excitable tissue b/c of irritability and conductivity  Irritability- ability of dendrites and neuron cell body to respond to a stimulus and convert it to a neuronal impulse  Conductivity- transmission of the impulse along an axon  Resting membrane Potential:  At rest all cells, including neurons, are negatively charged on the inside of the cell with respect to the charge that exists outside the cell  due to unequal distribution of charged ions o Neurons are polarized  The electrical charge difference is called the resting membrane potential o The magnitude ranges from -5 to -100mV depending on the cell type but its generally around -40mV to -75mV  Negatively charged anions are fixed inside the cell, which attract positively charged cations outside the cell  The magnitude of resting potential depends on o The permeability of the plasma membrane to different ion species o The different in ion concentration between muscular and extracellular fluids (potassium inside cell, calcium chlorine and sodium outside cell) o The permeability of a neuron to ions is regulated through ion gated channels  ions can move freely when the channels are open  At rest both most ion channels are closed to maintain a positive charge outside the cell and a negative charge inside the cell o Some potassium channels are still open “leaking” into the extracellular space  Negative membrane potential is a resting neuron o Higher permeability of the membrane for potassium than sodium o The concentration gradient for potassium from inside to outside the cell  The cell membrane has a sodium/potassium pump (using ATP) to maintain the concentration gradients for resting membrane potential  Action Potential:  When a stimulus reaches the neuron membrane, sodium gates open making the inside of the cell more positive  depolarization  When depolarization reaches threshold (a charge required in order to cause an action potential) o Sodium channels open flow into the cell to reach threshold propagates down the axon  Action potential: nerve impulse o once generated a sequence of ionic exchanges occurs along the axon to propagate the nerve impulse  the propagation occurs in a sequential fashion along the nodes of Ranvier  repolarization occurs proceeding depolarization o potassium channels open, causing potassium to leave the cell to reestablish a negative charge and sodium gates close o this quickly restores the negative resting membrane charge o the sodium potassium pump begins to reestablish ion concentration gradients (high potassium inside the cell, high sodium, calcium, and chlorine outside the cell)  All-or-None:  If a nerve impulse is initiated  the impulse will travel down the axon with a decrease in voltage o A neural impulse is just as strong after traveling the length of the axon as it was at the beginning  If initiated the nerve impulse will act with the same intensity the entirety of the axon  Neurotransmitters and synaptic transmission:  Synapse: small gap between the axon terminal of a presynaptic neuron and a dendrite of a postsynaptic neuron  Synaptic Transmission: occurs when sufficient amounts of s specific neurotransmitter is released from synaptic vesicles contained in the presynaptic neuron o Synaptic vesicles are released into the synaptic cleft (space between the two membranes) o Neurotransmitters from the vesicles attach to the target membrane and cause depolarization of the next membrane  Excitatory Postsynaptic Potentials (EPSPs): o After release of neurotransmitter into the synaptic cleft they bind to receptors on target membrane  produces graded depolarization’s on dendrites and cell bodies o If sufficient amounts of neurotransmitter is released  post synaptic neuron is depolarized to threshold  action potential is generated o Can cause postsynaptic membrane to reach threshold 2 ways:  Temporal summation  Spatial summation o Temporal summation: the summation of EPSPs over a short time period o Spatial summation: concurrent EPSPs come into a postsynaptic neuron form numerous different excitatory inputs o Acetylcholine: common excitatory neurotransmitter at nerve/muscular junction (excitatory but also inhibitory)  Inhibitory Postsynaptic Potentials (IPSPs): hyperpolarization of the membrane o Neuron develops a more negatively charged resting membrane potential further from threshold o This makes it harder for the neuron to depolarize  Sensory Information and Reflexes: o Proprioceptors: receptors that provide the CNS with information about body positions  Muscle spindles, Golgi tendon organs, joint receptors o Joint Proprioceptors:  Kinesthesia: conscious recognition of position of body parts with respect to one another as well as recognition of limb-movement rates  Extensive sensory devices in and around joints  3 principles:  Free nerve endings (most abundant) o The receptors are stimulated at the beginning of movement  they adapt at first but then transmit a steady signal until movement  Golgi-type receptors o Found in ligaments around joints o Act similar to free nerve endings  Pacinian corpuscles o Found in tissues around joints and adaptation presumably helps detect the rate of joint rotation o Muscle Proprioceptors:  Chemoreceptors, muscle spindles, and Golgi tendon organs  Chemoreceptors: specialized free-nerve endings that send info to the central nervous system response to changes in muscle pH, concentrations of extracellular