Download here - TurkoTek

Part 2 Physiology 206 Notes
Muscle
- 3 Major categories: 1.) Skeletal- Voluntary- Striated Muscle
2.) Smooth- Involuntary- Visceral
3.) Cardiac- Heart Muscle
- All Muscles contact.
- Muscle is a mechanical device.
 Requires energy.
 Real device; efficiency is NOT perfect; doing work generates heat.
Examples: Shivering when cold. & Exercise rises body temperature.
Skeletal Muscle
- Known since mid-19th Century that it has striations.
- Striations are made from the arrangement of proteins.
Vocabulary
- Cell Membrane = Sarcolemma
- Endoplasmic Reticulum = Sacrcoplasmic Reticulum
- Muscle Cell = Muscle Fiber
 Within it are Myofibrils- Visible manisfestations of proteins.
Proteins
1.) Actin- Thinner- known as thin filaments
2.) Myosin- Thicker- known as thick filaments.
** In muscle of Bundles **
-- Overlap one another.
-- They are attached to one another.
** Gives rigidity- makes hard to pull apart.**
- When Muscle fiber contracts, the thick and thin filaments stay the same size, they just get closer to
one another.- Known as Sliding- Filament Mechanism.
 Energy source is ADP.
 Provides energy for contraction.
 Gets energy from mitochondria;* Muscle cells have lots of Mitochondria.*
Two things Muscle can do
1.) Isometric Contraction- Can generate force without shortening.
2.) Isotonic Contraction- Can shorten without generating force. (At same tension)
 Rarely do any happen in pure form. Mostly approximation.
 Example: Piano player starts with isometric, then turns to isotonic.
Isometric Contraction
-Force low, Velocity High.
-Force high, Velocity Low.
Physical Definition of Work- Move Force through a distance.
 By definition, Isometric does no work.
Power- Rate at which you do work.
 By definition, Isometric doesn’t generate power.
** Maximum Ability to do work at high rate- 1/3 of 0 velocity and max velocity. **
Muscle
--- If you stimulate again, before muscle is relaxed, it can stay contracted; this is called Tetany.
--- Sensation that leads to it is called Tetanic Stimulation
Average- 50-55 Stimulations per second
--- Electric current in US-60 stimuli per sec.(cycle current)
--- Most of the rest of the world-50 stimuli per sec.
 Reason US does this-Historical Meaning-it was believed that anything less than 60 cycles,
would flicker.
 Truth is that you can see no flickering with cycles all the way to around 40 cycles.
Twitch- either it contracts or it doesn’t- NO halfway!
Neural Control- Helps to make fine movements; Brain sends out instructions to how many Motor Units to
Send out.
Motor Unit = 1 Motor Neuron & all the muscle cells it stimulates
- 1 Motor Unit innervates more than one cell
- Motor Nerves that make fingers work have small motor units
- In thigh, the motor units include several hundred cells-generate great power.
** Reason we play piano with fingers, not heels! **
Smooth Muscle
--- Differences between striated:
1.) Doesn’t have striations
Actin & Myosin present, but elements are not lined up in registered order, so
do not see the visible manifestations of striations.
2.) Smooth Muscle cells are electrically connected to one another; transmit
Depolarizations to cells; immediately around it, which sends a wave propagated out.
3.) Transmit action potentials from one to the next.
4.) Strength are controlled by hormones and Neurotransmitters
5.) Does contract Spontaneously (Skeletal Muscle doesn’t)
 Smooth have membranes that are leaky,so when a smooth muscle cell
rests,it never has a stable action potential,so it drifts up until cell depolarizes.
* Reoccur at regular intervals *
 The rate of leakiness can be modified by neuron or hormone.
--- Muscle use energy to do work
- Uses ATP for energy
- Source for ATP come from Mitochondria
- During Aerobic (Continue to do for long time) Respiration- uses oxygen in Mitochondria to
produce ATP; can generate 2/3
- If goes over 2/3,use anaerobic pathway-give ATP that comes from glucoseby-product- Lactic Acid.
Lactic Acid- causes muscle fatigue; muscle refuses to contract anymore.
 Reduce level of activity; anaerobic comes in and replaces oxygen & gets rid of Lactic Acid.
Muscle Fiber Types
--- Red Muscle- Looks dark; Lots of Myoglobin- Red protein; carries oxygen down to it- creates reservoir
of
oxygen, so when you work to the point where you do too much, you can go a little longer
because of stored oxygen.
--- White Muscle- Not able to sustain aerobic as long; less Myoglobin; more Actin & Myosin; meaning
more power, but because no reservoir of oxygen; fatigues quickly.
