Sum of all the pressures that each gas would exert independently
Q OF DAY: How and by what process does O2 enter the lungs and CO2 leave the lungs?
Diffusion and partial pressure
Partial pressure of O2 in atmosphere is HIGHER than the P.P. of 02 in alveolar air and blood. Therefore, it must move DOWN concentration gradient. ***ONE WAY VALVES PREVENT BLOOD FROM MOVING BACKWARDS WHEN TRAVELING FROM CAPILLARIES TO HEART!
What is the driving force to breath?
Levels of CO2
How is most 02 transported in the blood?
bound to hemoglobin
a protein contained in red blood cells
How many oxygen molecules can 1 Hb carry?
Hb bound to O2
Hb not bound to 02
Veins (at rest): 40 mmHg Arteries: 100 mmHg
What two factors alter 02-Hb Dissociation Curve?
Low pH: affect on O2-Hb Dissociation Curve
SHIFTS TO RIGHT!!!! more acidic "bohr Effect" b/c more H+ ions from glycolysis Facilitates more 02 UNLOADING
High pH: affect on O2-Hb Dissociation Curve
SHIFTS TO LEFT!!!! More alkaline Facilitates tighter bonding of O2 and Hb with LESS O2 unloading **This makes sense because a high pH makes the graph move 'higher' or to the left!
High Temperature: affect on O2-Hb Dissociation Curve
MOVES TO RIGHT!! MORE O2 UNLOADING.
Low Temperature: affect on O2-Hb Dissociation Curve
MOVES TO LEFT!!!!!!! facilitates tighter bonding
Main stimulation to breathe?
increase in CO2
Why does ventilation increase overtime on a hot/humid environment?
Increase in body temperature
Why are hydrogen ions (H+) bad?
Interfere with actin and myosin
Inflection point where Ve increases exponentially Occurs ~50% VO2 max
Low PO2 level
What are some of the effects of endurance training on Ventilation During Exercise?
Does exercise training have an effect on lung structure and function at rest?
Does the pulmonary system limit exercise performance?
No (Not at sea level or in disease free individual) Our lungs are overbuilt!
Low heart rate *Reduction in the simulation from the sympathetic nervous system and increased stimulated parasympathetic system.
Q OF DAY: You go to the doc and your HR is 40 beats/min. The doc wants to admit you to the hospital, WhY?
exercise training can lead to changes in the EKG that can be confused with symptoms of heart disease. **Bradycardia- pathalogical condition indicating the heart isnt functioning properly and may require a pacemaker. They are confusing your exercise training w. having a pathological condition.
3 Main Functions of the Cardiorespiratory System
1) Transport O2 and nutrients to tissues 2) Removal of CO2 waste from tissues 3) Regulates body temperature
Because the circulatory system works hand on hand with the respiratory system.
What creates the pressure to pump blood in the body?
Where does the exchange of O2, CO2, and nutrients with tissues take place?
Includes all events associated with blood flow through the heart during one complete heartbeat. *Includes atrial systole and diastole followed by, ventricular systole and diastole. Recorded by EKG
CONTRACTION PHASE 2/3 blood is ejected from ventricles per beat
Relaxation Phase Refill with blood
At rest, which is bigger: Diastole or Systole?
During exercise, which is bigger: Diastole or Systole?
amount of blood pumped by each ventricle in one minute
CO= heart rate (HR) x Stroke Volume (SV) beats/min x L/beat = L/min
End Diastolic Volume (EDV)
Amount of blood in ventricle at the END of diastole (Preload)
End Systolic Volume (ESV)
Amount of blood remaining in ventricle after contraction
Amount of blood ejected with every heartbeat SV= EDV - ESV
3 Regulations of Stroke Volume
1)End Diastolic Volume or preload: amount ventricles are STRETCHED by blood volume at end of diastole. more stretch=more contractile Force 2) Average aortic Blood PRessure: pressure the heart must pump against to eject blood. 3) Strength of the ventricular Contraction/ Contractility: increase Ca2+ in cytoplasm
Frank-Starling Law of the Heart
Amount of blood returning to heart (venous return) is most important factor affecting preload.