potassium and changes in O and2CO 2  May play a role in cardiopulmonary regulation  Muscle Spindle: length detector  Muscles that require the highest degree of control contain the most amounts of spindles (ie. The hands)  Composed of several thin muscle cells that are surround by tissue sheath  Insert into connective tissue within the muscle  Primary endings: respond to changes in muscle length Secondary endings: provides CNS with information concerning static muscle length  Golgi Tendon Organ (GTOs): Continuously monitor the tension produced by muscle contraction Located within the tendon Serve as safety devices that help prevent excessive force during muscle contraction Play and importance in the performance of strength activities Responsible for a reflex known as the inverse stretch  Muscle Chemoreceptors: Chemoreceptors are free nerve ending and are sensitive to changes in the chemical environment surrounding muscle They send information to the CNS through slow conducting fibers (group III myelinated and group IV unmyelinated)  Withdrawal reflex: reflex arc is a nerve pathway from the receptor to the CNS and from the CNS along a motor pathway back to the effector organ used in response to sensory input and is not dependent on higher brain centers pathway o sensory nerve (pain receptor) sends a nerve impulse to the spinal column o interneurons within the primal cord are excited and in turn stimulate motor neurons o the excited interneurons cause depolarization of specific motor neurons which control the flexor muscles necessary to withdraw the limb from the point of injury reciprocal inhibition= simultaneous excitatory and inhibitory Somatic Motor function and motor Neurons: o somatic: the outer regions of the body o motor neuron: somatic neuron that innervates skeletal muscle fibers (also called an alpha motor neuron o motor unit: each motor neuron and all the muscle fibers it innervates o motor unit recruitment: progressive activation of more and more motor neurons o size principle: order and sequential recruitment of larger motor neurons Vestibular Apparatus and Equilibrium: o Vestibular apparatus: maintains general equilibrium/balance in the ear Motor Control Functions of the Brain: o the brain stem= at the base of the skull, responsible for metabolic functions, cardiorespiratory control and highly complex reflexes o cerebrum= large dome of brain divided into left and right hemispheres  motor cortex= final relay point upon which subcortical inputs are focused o cerebellum= coordination and monitoring complex movement  lies beyond pons and medulla Autonomic Nervous System: o Maintains homeostasis o Sympathetic division: activates the organ o Parasympathetic division: deactivates the organs Chapter 8: Structure and Function Skeletal Muscle Structure o Epimysiumperimysium endomysium o Sarcolemma= is the membrane surround the muscle fiber. Beneath the sarcolemma is the sarcoplasm that contains myofibrils  Myofibrils= contain the contractile component actin (thin) and myosin (thick).  A-band = (myosin and actin overlap. I-band (actin only).  H-band (myosin only)  Sarcoplasmic reticulum= stores and releases calcium ions to initiate contraction.  T-tubules = connect to the SR. Plays a major role in communicating the action potential to the inside of muscle fiber Muscular Contraction o Reduction of distance from z-line to z-line o A bands move closer, but do not shorten o I-bands shorten, H-bands shorten o Nerve impulse at neuromuscular junction  depolarization of axon triggers exocytosis of Ach released into synaptic cleft, binds to receptors on muscle fiber  influx of Na into cell causing depolarization wave  action potential 2+ 2+ propagated to inferior by t-tubules  SR releases Ca  Ca binds to troponin  tropomyosin is moved exposing active site on actin  actin and myosin interact to form cross bridge  ATP released from head of myosin and causes power stroke  Sarcomere (z-lines) shorten for contraction  ATP is hydrolyzed to break cross bridge and cycle repeats. o The amount of Ca 2+is the controlling factor for muscle contraction. Ca 2+is continuously pumped back to the SR… used ATP. Muscle Fiber Types  Physiological  Biochemical  Type  Slow twitch  High oxidative  Type 1 fatigue capacity resistant  Low glycolytic (anaerobic) capacity  Fast fatigable  Low oxidative  Type 2A and high glycolytic  Fast twitch  High oxidative  Type 2B fatigue and high resistant glycolytic Force Velocity Relationship o for muscles to shorten it must generate force greater than the load. The lighter the load the faster the contraction. Length Tension relationship o the strength of a muscle contraction is influenced by the frequency of stimulation, thickness of each muscle fiber, and initial length of fiber. o Too litter overlap yields less tension because fewer cross bridges can form. No overlap there is no force that can be generated. Muscle Actions o Isometric actions: a static exercise. Exerted force does not cause load to move, Length of fibers is constant o Dynamic exercise (isotonic): movement of body part  Concentric: muscle shortening  Eccentric: muscle lengthening ▯ ▯ ▯ Chapter 9: Cardiovascular System ▯ Structure and blood flow of the heart o Vena Cava – right atrium – tricuspid valve – right ventricle – pulmonary valve – pulmonary artery – pulmonary vein – left atrium – bicuspid valve – left ventricle – aortic valve – aorta o Pulmonary circuit: blood delivered from right atrium to lungs o Systemic circuit: oxygenated blood pumped from left side to various tissues o Blood travels away from the heart in arteries and to the heart in veins. o Arteries – arterioles – capillaries – venules – veins Cardiac Cycle o Systole = contraction, Diastole = relaxation o Diastole- Relaxation and filling o Ventricular filling, blood flows from atrium to ventricle  Up to 70% filled passively  Atrial contraction “atrial kick”  Occurs in late diastole, P-wave  If ventricle is filling there is more pressure in the atrium causing the blood to flow to the atrium o Isovolumetric contraction period  No valves open, contraction leads to a build up of pressure to overcome the aortic pressure and pump out the blood. o Ventricular Ejection Period  Ventricular pressure is greater than aorta, valves are open allowing blood to go out of the heart  P > P = ejection vent aorta  Ventricular volume decreases because blood was ejected into aorta then out of the heart  This period will end when the pressure in the ventricle becomes less than the pressure in the aorta causing the valves to close o Isovulumetric relaxation period  Valves will be closed and the pressure is decreasing (relaxing)  When atrial pressure is greater than ventricular pressure this period ends.  Electrical Activity of the heart o SA nodes serve as a pacemaker. When the SA node reached depolarization threshold the depolarization spreads over aorta resulting in atrial contraction. The wave of atrial depolarization must be transported by the AV node located on the floor of the right atrium. The AV node connects atria with ventricles with a pair of left and right bundle branches. When it reached the conductive pathway it branched to purkinje fibers that spread depolarization throughout ventricles. o P wave: depolarization of atria o QRS complex: depolarization of ventricles o T wave: ventricular repolarization.  What is cardiac output? (Q) o Amount of blood pumped per unit time o HR x SV= Q (heart rate x stroke volume) o Stroke volume: amount of blood ejected per beat. EDV-ESV=SV o To increase SV you would need to increase systolic volume or decrease diastolic volume  Factors affecting SV o Preload o The amount of blood returning to the heart before it contractions. Same things as EDV (end diastolic volume) o Venous return o How does blood return to the heart via veins? What affects venous return?  Venous tone  Increases SNS=Venocontrisction  Posture  Supine position = greater end diastolic volume because the body doesn’t have to go against gravity  Skeletal muscle pump, contracts muscles to squeeze vein and push blood through valves to prevent backflow in veins  If you immediately stop exercise, the muscles are not contracting and blood will not be moved back into the heart and to the brain causing yo to faint so the body does not have to work against gravity  Respiratory muscle pump; as lungs expand veins are compressed to pump blood through them o Contractility  Frank Starling Method  When you increase end diastolic volume the ventricle stretches and then forces a recoil which causes a more forceful contraction and ejects more blood  As heart fills it stretches causing it to want to recoil and cause contraction o This increases volume which in turn increases stroke volume  Other means of contractility = SNS stimulation o Increase epinephrine and norepinephrine which causes a greater contraction o Afterload  Resistance to ventricular emptying  Afterload increase – cardiac work increases  We measure afterload by blood pressure  Acute increase in afterload  increase ESV  decrease in SV  Poiseuille’s Law o Blood Flow= DPr^4(pi)/ nl(8) o Resistance is directly proportional to length of vessels and viscosity of blood (n) ▯ ▯ Chapter 10: Respiration during Exercise Explain the principle function of the pulmonary system. o The primary function is to provide a means of gas exchange between the environment and the body. Pulmonary respiration refers to ventilation (breathing) and the exchange of gases (O2 and CO2) in the lungs. Pulmonary systems plays a key role in maintaining blood-gas homeostasis (O2 and CO2 tensions) during exercise. o Ventilation= mechanical process of moving air into and out of the lungs o Diffusion= random movement of molecules from an area of high concentration to an area of lower concentration Outline the major anatomical components of the respiratory system. o Major organs of the respiratory system: the nasal cavity, nostril, hard palate, soft palate, pharynx, epiglottis, esophagus, larynx, trachea, left lung, right lung, primary bronchus, secondary bronchus and segmental bronchus. o The lung structure is designed to maximize surface area and minimize diffusion distance. o Air passes from mouth  trachea  right and left bronchi  bronchioles  terminal bronchioles (the smallest airways without alveoli)  respiratory bronchioles  alveoli. o Conducting zone: conducts air to respiratory zone. Humidifies, warms and filters air. Composed of the trachea, bronchial tree and bronchioles. o Respiratory zone: exchange of gases between air and blood. Composed of the respiratory bronchioles and alveolar sacs. o The blood gas barrier: alveolar wall  capillary wall  plasma  erythrocyte (RBC) membrane o Blood vessels and blood flow in the lung: pulmonary artery (deoxygenated blood)  pulmonary capillaries  pulmonary vein (oxygenated blood)  Pulmonary artery receives the whole of the cardiac output o RBC spends about 0.75 seconds, traversing 2-3 alveoli through the pulmonary circuit  List major muscles involved in inspiration and expiration at rest and during exercise. o Inspiration: the most important muscle is the diaphragm.  