Examples:
Bird flying; 3 or 4 power strokes and then soar- White Muscle
Red Muscle-Leg muscles; capable of sustained contractions.
--- In Humans, muscles are made of intertwined red and white muscles.
Ex.- Way Kitty Hunts, mostly white muscle, stationary til ready to pounce.
- Dog mostly red muscle animal-can run all the time;barks because he wants it to run.
--- With exercise, Hypertrophy of muscles used
 Increase in vasculatorblood vessels increase; more blood glow to exercised muscle.
--- When don’t use the muscle, Atrophy- Muscle gets smaller, and loses tone.
Cardiac muscle
- Heart has four chambers
- Heart is a pump, mechanical device
Three main types of muscle make up heart:
1.) Ventricular muscle- big and strong- pumping
2.) Atrial muscle- weaker
3.) Conducting muscle
--- Cardiac muscle has striations like skeletal muscle.
--- Unlike skeletal muscle, action potentials can pass through many cardiac cells like smooth muscle
--- Syncytion- cells communicate, so they will act as a unit
1.) Ventricular Syncytion
2.) Atrial Syncytion
** Action potentials of one syncytion don’t travel to other ones **
--- Cells not very leaky; -80mV
--- Cardiac muscle produce action potentials
- have long duration
- remains depolarized for some time
- refractory period roughly as long as Plateau
~ Atrial- 150 milliseconds- plateau duration, 7 per second/ Maximum rate-400/per minute
~ Ventricle- 300 milliseconds- plateau duration; 3 per second/ Maximum Rate- 180/per minute
--- Have Actin & Myosin act the same way skeletal actin and myosin work
--- When heart contracts, it will be propagated through the Syncytion that it started in.
--- Cardiac Cycle- Heart alternately contracts (Systole) and relaxes (Diastole)
- when heart contracts, blood leaves into arteries
- when relaxes; blood refills; heart is closed system
- fluid always moves downhill in concentration gradient
- each step, next one has to have less pressure than the one before it
- valves are one-way; if pressure exceeds on the one side, the valve will open
- valves are the reason the system flows Unidirectional
- when heart contracts, there can be periods when t just gains pressure, and valves remain
closed, constricting Isometrically
- Period of isometric contraction- the beginning of systole creates tension, without shortening.
- Period of ejection- when blood is actually pushed out of ventricle.
--- Left Ventricle- diastole- 0mm
- Maximally contracted; end of systole- 120mm Mercury
 Pressure in Aorta goes up to 120 mm mercury
 Aorta’s elasticity sends blood in systematic circulation
 Pressure in aorta then decreases
** Blood Pressure reads Systolic/Diastolic **
--- Atria- relatively thin walls; not able to generate great pressure; maximum pressure much smaller than
ventricles.
** Average- 50-60 bpm (beats per min) **
--- End-Diastolic Volume = 200 ml (not exact)
--- End Systolic Volume = -75 ml
 Stroke Volume- the difference is what the heart pumps out with each stroke
--- Stroke Volume x number of Strokes = total amount of blood pressure
- Average: 60 strokes/min.
- Average: 5 liters leave heart per stroke
--- Spread of Depolarization
~ Action potential in one part of one atria, and propagates through cell until it goes through the
atria in less time than the refractory period, so when it gets back to original, can’t be stimulated,
so entire atrium is contracted.
~ In ventricle conducting fiber to bring depolarization to ventricle from atrium, and then is
Propagated through cells and conducting fibers, which speeds it up.
** This is very important; allows entire heart to be contracted! **
- Normal Cardiac Output
= 5000 ml/min.
--- Starling’s Law of the Heart
- Amount of blood that heart will eject in the next stroke will be equal to the amount of blood that
entered on the last stroke.
- The pipes are elastic; can constrict or relax.
- If pipe gets bigger, more fluid will flow through it, even at same pressure.
- If heart pumps and certain vessels relax, more blood will flow to that tissue.
- Most circumstances, this is totally separate of pressure.
- If you vary the amount of blood you let flow through tissues, the heart will compensate.
--- Fluids & Pipes
- Flow = Pressure
Resistance
~ Discovered by Poiseville Civil Engineers Sewer System in Paris.
1.) Pressure
2.) Resistance- rules are:
- Longer Pipe- greater resistance (garden hose); directly proportional; double
hose; double the pressure.
- Bigger Diameter- less resistance- drops 1/16th if doubled
Resistance = ___1___
Diameter 4
- In our bodies,our pipes can change their diameters,meaning they can change their resistance,
meaning they can change flow.