How long does it take the heart to pump your entire blood volume?
How many liters of blood are in the human body?
How can you enhance contractility?
-Circulating epinephrine and norepinephrine -Direct sympathetic stimulation of heart - Increase in contractility is due to greater Ca2+ into cytoplasm
What factors influence CO or Q?
Training Status (Trained vs. Untrained) Gender Age
How does exercise training influence CO?
Exercise increases blood volume, venous return, and therefore preload.
2 Major adjustments of blood flow during exercise
1) Increased cardiac output 2) Redistribution of blood flow from inactive organs to active muscle
How much of blood flow will go to active muscles/tissues during exercise?
How is exercise cardioprotective?
1)Reduce incidence of heart attack 2)improves survival from heart attack *Reduces amount of myocardial damage from heart attack
What determines patient's chance of recovery?
# of cardiac cells that are destroyed during heart attack
Can indv'ls with cardiovascular disease decrease their chances of death by exercising?
Who is more resistant to fatigue, men or women?
WOMEN! they have less type IIx fibers, which fatigue sooner. However, even in the same muscle fiber, women fatigue less. *In a study done in 1999 by Fulco et al., they discovered women have more capillaries, oxidative metabolism, and more mitochondria.
Q OF DAY: Blood pressure can be increased by which of the following factors?
A) ^ Blood volume B) ^ Blood viscosity C) ^ Heart Rate D) ^ Stroke Volume E) ^ Peripheral Resistance
increase muscle size (diameter)
Left Ventricle (LV) hypertrophy due to: DISEASE
Less compliant Holds LESS blood LESS ejection fraction
Left Ventricle (LV) hypertrophy due to:EXERCISE
MORE compliant holds MORE blood HIGHER ejection fraction
Force exerted by blood against arterial walls and is determined by how much blood is pumped and the resistance of blood flow. *Used as indication of health
Difference b/n systolic and diastolic * HIgh value may be indication of heart disease
Mean Arterial Pressure (MAP)
Average pressure in the arteries Determines rate of blood flow through the systemic circuit MAP= DBP + 0.33(SBP-DBP) *estimate
Blood pressure over 140/90 mmHg
2 Types of Hypertension and their causes
1)Primary (Essential) Hypertension: cause= unknown; 90% cases of hypertension 2) Secondary Hypertension: Cause= result of some other disease process "secondary" to another disease
Risk factors for Hypertension
Left ventricular hypertrophy atherosclerosis kidney damage Stroke
build up of plaque in coronary artery
Factors that influence arterial blood pressure
cardiac output Total vascular resistance=sum of resistance to blood flow by systemic circulation MAP= CO x TVR
What regulates blood pressure: SHORT TERM?
Sympathetic Nervous System/ SNS -Baroreceptors (Pressure Receptors) in aorta and carotid areries Increase BP = Decrease SNS activity Decrease BP = Increase SNS activity
What regulates blood pressure: LONG TERM?
Kidneys- via control of blood volume
How many voluntary skeletal muscles does the human body contain?
3 Major Functions of skeletal muscle:
1) Force production for locomotion and breathing 2) Force production for postural support 3) Heat production during cold stress
threadlike protein filaments that make up muscle fibers
2 Major types of contractile proteins:
Actin (Part of thin filament) Myosin (Part of thick filament)
Connects muscle to bone
Connects bone to bone
Where shortening occurs *Functional unit of skeletal muscle contraction Includes: Z line, M line, H zone, A band, I band
storage site for calcium
extend from sarcolemma to sarcoplasmic reticulum
Muscle Contraction/ Sliding Filament Theory
Muscle shortening occurs due to the movement of the actin filament over the myosin filament, which results in a reduction of Z line to Z line of sarcomere. This results in a formation of cross-bridges between actin and myosin filaments (power stroke) Figure
Ca2+ binds to troponin -> causes shift in tropomyosin to uncover the active site -> cross bridge forms strong binding state
Excitation- Contraction Coupling
sequence of events in which a nerve impulse (action potential) reaches the muscle membrane and leads to muscle shortening by cross-bridge activity.