Force abdominal contents downward and forward, ribs are lifted outward. Increasing volume of thorax, reducing intrapleural pressure and intrapulmonary pressure.  During rest diaphragm does most of the work.  During exercise the external intercostal muscles, pectoralis minor, the scalene muscles and sternocleidomastoids assist in breathing o Expiration:  During rest, there’s no muscular effort because lungs and chest walls are elastic and return to their equilibrium position after expanding during inspiration.  During exercise, the important muscles involved are the rectus abdominis and internal oblique’s. When they contract the diaphragm is pushed upward and the ribs are pulled downward and inward. This causes an increase in intrapulmonary pressure and expiration. ▯ ▯ ▯ Chapter 11: Acid- Base Balance During Exercise: ▯ Ion: any atom that is missing electrons or has gained electrons Hydrogen ion: formed by the loss of an electron Acid, Bases, and pH o Acid: a molecule that releases hydrogen ions and thus can raise the hydrogen ion concentration of a solution above that of pure water.  Strong acids= acids that give up hydrogen ions (ionize) more completely o Base: a molecule that is capable of combining with hydrogen ions and therefore lowers the hydrogen ion concentration of the solution.  Strong bases= bases that ionize more completely. o pH: the negative logarithm of the hydrogen ion concentration (H+). o Acidosis: Hydrogen ion concentration increases, pH declines and the acidity of the blood increases o Alkalosis: Hydrogen ion concentration decreases, pH increases and the solution becomes more basic  Hydrogen Ion Production During Exercise o 3 important contributors to exercise-induced muscle acidosis are:  Production of carbon dioxide and carbonic acid.  Production of lactic acid and lactate.  ATP breakdown.  Importance of Acid-base regulation During Exercise o Heavy exercise results in the production of large amounts of hydrogen ions. Hydrogen Ions attach to other molecules and alter their shape and size. This change can alter molecule in a positive way and influence metabolism. o Increase in intramuscular hydrogen ion concentration can impair exercise performance in two ways:  Reduces muscle cell’s ability to produce ATP  Hydrogen ions compete with calcium ions for binding sites on troponin, which hinders the contractile process.  Acid Base Buffer Systems o Buffer: resists pH change by removing hydrogen ions when the hydrogen ion concentration increases. o Intracellular Buffers  The most common intracellular buffers are proteins and phosphate groups.  Intracellular phosphocreatine has been show to be a useful buffer at the onset of exercise.  Bicarbonate in muscle has been demonstrated to be a useful butter at the onset of exercise. o Extracellular Buffers  The blood contains three principal buffer systems  Proteins o Contain ionizable groups that are weak acids and act as buffers. o Blood proteins are found in small quantities so as buffers are more limited during heavy exercise.  Hemoglobin o Particularly important protein buffer and is a major blood buffer during resting conditions. o 6 times the buffering capacity compared to plasma proteins due to its high concentration. o Deoxygenated hemoglobin is a better buffer than oxygenated hemoglobin.  Bicarbonate o The most important buffer system in the body.  Respiratory influence on Acid-base Balance o The respiratory system is an important regulator of blood carbonic acid and pH. o Respiratory system provides the body with a rapid means of regulating blood pH by controlling the amount of CO2 present in the blood.  Regulation of Acid-base balance via the kidneys o Kidneys do not play an important role in acid-base regulation during short- term exercise. o Kidneys regulate hydrogen ion concentration by increasing or decreasing bicarbonate concentration. When the hydrogen ion concentration increases in body fluids, the kidney responds by a reduction in the rate of bicarbonate excretion. o When the pH of body fluids rises, the kidneys increase rate of bicarbonate excretion. o The kidney mechanism occurs in the tubule portion of the kidney. ▯ ▯  Regulation of acid-base balance during exercise o During the final stages of an incremental exercise test or during near- maximal exercise of short duration, there is a decrease in both muscle and blood pH primarily due to the increase in the production of hydrogen ions by the muscle. o The amount of hydrogen ions produced during exercise is dependent on:  Exercise intensity  The amount of muscle mass involved  The duration of work o How does the body regulate acid-base balance during exercise?  Because working muscle are the primary source of hydrogen ions during exercise, it is logical that the first line of defense against a rise in acid production resides in individual muscle fibers. o Respiratory Compensation: The overall process of respiratory assistance in buffering lactic acid during exercise for metabolic acidosis. ▯ ▯ ▯


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