Nerve Physiology

 Nervous System- one of the major control organ systems of the body
o Regulate and control and command all parts of the body because of highly specialized cells (neuron)
o Membrane potential- the special property of charge separation across the membranes of neurons which
enables neurons to generate signals
 The Human Nervous System
o Central Nervous System
 Brain
 Spinal Cord
o Peripheral Nervous System- connect the brain and spinal cord with the body’s sense, organs, muscles,
glands, and other functional tissues
 Cranial Nerves (12 pairs) (from the brain)
 Spinal Nerves (31 pairs) (connecting the spinal cord to the body)
 Neuron- functional unit
o Serve as integrators
o Operate by generating electrical signals that mo0ve from one part of the cell to another part of that
same cell or nearby cells
 Electrical signals cause release of neurotransmitters for communication
o Consists of:
 Cell body (soma)- contains nucleus and ribosomes
 Dendrites: Highly branched
outgrowths that receive incoming
info. from other neurons (increase
surface area so more signals can be
intercepted)
 Dendritic spines: further increase
surface area
 Axon: long process that extends form
the cell body to carry messages to
target cells (can range from microns
to a meter!)
 Axon hillock (initial segment): region
of the axon that arises from the cell
body
 Initial segment is where
most electrical signals are
generated
 Collaterals: branches from the axon
 The greater the axon and its collaterals, the greater influence the axon has
 Axon terminal: ends of axon branches which release neurotransmitters from the axon
 Varicosities: neurons can release their chemical messengers from these as well as axon
terminals
 Myelin: covers axons in sheath-like covers consisting of about 20-200 layers of highly modified
plasma membrane to speed up conduction of electrical signals along axon
 Also helps to conserve energy
 Axonal transport: movement of the axon, various organelles, and other stuff to move between cell body and axon
terminals
o Depends on scaffolding of microtubule “rails"
o Motor proteins: Kinesins and dyneins (use ATP hydrolysis)
 Kinesin transport: mainly occurs from the cell body to the axon terminals (anterograde)
o Important for moving nutrients, enzymes, mitochondria, neurotransmitter-filled vesicles, and more
 Dynein transport: (retrograde: opposite direction of kinesin) carries recycled membrane vesicles, growth factors,
and more to affect morphology, biochem., and connectivity
 Functional Classes of Neurons:
o Efferent neurons: take information away from CNS towards the
rest of the body
 Cell bodies and dendrites are within CNS
 Axons extend into periphery
o Afferent neurons: take information from the body towards the
CNS
 Single process from the cell body splits into a long
peripheral process (axon) in the PNS and a short
central axon in the CNS
o Interneurons: connect neurons within the CNS (99% of all
neurons)
 Function as integrators and signal changers
 In CNS
 Integrate afferent and efferent neurons into reflex
circuits
 Proportional: 1 afferent neuron : 10 efferent neurons : 200,000 interneurons
o Sensory receptors: respond to various physical or chemical changes in the environment by generating
electrical signals
 Located on the peripheral end (farthest away from CNS) of the afferent neuron
o Nerves: afferent/efferent neuron axons, myelin, connective tissue, and blood vessels
o Synapse: specialized junction between two neurons where one neuron alters the electrical and
chemical activity of another
 Signal transmitted by neurotransmitters
o Presynaptic neuron: neuron that conducts a signal toward a synapse
o Postsynaptic neuron: neuron conducting signals away from a synapse
 Glial Cells (glue)
o Oligodendrocytes: (type of glial cell) myelin forming cell in the CNS
o Schwann cells: (also glial cell) myelin forming cell (1-1.5 mm long segments) in the PNS
o Nodes of Ranvier: spaces between adjacent sections of myelin where axon’s plasma membrane is
exposed to extracellular fluid
 Surround the axon and dendrites of neurons
 Provide physical and metabolic support
o Glial cells can divide (can also cause tumors in CNS)
 Types of Glial cells
o Oligodendrocytes: form myelin sheaths of CNS axons
o Astrocyte: help regulate composition of extracellular fluid in CNS (remove K+) and neurotransmitters
around synapses.
 Stimulate the formation of tight junctions between cells that make up walls of capillaries in CNS
 Forms a blood-brain barrier: more selective filter for substance exchange
 Sustain neurons metabolically i.e. providing glucose and removing toxic ammonia
 Guide CNS neurons to their ultimate destination
 Stimulate neuronal growth
o Microglia: specialized macrophage-like cells that perform immune functions in the CNS
 Contribute to synapse remodeling and plasticity
o Ependymal cells: line fluid-filled cavities within brain and spinal cord
 Regulate production and flow of cerebrospinal fluid
o Schwann cells: (glial cells of PNS) produce the myelin sheath of the axons in the PNS
 Neuronal Growth and Regeneration: Embryoinic development:
o 1. Series of cell divisions of precursor stem cells
o 2. Develop into neurons or glia
o 3. Neuronal daughter cell differentiates and migrates to final location
o 4. Starts sending out dendrites and axons
o Growth cone: forms tip of each extending axon and finds correct route and final target
 Axon routes depend on:
o Attraction, supporting, deflection, inhibition of molecules
o Once target of growth cone is reached, synapses form
 50-70% of neurons undergo apoptosis in the developing CNS
 Plasticity: ability to modify its structures and function in response to stimulation or injury
o Involves remodeling of synaptic connections
o Varies with age
 Basic shapes and formations of major neuronal circuits in mature CNS don’t change once formed
o Creation and removal of synaptic connections continues throughout life
 Regeneration of Axons:
o Axons can repair themselves and restore function as long as damage occurs outside the CNS and
doesn’t effect the cell body
 Axon that is still attached to a cell body creates a growth cone and starts outgrowth of a new
axon
 Axons grow about 1 mm per day
 Basic Principles of Electricity:
o Electrical potential: separated electrical charges of opposite sign have the potential to do work if they
are allowed to come together (Potential difference (potential))
o Current: movement of electrical charge
o Resistance: obstructing electrical charge
o Ohm’s law: I = V/R
 I = current
 V = voltage
 R = resistance
o Insulators: high electrical resistance = reduce currant flow
o Conductors: rapid current flow (low resistance)
o Resting membrane potential: inside of cell negatively charged
 Small excess of negative ions inside the cell and excess of positive ions outside the cell
o Magnitude of resting membrane potential depends on:
 1. Differences in specific ion concentrations in the intra/extracellular fluid
  2. Differences in membrane permeabilities to different ions (open channels available for
different ions)
 Equilibrium potential: membrane potential at which two fluxes for one ion become equal and
opposite
 The magnitude of the equilibrium potential for any ion depends on the concentration
gradient for that ion across a membrane
 The larger the concentration gradient, the larger the equilibrium potential
 Nernst equation: describes equilibrium potential for any ion:
 predicts how much electrical force is req across a membrane to balance the tendency
of an ion to go down its electrical membrane
 Goldman-Hodgkin-Katz (GHK) equation - calculates Vm, if conditions are known
 an expanded version of Nernst eqn that takes into account individual ion
permeabilities that generate the Vm
 Forces acting on K+ when membrane is at (a) Resting Potential and (b) the K+ equilibrium
potential
 @Vm = -70 mV, both conc and electrical gradients favor inward movement of Na+
into nerve cell
 Graded Potentials and Action Potentials:
o Excitability: (excitable membranes) channels give a cell the ability to produce electrical signals that can
transmit info between different regions of a membrane
o Electrical signals can be graded or action
o Graded potentials:
 Important for signaling over short distances
 Changes in membrane potential that are confined to a small region of the plasma membrane
 Magnitude of graded potentials can vary and depend on magnitude of initiating events
 Charge flows between the place of origin and adjacent regions of the membrane still at resting
potential
 Can occur in depolarizing or hyper polarizing direction
 Decremental: flow of charge decreases a the distance from the origin increases due to open
leak channels (allow ions to leak through causing decrease in current)
 Summation: stimuli can add up and can add to the potential before it has died away due to
decrementation (which will allow it to travel farther)
 Polarization states:
 Polarized: outside and inside of the cell have different net charge
 Depolarize: potential becomes less negative than the resting level (closer to 0)
 Overshoot: reversal of the membrane potential polarity (inside of the cell becomes
polarized relative to the outside)
 Repolarize: depolarized membrane potential returns to its resting level
 Hyperpolarize: potential is more negative than resting level
o Action potentials:
 Long distance signals i.e. neuronal muscle cell communication
 Very rapid and large changes in voltage (1-4 milliseconds)
 Not proportional to the magnitude of the stimulus
 Magnitude depends on number of action potential cycles per unit time
 Action potentials are not decremental
 Voltage-gated ion channels: allow membrane to undergo action potentials
o i.e. Na / K channels
o Membrane depolarization tends to open the channels
o 1. Na channels respond faster to changes in voltage so they open before K channel (when depolarized)
o When depolarized, K channels close slower
o 2. Inactivation gate: limits the flux of Na by blocking the channel shortly after depolarization opens it
o When repolarized, channel closes, which forces the inactivation gate back out, allowing channel to
return to closed state