2 Steps of EXCITATION
1. Action potential in motor neuron causes release of acetylcholine into synaptic cleft. 2. Acetylcholine binds to receptors on motor end plate, leads to depolarization that is conducted down transverse tubules, which causes release of Ca+2 from sarcoplasmic reticulum (SR).
5 STEPS OF CONTRACTION
1. At rest, myosin cross-bridges in weak binding state. 2. Ca+2 binds to troponin, causes shift in tropomyosin to uncover active sites, and cross-bridge forms strong binding state. 3. Pi released from myosin, cross-bridge movement occurs. (Pi=inorganic phosphate) 4. ADP released from myosin 5. ATP attaches to myosin, breaking the crossbridge and forming weak binding state.
Decrease in muscle force production and characterized by a reduced ability to do work
Contributing Factors to Muscle Fatigue: High Intensity
accumulation of H+, ADP, Pi, and free radicals. *Result: Deprivation of muscle homeostasis and impairs force production.
Contributing Factors to Muscle Fatigue: Long-Duration Exercise
*Muscle Factors: Accumulation of free radicals Electrolyte imbalance Glycogen depletion *Central Fatigue: Reduced motor drive to muscle from CNS
3 types of skeletal muscle fibers
Fast Fibers: type IIx type IIa Slow Fibers: type I
Type IIx Fibers
Fast-Twitch fibers fast glycolytic fibers non oxidative metabolism
YES!! *Maximal force per cross sectional area -10-20% higher in fast fibers (IIa, IIx) compared to slow fibers(types I) -Force production related # of myosin cross bridge. ~Fast fibers contain more cross bridges per cross sectional area
Distance runners: more Slow fibers or Fast fibers?
Sprinters: more Slow fibers or Fast fibers?
Non-athletes: more Slow fibers or fast fibers?
number of muscle fibers
Muscle Atrophy: Initial Atrophy
due to reduction in muscle protein synthesis
Muscle Atrophy: Subsequent Atrophy >2 days
due to increased muscle protein breakdown
Is atrophy permanent?
NO! Can be reversed by returning the muscle to 'normal' use *Resistance exercise is extremely important
Application of force without joint movement
variable resistance exercise/ movement of body parts eg- nautilus equipment
2 types of hypertrophy
1) Transient 2) Chronic Hypertrophy
increased muscle size that develops during and immediately following a sigle exercise bout. *Why someone looks bigger right after exercise, but the sixe goes away in an hour or so... -Results from fluid accumulation/edema in the interstitial spaces of muscle and only lasts a short time
increase in muscle size that occurs with long-term resistance training. actual structural changes in the muscle from an increase in size of muscle fibers or increase in number of muscle fibers.
How is it an individual can lift more weight but not get bigger?
increase # of motor units
Delayed Onset Muscle Soreness *Microscopic tears in muscle fibers/connective tissues *Result: pain within 24-48 hours after strenuous exercise
Steps leading to DOMS
-Strenuous muscle contraction (eccentric) results in muscle damage -Membrane damage occurs -Calcium leaks out of SR and collects in mitochondira *Inhibits ATP production -Results in inflammatory process -edema and histamine stimulate pain receptors
maintenance of a constant or unchanging 'normal' internal environment during unstressed conditions
constant internal environment Balance achieved between the demands placed on the body and the body's response to those demands (EX-exercise)
pWhat happens to mean pressure when arterial pressure fluctuates?
Mean pressure REMAINS CONSTANT
Biological control system
series of interconnected components that maintain a physical or chemical parameter at a near constant value
Detects changes in variable
HYPOTHALAMUS; assesses input and initiates response; center to integrate response
changes internal environment back to 'normal' PRODUCES DESIRED EFFECT
response of central system is negative/opposite of stimulus reverses the initial disturbance in homeostasis **99% of items in our body work on negative feedback!
Response increases the original stimulus
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