- Autoregulation- keeps oxygen constant even when metabolic rate changes.
* Anytime, flow is from higher to lower pressure. *
--- Circulation’s function is to bring all tissue nutrients and oxygen, and to carry away waste products
produced.
** Capillaries are porous- can let some
leak out stuff, but not big enough
for cells or proteins. **
--- The leaked out stuff:
- Will lessen the volume is capillaries causing a reduction in pressure.
- Since allowed fluid, but not protein, the protein concentration goes up (20%).
- Consequence of that is that an osmotic pressure has been made, and is going
to pull fluid to venule.
- Metabolic waste product will go from cell to interspacial space, and nutrients
get into cells- this is how capillaries give cells nutrients, and transport the cell’s
wastes away from cell.
(When you hit your thumb with a hammer, you make holes in capillaries, causing the stop of osomotic
pressure, so it can’t get to venule, so it can’t get out, so all the stuff gets into the interspatial fluid, causing
thumb to get bigger.)
** Missed the first half of class, so missing something here. **
--- Reflex Method
- Carotid Artery-Pressure receptor, when changes, sends receptors to brain, which changes balance
between sympathetic & parasympathetic.
- Monitors changes in pressure.
- Receptors fatigue, which is not good for long term adjustments.
** On a day to day basis, maintain an average Blood Pressure, receptors can’t do this. **
Renal-Body Fluid System for Blood Pressure Control
Hypertension- Chronically Elevated pressure; set point gets shifted.
- 90% is called Essential Hypertension- No knowledge why it has happened.
- Much more prone to Stroke.
- More capillaries get damaged- lose kidney mass.
- Promote the deposition of plaque of the artierals.
Cardiovascular Information
- Artierals- where pressure drop is greatest & where you do most regulation.
- If constrict arterial, pressure toward heart will get higher, and pressure toward vein will go down.
- Constrict everywhere in tube, pressure becomes equal.
- One way to regulate artierals pressure is to have autonomic nervous system regulate constriction
and dilation.
Shock
- Blood flow has gotten low enough, so you are not adequately providing tissues with nutrients.
Causes:
1.) Hypovolemic-reduction in plasma vol., which reduces venus return, which reduces cardiac output.
a.) Hemorrhage- Hemmorrhagic Shock
b.) Dehydration
2.) Cardiogenic- Anything is because cardiac output goes down because of inadequate heart working.
3.) Neurogenic- if shock originates in nervous causing artierals dialate and pressure goes down, which
reduces cardiac output.
a.) Anethestisia can cause this.
b.) Pain can activate.
4.) Can be a combination of all of these.
Cardiac Failure- Cardiac output, in some people, falls below 5L per minute.
- Blood accumulates in tissues, causing swelling.
- Place it accumulates is in the lungs- Congestive Heart Failure
Heart Attack
- Damage done to heart muscle, due to loss of blood supply to some part, then it dies.
~ it can be up to 90% clogged, but if goes above that, heart muscle dies.
~ Either you die
~ Or you have scar tissue on the heart, which will eventually lead to Heart Failure.
Infarction- killing of muscle
Infarcted- dead muscle
Causes:
1.) Clot breaks loose, and eventually blocks vessel.
2.) Deposition of plaque on vessel walls.
Damage:
1.) Sometimes infarcted muscle becomes elastic, causing blood, that used to be pumped out, to go
Elastic, causing stroke change, causing change in cardiac output, called Systolic Stretch;
increases end systolic volume.
2.) Cardiac Tamponnade- infarcted part creates hole, causing blood to get into the pericardial sac,
Restricts the amount the heart can expand, reducing the diastolic volume, stroke volume
down, cardiac output down.
3.) Ventricular Fibrillation- damaged area can become hyperactive, causing an irregular rhythm,
So there is never a time when heart is completely relaxed or completely constricted, causing a
change in cardiac output.
 Defibrillator- simultaneously depolarizes entire heart, so entire heart is in refractory,
so hyperexciteable has calmed down.
Respiratory System
--- Main functions:
- Brings in Oxygen we need
- Gets rid of CO2 we don’t want
 automatically effects pH
--- Subfunctions:
- Moisturizes air
- Speech
- Maintance of water balance- body temperature
~ Humans control body temperature by sweat.
~ Most animals don’t sweat; they use panting- cooling by using lungs
--- Ventilation- set of mechanic process in which we bring air in and out
--- Gas Exchange- at level of cell, we use up oxygen, and release Carbon Dioxide.