o 1. Begins with depolarizing stimulus which opens voltage-gated ion channels

o 2. Membrane reaches a critical threshold potential and creates a positive feedback loop
o 3. causes overshoot and membrane becomes + on the inside and - on the outside
o 4. Membrane potential reaches peak value
o 5. Cell rapidly repolarizes towards its resting value
o 6. Hyper polarization occurs because K channels close slowly (afterpolarization)
o 7. Resting membrane potential is restored after K channels close (negative feedback

o Threshold stimuli: stimuli that are just strong enough to depolarize the membrane
o Subthreshold potentials: (caused by sub threshold stimuli) weak depolarizations not strong
o enough to generate an action potential
o All-or-none: action potentials either occur maximally or they don’t occur at all
o Absolute Refractory period: during an action potential, a second stimulus will not produce a second
action potential no matter how strong the stimulus
 A whole cycle must finish before a second can begin
o Relative refractory period: following the absolute refractory period, there is a interval during which a
second action potential can be produced (only if the stimulus is high)
 refractory periods are a way of regulating the number of action potentials that can occur at a
given time
o Action potential propagation: a new action potential produces local currents that depolarize the region
adjacent to it to produce another action potential at the next site
 i.e. like setting of a trail of gunpowder
 Also means that action potential trail can only go forward and not back (gun powder
cannot be re- lit)
 Propagation of the “message” stops when the end of the axon is reached
 Faster propagation occurs with a larger diameter of the axon and if it is myelinated
(due to more ions flowing through and less leakage)
o Receptor potential: in affarent neurons, initial depolarization to threshold is achieved by a graded
potential
o Synaptic potential: depolarization to threshold is due either to graded potential generated by synaptic
input to a neuron
o Pacemaker potential: spontaneous change in neurons membrane potential
 Synapse: specialized junction between two neurons
o Electrical activity in a presynaptic neuron influences activity of a post synaptic neuron
 Consist of connections to presynaptic and postsynaptic neurons along with extracellular space
between cells
o About 100 trillion synapses in the CNS
o Synapse activity can effect the chance that a postsynaptic neuron with fire action potentials by inducing
a brief graded potential in the postsynaptic membrane
 This leads the membrane to either become depolarized and then hyperpolarized (excitatory
synapse) or stabilized at its resting potential (inhibitory synapse)
 Convergence: many synapses from different presynaptic cells can affect a single postsynaptic cell
 Divergence: single presynaptic cell can send branches to many postsynaptic cells
 Electrical Synapses:
o Plasma membranes of the presynaptic and postsynaptic cells are joined by a gap junction allowing local
currents from action potentials to flow across the junction through connecting channels from one neuron
to another (depolarizes the membrane of a second neuron to threshold to continue propagation of AP)
o Very rapid communication
 Chemical Synapses:
o Axons of presynaptic neurons end in slight swellings to hold synaptic vesicles which contain
neurotransmitters
 Postsynaptic density: high density postsynaptic membrane adjacent to axon terminal containing membrane
proteins
 Synaptic cleft: extracellular space that separates presynaptic and postsynaptic neurons and prevents direct
propagation of the current from pre to post’
o Signals are transmitted by neurotransmitters released from presynaptic axon terminal
o Permit integration of multiple signals at a given cell
 Neurotransmitter Release:
o Active zones: release regions to which vesicles are docked on the presynaptic membrane
 Neurotransmitter is released when action potential reaches the presynaptic terminal
membrane
o SNARE proteins: loosely docked vesicles in the active zones by interaction of a group of proteins which
are anchored in the vesicle membrane
 Ions entertain during depolarization bind in the vesicles which trigger a conformational change
in the SNARE complex leading to membrane fusion and neurotransmitter release
o Vesicles can either:
 1. Fuse with membrane (contents enter cell)
 2. “Drop off” contents and return back to axon terminal
 Structure of the Nervous System:
o Nerve: group of many axons traveling together to/from same place in the PNS
o Pathway (tract): group of axons travelling together in the CNS
 o CNS pathways:
 1. Long neural pathways: neurons w long axons that carry info between brain and spinal cord
 2. Multi-synaptic pathways: neurons with branching axons and lots of synaptic connections
o Ganglia: neuron cell bodies in PNS
o Nucleus: neuron cell body in CNS
 Brain:
o Cerebrum:
 Majority of the forebrain
 Consists of 2 hemispheres
 Functions:
 perception
 Skilled movements
 reasoning
 Learning
 memory
 Cerebral Cortex consists of 4 lobes:
 1. frontal
 2. parietal
 3. Temporal
 4. Occipital
 Gray matter: primarily cell bodies and dendrites
 White matter: primarily axons
 Cerebral structures:
 1. Cerebral Cortex:
o Highly folded gray matter
o Responsible for consciousness
 2. White matter tracts: consists of axons and corpus callosum (massive bundle of
axons connecting hemispheres of the brain)
 3. Subcortical nuclei:
o Basal nuclei: deep collections of gray matter (cell bodies) that play a large
roll in movement and posture
o Movement control
o Posture
o Diencephalon:
 1. Thalimus:
 Synaptic relay center
 Receives afferent inputs to cerebral cortex
 Controls arousal and attention
 2. Hypothalamus:
 Homeostatic control center
 Autonomic and endocrine control
 3. Epithalimus:
 Contains pineal gland: plays role in biological rhythms
o Limbic system: learning, emotions, and behavior
 Consists of:
 Frontal lobe
 Temporal lobe
 Thalamus
 Hypothalamus
o Cerebellum:
 Fine tuning
 Coordination of movements
 Balance
o Brainstem:
 Functions:
 Eye movement
 Cardiovascular and respiratory control
 Swallowing and vomiting control
 Regulation of sleep and arousal
 Contains reticular formation
 The Spinal Cord
o Structure: central core contains gray matter (cell bodies and dendrites)
o Gray Matter:
o Ventral horn (front): contains cell bodies for exiting EFFERENT neurons
o Dorsal horn (back): where afferent neurons enter the CNS from the PNS (using synapses)
o White Matter: (axons)
 Afferent: ascending tracts
  Efferent: descending tracts
o Dorsal roots: entrance for afferent axons from the dorsal side of the cord
o Dorsal root ganglia: contain cell bodies of afferent neurons that enter through the roots
o Ventral roots: exit for axons of efferent neurons
o Spinal nerve: where dorsal and ventral roots meet carrying information two ways (afferent and
o efferent)

 Peripheral Nervous System:

o Afferent division:
 Relays sensory information from PNS to CNS
o Efferent division:
 commands from CNS to PNS effectors
 1. Somatic motor
 Innervate skeletal muscle
 Single neuron linking CNS and effector (muscle)
 Neurotransmitter: acetylcholine ; which binds to cholinergic receptors and excites
skeletal muscles
 2. Autonomic branch
 Two-neuron chain connected by a synapse between CNS and effector organ
 Innervates smooth and cardiac muscle, glands, GI neurons
 Can be excitatory or inhibitory
 Sympathetic NS
 Parasympathetic NS
 Enteric NS
 Autonomic NS:
o Efferent innervation of tissues other than skeletal muscles
o Enteric nervous system: neuronal network in the wall of the GI tract
o Made up of two neurons in series that connect CNS and effectors
o Autonomic ganglion: cell cluster outside the CNS to where the synapse
connects
 Autonomic NS is divided into sympathetic/ parasympathetic NS:
o both sympathetic and parasympathetic divisions use acetylcholine as the neurotransmitter between pre
and postganglionic neurons in autonomic ganglia
 Postganglionic cells have mostly nicotinic acetylcholine receptors
 Parasympathetic division uses acetylcholine as neurotransmitter between postganlionic neuron
and effector
 Sympathetic division uses norepinephrine is transmitter between postganglionic neuron and
effector
o Sympathetic:
 Neurons leave the CNS from the thoracic and lumbar regions of the spine
 Sympathetic trunks: two ganglia chains on each side of the cord
 Preganglionic sympathetic neurons leave spine first thoracic and second lumbar segment
 Sympathetic trunks span entire length of cord
 Typical for sympathetic activity to occur body-wide
 Fight-or-flight (physical or psychological stress)
 o Parasympathetic:
 Neurons leave the CNS from brainstem and sacral portion of spine
 Parasympathetic ganglia lie in close proximity to organs and post- ganglionic neurons
innervate
 Tends to activate specific organs
 Rest-or-digest state
o Adrenal medulla: postganglionic neurons in the sympathetic division don’t develop axons but instead
form part of an endocrine gland
o Dual innervation: innervated by both sympathetic and parasympathetic fibers
 Protective Elements associated with the brain:
o Meninges: membranous coverings between soft neural tissues and bones that house them
 1. Dura mater: next to the bone (thick)
 2. Arachnoid mater: in the middle
 3. Pia mater: next to the nervous tissue
o Subarachnoid space between arachnoid mater and Pia mater is filled with cerebrospinal fluid (CSF)
o Choroid plexus: ependymal cells that make up specialized epithelial structure which produces CSF and
completely replenishes it 3 times a day
 CSF flows to the top of the outer surface of the brain where it enters the bloodstream through
one-way valves
 CNS floats on a cushion of CSF
 Hydrocephalus: “water on the brain” protects brain and fluid can absorb shock
 Glucose is the main ATP supplier in the brain
 Brain receives up to 12-15% of total blood supply
 The Blood Brain Barrier: regulation of substances that reach neurons
 Formed by cells that line smallest blood vessels in the brain
 Contains tight junctions (no movement)
 Substances that dissolve readily in the lipid components of the plasma membranes enter the
brain quickly
 Extracellular fluid of the brain and spinal cord is a product of chemically different form of blood