--- Path Air Takes:
- Respiratory (Pulmonary) Airway- passage ways in which air gets inside
- Pharynx
____
- Trachea- branches out
 have cartilage in walls; keeps them open & from collapsing!
- 2 Bronchi- branch out___
- Bronchioles (muscle in walls)- offers most resistance to flow & most control.
- Terminal Bronchioles
- Alveoli
--- Lungs are surrounded by sac, Pleural Membrane & thin layer of fluid- comes between lung & thoracic
cage.
 Allows less friction in the lungs, when they move.
--- Rules of Flow:
-- Air always moves from high pressure to low pressure- Atmospheric & alveoli pressures
 Atmospheric pressure around 760 mmHg
 In real life it varies.
 To measure alveolar pressure, use the difference + or – above or below ATM.
For most people:
--- Inspiration- Active
--- Expiration- Passive
--- Two elastic lungs- tendency to collapse
norm lungs don’t collapse because encased in airtight compartment;balances due neg. pressure
 If you put hole into Thoracic Cavity, lungs will collapse.
-- Contract diaphragm increases thoracic volume, thoracic cavity becomes more negative, so lungs
expand; alveoli pressure reduces, so it brings in air from outside.
--- How Thorax makes Volume Change
- Contracting Diaphragm
- Have muscle between ribs,on the outside-make chest cavity larger-External Intercostal Muscle
 These are used for more strenuous activities.
- By Contracting Pectorial Muscles, even more strenuous.
- All will increase depth of inspiration
- Normal expiration, simply relax diaphragm and External Intercostal Muscle.
- When more strenuous, expiration contracts Internal Intercostal Muscles & Abdominal Muscles.
- When using abs, guts get pushed against diaphragm and diaphragm pushes against thorax.
- Stitch in side is due to the fatigue of the Internal Intercostal Muscles.
- Spinal injuries will prevent External Intercostal Muscles to work, but diaphragm will still work.
--- How to Change Respiratory Rate
1.) Amount of pressure.
2.) Amount of resistance to flow present; diameter of pipe 16 fold change.
 Bronchioles can change the amount of resistance using Autonomic Nervous System
- Sympathetic dialation of Bronchioles
- Parasympathetic constriction of bronchioles
** Exact Opposite of what they do in smooth muscle. **
--- Chronic Obstruction Pulmonary Disorders (COPD)
 Airway is fairly constricted, so the person has to work extra hard to breathe.
 People have to work hardest to exhale (which is normally passive)
 Normal People used 3 to 5% energy to breathe & about 100 Calories
 COPD people can use up to 30% energy & up to 500 calories.
--- When oxygen tension goes down, smooth muscle relaxes; tension goes up; smooth muscle constricts.
--- In lungs, oxygen goes down, greater blood flow to carry oxygen, & more air can enter them because
bronchioles relax.
--- Elasticity of Lungs
- Would collapse if nothing acting on it
- The lungs wall is itself sort of elastic.
- Alveoli have surface tension in them.
 Surface Tension- Water molecule, at surface, are subjected to unbalanced forces.
- As a result, surface actually has tension; compress film on surface.
Example: Belly Flop in pool
 LaPlace- discovered that the surface tension is greater, as the sphere gets smaller.
- Pressure goes up, when diameter gets smaller.
Example: Reason why it is hard to get balloon started; pulling it will do nothing.
 Alveoli are like tiny spheres, and LaPlace’s Law says that alveoli will want to collapse.
 Pulmonary Surfactant-without this we wouldn’t be able to breathe because the surfactant
reduces the surface tension, so it can overcome the pressure in alveoli.
~ In development, don’t start producing until 7 months.
--- Basic Volume Parameters
 In average size person, -Max Inflated Lung Volume = 5700 ml- Total Lung Volume
-Max Deflated Lung Volume = 1200 ml- Residual Volume
~ During normal breathing cycle between 2700-2200 ml (12-13 times per minute).
500 ml = Tidal Volume- amount of air you move in normal breathing.
3000 ml = Inspiratory Reserve Volume = amount of air you can intake after norm.
1000 ml = Expiratory Reserve Volume = amount of air you can exhale after norm.
 Can combine these into Capacity
Tidal Volume + Inspiratory Reserve = Inspiratory Capacity
Tidal Volume + Expiratory Reserve = Expiratory Capacity
Sum of everything = Vital Capacity
--- FEV1- Forced Expiration in One Second
 Have person inhale as deeply as they can
 then have them exhale as fast & hard as they can
 Measure amount of air per second
 Average: 80 % will come in 1 second; 100% by 3 seconds.