Endocrine System

 Endocrine system function:

o communication across the body
o Regulates body processes
o Essentially an efferent pathway

o
 Consists of:
o 1. Endocrine glands/cells : produce hormones
o 2. Hormones: hormones enter the blood
o 3. Blood: blood delivers hormones to effectors
o 4. Target cells (effectors)
 Basic characteristics:
o Responses are slow but tend to last long
o Single gland can secrete more than one hormone
o A hormone can be secreted by multiple glands
o Many glands have primary endocrine function
o Organs with other primary functions also have an endocrine component
 Major structural classes of hormones:
o 1. amines
 i. Thyroid hormones (from thyroid gland)
 Derived from AA tyrosine (depend on how many iodines are bound (T3/T4))
 ii. Catecholamines (from the adrenal medulla)
 Epinephrine (Epi) and norepinephrine (NE)
 iii. Dopamine (from hypothalamus)
o 2. Peptides and proteins: most numerous and mostly polar
  Synthesized polypeptides in cytosol
 Preprohormones (rough endoplasmic reticulum)
 Pro hormones (Golgi apparatus)
 Secreted via exocytosis
 Water soluble (hydrophilic): transported and dissolved in plasma volume
o 3. Steroids: synthesized from cholesterol by gonads, adrenal cortex, and placenta (pregnancy)
 Non-polar molecules (easily diffusible)
 Hydrophobic so they need to be bound to a transport protein (plasma proteins)
 Adrenal Glands
o 1. Adrenal medulla
 Modified sympathetic ganglion
 Releases catecholamines (Epi and NE) in response to sympathetic activation
o 2. Adrenal cortex
 Outer region of adrenal glands
 Produces steroids
o i. Aldosterone: regulates ion (Na, K, H) balance and water balance
o ii. Cortisol: regulates metabolism of glucose and nutrients
 Stress response
o iii. DHEA androstenedione: important in sexual development
 The Gonads:
o Produce steroids that are important for sexual development and reproduction
o Cholesterol based
o 1. Testes:
 Mainly testosterone (often converted into estradiol (aromatase)
 Small amounts of estrogen
o 2. Ovaries:
 estrogen
 Small amount of testosterone
 Progesterone can be secreted by corpus luteum: ovulation
 placenta
 Adrenal cortex
 Hormone transport and metabolism:
o Catecholamines: hydrophilic: dissolved and transported in plasma volume
o Steroid/ Thyroid hormones:
 Poor solubility in water (hydrophobic) : attach to plasma protein (as transport)
 Free hormone + binding protein = hormone protein complex
o Plasma hormone concentration is affected by:
 1. Rate of secretion into blood
 2. Rate of removal from blood
o i. Cellular uptake
o ii. Hormone clearance: degradation, excretion in liver and kidneys
o iii. enzymatic breakdown:
 catecholamines (peptide hormones) breakdown in hours
 Steroid/ thyroid hormones are available for hours and break down in days
o iv. Metabolism also activates hormones
 Factors affecting how well cells respond to hormones:
o 1. Hormone receptor concentration
o 2. Permissiveness : must chemically fit into the cell
 Cellular Effects of Polar Hormones: (peptides/ proteins)
o Activation of a second messenger system
o Rapid non-genomic effects (like changing enzyme activity)
o Longer lasting genomic effects (like transcription and translation)
 effects of polar hormones are short (minutes to an hour) due to rapid metabolism of hormone
 Cellular Effects of Non-Polar hormones:
o Steroid, thyroid hormones bind to intracellular receptors
o Forms hormone receptor complex
o Change in transcription and translation rates
o Long lived (hours to a day)
o Can also exert non-genomic effects by binding to plasma membrane receptors
 Regulation/Control of Hormone Secretion:
o 1. Humoral Control: Ion/ nutrient concentrations are the stimulus for hormone release
o 2. Neural Control: neurotransmitter release from autonomic neurons influence the release of of many
endocrine glands i.e. catecholamine from adrenal medulla
o 3. Hormonal control: one hormone can signal the release of a second hormone from a different
endocrine gland
 tropic hormone: causes release of a different hormone
 Hypothalamus (homeostasis center) is the master control center for many of the hormonal systems in the body
and works closely with the pituitary gland (hypophysis)
o 1. Posterior Pituitary Gland (PPG)
 Outgrowth of the hypothalamus (neurohypophysis)
 Neural control of hormone release
 Released into the blood
 Hormone receptors on the cell membrane
 Cellular effects: activating enzymes and opening ion channels
 PPG hormones: peptides
 1. Oxytocin: maternal behavior, emotional connections (“cuddle hormone”)
o a. Breasts - results in milk ejection during lactation
 in response to stimulation of nipples during nursing of infant
 sensory cells in nipples send neural signals = oxytocin
o b. Uterus - during labor in a pregnant woman
 stretch receptors in cervix send signals to hypothalamus = oxytocin
 present in males, but function uncertain
 recent research suggests that oxytocin may be involved in various
aspects of memory and behavior in male and female mammals,
possibly inc humans (pair bonding, maternal behavior, love)
 2. Vasopressin: raises blood pressure and increases water reabsorption into the
blood in the kidney
o stimulates contraction of smooth muscle cells around blood vessels
o constriction of blood vessels, increase blood pressure
o also acts within kidneys to decrease water excretion in urine (retain fluid)
o helps during dehydration
o also known as antidiuretic hormone (ADH)
o Diuresis - loss if excess water in urine
 How PPG hormones get excreted
 i. Hormones synthesized in hypothalamic nuclei
 ii. They travel in vesicles through axons in infundibulum
 iii. Then they get stored in the PPG until neural depolarization
 iv. Hormones released into blood
o 2. Anterior Pituitary Gland (APG)
 Hypothalamus controls the release of anterior pituitary hormones via releases of
hypophysiotropic hormones
 Hormones synthesized in hypothalamic nuclei
 Portal system (transport mechanism: capillary to vein back to capillary)
 Advantage is that it strictly keeps communication between APG and hypothalamus
 APG hormones:
 1. Follicle Stimulating Hormone (FSH)
 2. Luteinizing Hormone (LH)
o **1 and 2 collectively known as gonadotropins: germ cell development, sex
steroid hormonesecretion
 3. Growth Hormone (GH): somatotropin
o Protein synthesis/ metabolism
o Effectors are liver and other cell that secrete insulin growth factor 1 (IGF-1):
makes sure that our body has nutrients
 4. Thyroid Stimulating Hormone (TSH, thyrotropin)
o Releases T3 and T4 from thyroid gland
 5. Adrenocorticotropic Hormone (ACTH, corticotropin): signal for adrenal cortex to
secrete cortisol
  These hypophsiotropic hormones:
o Diffuse into capillaries of median eminence
o Act on endocrine cells in APG to cause
o secretion or inhibition of a second hormone
 How APG hormones get secreted:
o i. 1st hormone released from hypothalamus
o ii. 2nd hormone released from the APG
o iii. Third hormone release from a gland that sends message to effectors
 Control mechanisms for hormone secretion:
o Long loop negative feedback vs. short loop negative feedback
 Mechanisms of endocrine disorders:
o 1. Hyposecretion: reduction in plasma hormone concentrations to cause impaired effector response
 Primary hyposecretion: defect in hormone-producing gland (3rd hormone in sequence)
 Partial destruction of gland
 Enzyme deficiency causes decrease in hormone synthesis
 Dietary deficiency of precursors
 Secondary Hyposecretion: too little stimulation by tropic hormone
 Lack of cellular signal to produce/ release hormone
 difference between primary and secondary hypo secretion can be identified by measuring
tropic hormone in plasma concentration
 If primary: high plasma concentration of hormone 2
 If secondary: not enough signal for the third gland in sequence
o 2. Hypersecretion: increased circulating hormone concentrations
 Primary hypersecretion: gland producing too much hormone
 Secondary hypersecretion: excessive stimulation by tropic hormone
 Can also be due to presence of a
hormone-secreting tumor
 Hyporesponsiveness: diminished response to
hormonal inputs i.e. insulin resistance (type II
diabetes)
 Caused by:
o Hormone receptor deficiency
o Defect in hormone receptors
o Enzyme deficiency
 Hyperresponsiveness: increased
response to hormonal inputs
 Thyroid Hormones: odine containing hormones
o 1. Triiodothyronine (T3): biologically active form
o 2. Thyroxine (T4): secreted form
o can be metabolized to T3 in tissues for many processes
o What they do?
 Thyroid hormone increases metabolic rate
 Contain Na/K -ATPases
 Permissive with catecholamines (EP / NEP)
 Helps with growth and development
o Hypothyroidism is caused by insufficient T3 / T4
o Hyperthyroidism is caused by excessive levels of T3/T4
 Responses to Stress:
o 1. Cortisol: released from adrenal cortex
 Hypothalamus receives inputs from sensory regions of NS and circadian rhythms
 Cortisol exerts long-loop negative feedback
 Cortisol helps with:
 Adequate energy availability (protein catabolism, fatty acid and glucose released into
the blood)
 Blood pressure maintenance (permissiveness)
 Immune response isn’t excessive and damaging
 Inadequate cortisol levels: adrenal insufficiency
o 2. Chatecholamine: release from adrenal medulla

Muscle Physiology

 Tissues: cells with similar properties working to perform a specific function

o 1. Skeletal muscle:
 Striated
 Attached to skeletons
 Control posture and movement
 activated by the somatic motor nervous system (voluntary)
 Recruitment: process of increasing number of motor units that are active in a muscle at a given
time
o 2. Smooth muscle:
 Surround hollow organs and body “tubes"
 activated by the autonomic NS (involuntary), hormones, autocrine agents, and paracrine
agents
o 3. Cardiac muscle:
 Striated with branched muscle fibers
 Coordinates heart beats
 activated by autonomic NS (involuntary), hormones, intrinsic pathways
 Muscle Contraction and Excitation:
o Muscle fibers generate tension when cross-bridges are formed between thick/thin filaments
(proportional)
o Excitation: activation from somatic motor neurons: straightening of the limb
o Contraction: leads to cross-bridge formation (tension)
 Thick Filaments:
o Composed of myosin
o 2 intertwined heavy chains (consisting of a head, tail, and hinge regions)
o Mysoin:
 Actin binding sites at cross- bridge formation between thick and thin filaments
 ATP binding sites act as an ATPase (myosin ATPase)
 4 small myosin light chains play regulatory roles
 Thin Filaments:
o Composed of actin with myosin binding sites
o Contains proteins tropomyosin and troponin (which regulate myofilament interactions and cross-
bridging)
 Skeletal muscle fibers (cells) characteristics:
o Membrane: sarcolemma
 Excitable (capable of depolarization) : straightening of the limb
 Continuous with transverse tubules (T-tubules)
 Contains nicotinic cholinergic receptors
 Flux is controlled by ions, glucose, lipids, AA’s
 Important function is compartmentalization
o Sarcolemma (Muscle cell):
 Multi nucleated (due to myoblast fusion during development)
 Myoblast: undifferentiated mono nucleated cells that fuse during development to form muscle
fibers
 Many mitochondria (high metabolic rate : lots of energy in skeletal muscle)
o Sarcoplasmic reticulum: surrounds each myofibril (thick and thin filaments arranged into myofibrils)
 Terminal cisternae (lateral sacs): Large Ca storage
 Large cells can span up to 20 cm long
 Fixed number at birth but they can grow (hypertrophy)
 Generally don’t divide
o T- Tubules: tubular structure that lies between the terminal cistern of adjacent segments of the
sarcoplasmic reticulum.
 Sarcoplasm:
 Contains:
o Organelles
 o Glycogen (stored in the liver and skeletal muscle)
o Intramuscular triglycerides
o storage
o ICF composed of 75% water
 Functional proteins:
 Thick and thin myofilaments
 Troponin
 Tropomyosin
 Satellite Cells:
 Differentiate into myoblasts
 Fuse with existing muscle fibers for muscle repair
 Role of motor Neurons
o skeletal muscle fibers are excited by somatic motor neurons
o 1 motor neuron diverges and innervates (supply with nerves) many muscle fibers
o Motor unit: motor neuron and all of its fibers
o Smallest functional unit of muscle contraction
o Alpha MN can innervate many muscle fibers
o Each fiber only innervated by 1 axon terminal of 1 alpha motor neuron
o Motor unit connected to muscle fibers via neuromuscular junctions
o NMJ- Synapse between a somatic motor neuron axon terminal and the motor end plate region on the
sarcolemma of the muscle fiber
 NMJ excitation:
 1. AP along alpha- MN leads to neurotransmitter (acetylcholine) release at NMJ
 2. Neurotransmitter binds to receptors (nicotinic receptors) on motor end plate
o Causes ion channels to open to allow for depolarization
 3. Depolarizing motor end plate potential which triggers AP
 4. AP propagates along sarcolemma and down T-Tubules
o Spreads excitation into the muscle fiber
 5. ACh is broken down by acetylcholinesterase
o End to excitation
o Choline gets recycled within axon terminals
o Sarcolemma depolarizes to prepare for the next motor end plate potential
(recharge)
 How is Calcium Released (to cause muscle contraction)?
o T-Tubules contain voltage-gated channels (dihydropyridine receptors (DHPR)) which open when AP
reaches them
o DHP channels mechanically linked to Ca channels on sarcoplasmic reticulum (Ryanodine receptors
(RyR)
o Opening of DHPR leads to opening or RyR, increases cytosolic Ca, which generates tension
 Ca Triggers Actin-Myosin Interactions:
o At rest, tropomyosin blocks actin-myosin interactions
o Held in blocking position by troponin
o Ca binding to troponin allosterically changes its shape which moves tropomyosin out of the way
o Now myosin can form cross-bridge with actin which generates tension
o Ca is released to saturate all binding sites on troponin, but is removed before all crossbridges are
formed
o Fibers generate tension due to interaction between thick and thin filaments
o Myosin heads pull thin filaments toward center of sarcomere which leads to sarcomere (fiber)
shortening
 The Cross-Bridge Cycle:
o In resting state, myosin head is considered “energized” and has ADP + P
o Cycle continues as long as Ca concentration is high
o Each myosin head undergoes cycle independently of others