 Person with COPD- FEV1 is lowered.
--- Restrictive
 Can exhale at same rate.
 Has reduced vital capacity.
--- Gas exchange only in alveoli.
--- The volume of the conducting zone of Respiratory System  Anatomical Dead Space- Avg.- 150mL
--- Tidal Volume = 500 mL
--- Only amount of fresh air is = 350 mL
--- The amount of air you put into and out your lungs Ventilation Rate- 12 x 500
 Body doesn’t really care about that
--- Cares how much gets to alveoli
--- Amount of fresh air that get to alveoli with each breath Alveolar Ventilation Rate 12 x 350
--- Total Ventilation being different the Alveolar Ventilation Rate has consequences when dealing with
Respiratory Rate.
 If respiration goes down, and tidal volume goes up, Alveolar Ventilation Rate will go up.
--- Can’t attach self to hose and go to bottom of pond and breathe because Anatomical Dead Space goes
above tidal volume, so don’t bring in any fresh air.
Exchanging Gases
--- Source of oxygen; disposer of CO2
--- In Alveoli, air diffuses between capillaries in lungs
--- Higher in CO2 on inside, so diffuse out
--- Higher in O2 on outside, so diffuse in
--- Blood comes in with lots of CO2 & leaves with O2
--- Systemic capillaries- oxygen is lower than inside, so diffuses out; CO2 diffuse in
--- Diffuse down concentration gradient
--- Have to have a way to determine concentration of gases & liquids
Gas Tension
--- In gas mixture,the total pressure mixture exerting is the sum of all the pressures of all the components.
 Ptot = P1 + P2 +…. + Pn
--- To determine equilibrium in liquid is the partial pressure of Oxygen
--- The reason oxygen will get into liquid is the partial pressure of O2
--- When liquid is at equilibrium, partial pressure in liquid is same as partial pressure in air.
--- For dissolved gas in liquid = to partial pressure in gas in mixture, in which it will be in
equilibrium with liquid- Gas Tension
--- If PO2 lower it will gain oxygen
--- If PO2 is higher it will lose oxygen
--- Since blood enters pulmonary capillaries from systemic capillaries, lower PO2 in air; so it will diffuse
out of air into capillaries.
--- Oxygen is a fat soluble compound
--- Dissolved 3mL of oxygen per Liter of blood in H2O
--- Can dissolve enough to bring 15mL of oxygen to body per minute.
--- This is not enough to complete the metabolism process.
--- Hemoglobin (Hb) is inside red blood cells (lots in there)
--- Oxygen sticks to it
--- Lets oxygen (not very fat soluble) get transported in the blood
Hb + O2  HbO2
Reversible action
--- Hemo load up in O2 in pulmonary capillaries
--- Hemo let go O2 in Systemic
- Approx. what it is like in Alveoli.
- Hemo goes to tissues and 30% of
oxygen gets released.
Bohr Effect- the curve relating amount of oxygen carried on hemo actually shifts position, in high
Concentration of CO2.
- In pulmonary, CO2 level is low, so more O2 is bound to hemo.
- In systemic, O2 level low, CO2 level high, even more O2 gets released in hemo because
there is more CO2, goes up to 20-25% Saturated, and released the amount of O2.
- Important thing about Bohr effect change is not CO2, but Hydrogen Ions on hemo, which
are directly related to CO2.
- When hydrogen ion level goes up, the hemoglobin releases O2 very readily.
- When goes down, hemo bind O2 with great affinity.
95%Total- CO2 is very water soluble; when CO2 placed into water, forms Carbonic Acid, and it
spontaneously forms bicarbonate- all of these are reversible.
- Small amount of CO2 bound to Hb
- Small amount of CO2 bound to serum albumin
- Tissue release CO2
- Diffuse out of cells mostly in bicarbonate
- It’s carried to lungs.
Control of Respiration
--- 2 Levels of Control:
1.) Nervous System- neural control (holding your breath)
2.) Chemical Control- will override the neural control (forcing you to breathe)
- Increase of H ion concentration; receptors in inspiration system get activated,
so takes breath.
---Do have receptors that notice if O2 is too low; but the hydrogen ion receptors kick in much faster. **
Shallow Water Blackout
--- Hyperventilate completely saturates with O2, but it usually is, so it didn’t increase O2 much
--- Did reduce the CO2 & H ion concentration.
--- Since CO2 level didn’t get high enough to trigger inspiration. It had to wait until O2 levels get to low,
so you pass out.
--- * Shows the H ion receptors trigger much faster than the O2 receptors.
--- In aquatic animals, most use O2 receptors.