o Total tension related to Toal # of myosin heads attached at once
 1. Myosin binding to Actin: If Ca increases, myosin head binds to thin filament
 In low Ca, nothing happens
 2. PowerStroke: Myosin- actin binding triggers release of ADP + P
 This triggers the conformational change of the myosin head that pulls the thin filament
towards the center of the sarcomere
 Causes “power stroke” (about 10 nm)
 3. Release: Cross-bridge is broken when ATP binds to myosin head
 4. Re-Cocking: enzyme myosin ATPase splits ATP into ADP + P
 Myosin head returns to energized conformation, ready to bind actin again and
continue cycle
 Types of Single-Fiber Contractions:
o Tension: force generated with a contracting muscle
o Load: external force that a muscle works against (resistance)
 Isometric Contraction: muscle develops tension but overall length doesn’t change
 Isotonic Contraction: load on the muscle remains constant
o Muscle length changes
o Concentric contractions (shortening) : if tension is greater than the load, muscle length shortens
o Concentric: powerstroke pulls thin filament toward center of sarcomere
o Eccentric contraction (lengthening): if load is greater than tension, muscle lengthens
o Powerstroke cannot finish due to resistance from external load
o Myosinhead stretches until it is ripped from thin filament
o Myosin head can bind again immediately because it was never detached by ATP- binding
 Muscle Twitch: mechanical response to a single AP
o Twitch phases:
 Latent phase
 Contraction phase
 Relaxation phase
 load - velocity - tension relationship
o Max. Shortening velocity occurs at 0 load
o Max vel. Is independent of # of cross-bridges
o As load increases, shortening velocity decreases
o Velocity vs load: load = max, isometric tension
o At max load, isometric tension shortening velocity = 0
o If load exceeds max, isometric tension, muscle is lengthened
o Isometric tension > concentric tension
 frequency - tension relationships
o When 2 AP arrive closely in time, it can create a temporal summation
o Unfused tetanus results when APs arrive prior to complete relaxation
o Fused tetanus when APs arrive prior to any relaxation
o Larger excitatory command to the motor neuron pool results in a higher firing frequency for the active
motor neurons/ motor units
o Recruits more motor units
 length - tension relationship
o Passive tension: force of muscle fiber recoil due to tint as muscle fiber lengthens
o Optimal length: maximal, isometric, active tension
o If length is greater than optimal length, tension decreases
 Metabolic Factors Affecting Tension
o 1. Phosphagen System: stored ATP and creatine phosphate
 Immediate use, highest power, low capacity
o 2. Oxidative phosphorylation: complete breakdown of CHO, fats into CO2 and water
 Most ATP produced within ETC
 Lowest power (12-25% of phosphate system), enormous capacity
o 3. Anaerobic glycolysis: sublate-level phosphorylation of ATP within glycolysis, pyruvate converted to
lactate
 Intermediate power (50% phosphate), intermediate capacity
 Fatigue: decline in muscle tension as a result of previous muscle activity
o Mechanisms of Fatigue:
 1. Ca2+ Handling→↓ rate of release, reuptake, and storage of Ca2+ by the SR
  2. Thin filament Ca2+ sensitivity→for a given amount of Ca2+ release, the thin filament
becomes less activated
 3. Inhibition of cross-bridge formation and power stroke → steps associated with cross-bridge
cycle inhibited by mass-action and metabolite-driven modulation (H+)
 4. Muscle damage→high tension and leaky SR cause damage/degradation of contractile
proteins
 5. Substrate depletion → CrP depletion for high-intensity exercise, glycogen depletion for long-
duration exercise
 6. Central command failure → afferent feedback causes CNS to limit excitation of motor
neurons
 Fast vs. Slow twitch fibers
o Influenced by type of myosin / myosin ATPase
o Fast myosin completes phases 1 and 4 (splitting ATP and rebinding to actin) of the crossbridge cycle 4x
faster than slow myosin
o Results in faster rise in tension (greater shortening velocity
 Dominant Metabolic Pathways:
o Oxidative vs. Glycolytic Fibers
o Oxidative: many mitochondria, myoglobin, capillaries
 Fatigue resistant
o Glycolytic: stored glycogen, high concentrations of glycolytic enzymes
 Rely on glycolysis for ATP production (not much)
 Fast fatiguability
 Factors determining WHOLE muscle tension:
o I. Tension developed by each fiber
 Action potential frequency
 Fiber length (length-tension relationship)
 Fiber diameter
 Fatigue
o II. Number of active fibers
 Number of fibers per motor unit
 Number of active motor units
 Motor neuron cell bodies are in the CNS
 Frequency modulation:
o A larger excitatory command to the motor neuron pool results in higher firing frequency for active motor
neurons
o A larger excitatory input will recruit more motor units
 Motor neurons are recruited in this order: (if not enough tension is generated, the next order of motor units will be
recruited)
o Slow oxidative
o Fast oxidative glycolytic
o Fast glycolytic

Respiratory System

 Functions:
o Primary:
 Regulate arterial carbon dioxide by:
 Providing gas exchange with the environment
 Consequential supply of oxygen
 Short-term regulation of blood pH (acidity)
o Secondary
 Speech
 Smell
 Eliminates heat and water (thermoregulation)
 Modifies some hormone systems eg. Renin-angiotensin-aldosterone
 Modifies thoracic vascular flow eg. Assists venous return on inspiration
 Processes:
o 1. Ventilation: exchange of air between atmosphere and alveoli by bulk flow (pressure gradient)
o 2. Exchange of O2 and CO2 between alveola air and blood in lung capillaries by diffusion
(concentration gradient)
o 3. Transport of O2 and CO2 through pulmonary and systemic circulation by bulk flow
o 4. Exchange of O2 CO2 between blood in tissue capillaries and cells in tissues by diffusion (delivering
oxygen to cells in tissues)
o 5. Cellular utilization of O2 and production of CO2 (cellular respiration, deliver oxygen to tissues)
 Ventilation:
o Ventilation is defined as the exchange of air between the atmosphere and alveoli. Air moves by bulk
flow from a region of high pressure to one of low pressure. Obeys Poiseuille’s Law
 n = viscosity (of air)– constant
  L = vessel length (i.e. airway length) – constant
 DP = air pressure gradient – dependent on:
 Rate of change of lung volume (according to Boyles Law) (e.g. effort on inspiration)
 r4 = 4th power of the vessel radius (i.e. Resistance (R) = 1/r4) – dependent on:
 Airway (bronchiole) smooth muscle tone (provides increased resistance in disease,
e.g. asthma)
 Muscles responsible for ventilation
o Inspiration:
 Driving air in, large change in thoracic volume, drop in pressure in the chest cavity therefore air
comes in
 At rest: External intercostal muscles pull ribs up and out
 Diaphragm contracts (prime muscle, flattens, increasing volume=drop in pressure)
 High ventilation: Sternum moves up and out
 Sternocleidomastoid and scalenes elevate sternum (connected to clavicle and lift rib
cage slightly more)
 Pectoralis minor elevates ribs
 diaphragm contracts more
o Expiration:
 Passive process, forces air out of the mouth
 Rest: elasticity of lungs recoils inward
 Diaphragm (cut) relaxed
 Lung (cut)
 Abdominal organs recoil and press diaphragm upward
 High ventilation: diaphragm relaxed
 Internal intercostal muscles pull ribs down and inward
 Abdominal wall muscles contract and compress abdominal organs forcing the
diaphragm higher
 Lung Design & Transmural pressures
o Thoracic cavity divided by mediastinum (contains major vessels, airways and heart)
o Pleural fluid lubricates the divide between parietal pleura (outer) and visceral pleura (inner)
o Whatever we do to the chest wall will affect the space between the space between the lung and chest.
o Transmural pressure=
 Alveolar pressure – intrapleural pressure
 Atmospheric pressure – intrapleural pressure
 Thoracic pressures during ventilation:
o Beginning of inspiration: the pressure in the alveoli is 0 which means there is no breathing. The
pressure within the interpleural space is -4, our chest is stable.
o Mid-inspiration: When we start breathing, we activate the respiratory muscles, act on the chest cavity,
adding force to make it larger. Chest cavity is expanding, pleural space increases and pressure drops
because there is a greater force pulling in one direction. Air flow goes in.
o End of inspiration: the chest is equal to pulmonary atmospheric pressure and there is no airflow. At the
expanded position, we have to relax and breathe out as the lungs and chest wall start to passively
collapse due to elastic recoil
o Mid-expiration: the lung is collapsing, this compressing alveolar gas. When we recoil, we reduce its
volume and greater volume pressure for air to flow outward.
 Inspiration:
o Diaphragm and external intercostals contract
o Thorax expands
o Interpleural pressure becomes sub atmospheric, pressure in
o lungs is reducing
o Increase in transpulmonary pressure
o Lungs expand
o Alveolar pressure becomes sub atmospheric
o Air flows into alveoli
 Expiration:
o Diaphragm and external intercostals stop contracting
o Chest wall recoils inward
o Interpleural pressure moves back toward pre inspiration value
o Transpulmonary pressure moves back toward pre inspiration value
o Lungs recoil toward pre inspiration size
o Air in alveoli becomes compressed
o Palv becomes greater than Patm
o Air flows out of lungs
 Factors that contribute to the ‘work’ of breathing
o Compliance (work of breathing) = The magnitude of the change in lung volume produced by a given
change in transpulmonary pressure
 Inverse of lung stiffness: a compliant lung is more easily inflated, increased compliance =
decreased stiffness
 o Primary determinants are:
 Elasticity: stretchability of lung and chest wall connective tissue components includes elastin
and collagen
 Surface tension: tendency for alveoli to collapse due to air-water interface. Air is coming into
contact with tissues that is a fluid interface. Surfactants lower the surface tension, which
increases lung compliance and makes it easier to expand the lungs.
o Surface tension work:
 Reduced by surfactant (lubrication)
 Disrupts fluid attractive forces within alveoli
 Inflating the lung with air requires more pressure generated, larger work
 Inflating the lung with a liquid, no surface tension, don’t have an air-fluid interface.
 Most of the breathing we do is to overcome surface tension.
o Elastic work:
 Altered with restrictive diseases
 Characterised by formation of non-elastic scar tissue, pulmonary fibrosis,
 cardiothoracic surgery (increasing stiff tissue)
 Symptoms are shallow breathing and elevated FEV1/FVC ratio
 How tidal volume and respiratory frequency may vary to alter minute ventilation (VE)
o The total ventilation per minute is equal to the tidal volume multiplied by the respiratory rate as shown in
equation:
o Minute ventilation = tidal volume X respiratory rate
 Gaseous Exchange and Transport
o Partial Pressure: The total pressure of a mixed gas is therefore the sum of each single gas pressure
o Gases diffuse down a pressure gradient to produce gas exchange
o In a mixed gas (air) each single gas (O2) behaves individually
o Atmospheric air consists of approximately 79% nitrogen and 21% oxygen, with very small quantities of
water vapour, carbon dioxide and inert gases.
o A gas concentration is proportional to its partial pressure
o The alveolar PO2 is lower than atmospheric PO2 because some of the oxygen in the air entering the
alveoli leaves them to enter the pulmonary capillaries.
o Alveolar PCO2 is higher than atmospheric PCO2 because carbon dioxide enters the alveoli from the
pulmonary capillaries.
 Diffusion and Gas Transport:
o O2 and CO2 equilibrate at similar rates
 CO2 rate limited by rate release from the blood
 Normal equilibrium within 1/3 of capillary transit
o Slower or nor equilibration suggests a limitation of diffusion/gas exchange
 Eg. Decreased blood transit time during exercise
 Eg. Decreased alveolar wall surface area available for diffusion
 Oxygen transport:
o Lungs to pulmonary capillary: Inspire oxygen which diffuses across the surface of the capillary wall, less
than 2% is dissolved in the plasma, 98% diffuses into red blood cells  combines with haemoglobin
o Tissue capillary to tissue: oxygen dissociates from haemoglobin  dissolve in a red blood cell  cross
into the plasma  then into the tissue  cell  mitochondria
 Carbon dioxide transport: more complex and greater than O2
o Tissue to tissue capillary: CO2 produced by the cell  passes across the cell membrane by diffusion 
passes into the capillary by diffusion  10% dissolved in plasma, 90% diffuses into red blood cells 
some remains dissolved in red blood cells, some binds to haemoglobin for transport back to the lung.
o 30% of the blood that moves to the lung is bound to haemoglobin, 60% binds with water turns to
carbonic anhydrase  dissociates to bicarbonate and a hydrogen ion  goes out into the plasma in
exchange for a chloride ion
 Determinants of Total Gas Exchange:
o Diffusion capability- according to Fick’s Law
 Particularly factors that affect the:
 Respiratory surface area
 Respiratory surface thickness
 Ventilation-Perfusion ratio
 Perfusion= cardiac output
 Haemoglobin:
o 1.5% of oxygen breathed dissolves in plasma
o Found only in red blood cells
o Contains 4 haem groups each containing an ion atom
o Tetrameric globular protein
o Accounts for and transports 98.5% of O2 in whole blood
o Provides increased blood O2 carrying capacity and increased efficiency by decreasing energy
expenditure of ventilation
 Oxygen-haemoglobin dissociation curve is sigmoid because each haemoglobin molecule contains four subunits.
Each sub unit can combine with one molecule of oxygen, and the reactions of the four sub units occur
sequentially with each other combination facilitating the next one.
 Cooperative binding gets towards the limit and then its harder for oxygen to find a molecule of haemoglobin that
isn’t full. It plateaus because its harder it slows down and most molecules are saturated.
 Bohr Effect
o Right shifted: tissue level is unloading more oxygen
 Increased PCO2
 Increased acidity
 Decreased pH
o Left shifted: lung level is less and is loading
 Decreased PCO2
 Increased pH
 Decreased temperature
 Regulation of Respiration
o Breathing depends entirely upon cyclical respiratory muscles excitation of the diaphragm and the
intercostal muscles by their motor neurons. Inspiration is initiated by a burst of action potentials in the
spinal motor neurons to inspiratory muscles like the diaphragm. Then the action potentials cease,
inspiratory muscles relax, expiration occurs as the elastic lungs recoil.
 Parts of the central nervous system involved in control of respiration
o Control of this neural activity resides primarily in neurons in the medulla oblongata, the same area of the
brain that contains the major cardiovascular control centres. There are two main anatomical
components of the medullary respiratory centre:
o The dorsal respiratory group (DRG) primarily fire during inspiration and have input to the spinal motor
neurons that activate respiratory muscles involved in inspiration.
o The ventral respiratory group (VRG) contains expiratory neurons that appear to be the most important
when large increases in ventilation are required such as during strenuous exercise. During active
expiration, motor neurons activated by the expiratory output from the VRG cause the expiratory muscles
to contract. Therefore, air rapidly moves out of the lungs rather than passive expiration.
o The medullary inspiratory neurons receive a rich synaptic input from neurons in various areas of the
pons, the part of the brainstem above the medulla. This fine-tunes the output of the medullary
inspiratory neurons.
o The pontine respiratory group help to smooth the transition between inspiration and expiration.
o Pulmonary stretch receptors lie in the airway smooth muscle layer and are activated by a large lung
inflation. Action potentials in the afferent nerve fibres from the stretch receptors travel to the brain and
inhibit the activity of the medullary inspiratory neurons.
 Roles of central and peripheral chemoreceptors in control of respiration
o Peripheral Chemoreceptors: stimulated by
 Significantly decreased PO2
 Increased hydrogen ion concentration
 Increased PCO2
 Located in carotid bodies and aortic bodies (aortic arch)
 Respond to changes in the arterial blood
o Central chemoreceptors: stimulated by
 Increased PCO2 via associated changes in H+ concentration
 Located in medulla oblongata
 Derived from arterial CO2
o The low arterial PO2 increases the rate at which the receptors discharge, resulting in an increased
number of action potentials travelling up the afferent nerve fibres and stimulating the medullary
inspiratory neurons. Therefore, increase in ventilation provides more oxygen to the alveoli and
minimizes the decrease in alveolar and arterial PO2.
o The peripheral chemoreceptors response to decreases in arterial PO2 as occurs in lung disease or
exposure to high altitude. Peripheral chemoreceptors are NOT stimulated in situations in which modest
reductions take place in the oxygen content of the blood but no change occurs in arterial PO2. Mild to
moderate anaemia in which arterial PO2 is usually normal, does not activate peripheral chemoreceptors
and does not stimulate increased ventilation.
o Chemoreceptors respond to an increase in PCO2 and increases in brain extracellular fluid H+
concentration. Central chemoreceptors are the more important, accounting for 70% of the increased
ventilation.
 Hyperventilation and hypoventilation effect control of respiration
o Hyperventilation:
 Increased breathing greater than the metabolic demand
 Decreasing carbon dioxide inhibits ventilation
 Doesn’t do anything to oxygen, only CO2
o Hypoventilation:
 Breathing is less than metabolic demand
 Retain CO2 in the arterial circulation and increases PCO2
 Stimulates ventilation
 PO2 can fall if you hold your breath, but will have no effect on ventilation until 60mmHg, the
urge to breathe is due to a build-up of CO
 How exercise and altitude effect control of respiration and therefore how physiological adaptation occurs
following exposure
o During moderate exercise the alveolar ventilation increases in exact proportion to the increased carbon
dioxide production, so alveolar and therefore arterial PCO2 does not change. The alveolar ventilation
increases relatively more than carbon dioxide production. During strenuous exercise, a person may
hyperventilate thus, alveolar and systemic arterial PCO2 may actually decrease. Hydrogen ion
concentration increases during strenuous exercise. There is an abrupt increase within seconds in
ventilation at the onset of exercise and an equally abrupt decrease at the end. Exercise stimulates
skeletal muscle to do the exercise and respiratory muscle to increase ventilation.
o Hyperventilation at Altitude;
 Caused by decrease of partial pressure of arterial oxygen acting on carotid body peripheral
chemoreceptors
 Reduced PaCO2 and compensatory increase PaO2 (increases oxygen content)
 Stimulates ventilation
 Hyperventilation gets rid of CO2