Lecture Exam #2 Flashcards
exercise response of expired ventilation rate
increases with a breakaway at AnT
effects of submaximal/maximal training on tidal volume
higher/higher
effects of submax/max training on expired ventilation rate
lower/higher
effects of submax/max training on pulmonary diffusion capacity
higher/higher
effects of submax/max training on respiratory rate
lower/higher
effects of submax/max training on carbon dioxide production rate
lower/hiher
effects of submax/max training on oxygen uptake rate
slightly lower/higher
what does an increase in exercise intensity and workload lead to
increase in metabolism, CHO, decrease in fat
increase in FT, decrease in ST
what does an increase in metabolism, CHO and decrease in fat lead to
increase pyruvate to acetyl CoA
increase in Krebs cycle activity
what does an increase in pyruvate to acetyl CoA and Krebs cycle activity lead to
increase in CO2 production
responsibility of chemoreceptors
detect increase in CO2 and decrease in pH from lactate, which stimulate breakaway at anaerobic threshold
why do trained individuals have a lower tidal volume during submax exercise than untrained individuals
they have an increased ability for gas exchange with circulation
decreased sensitivity of chemoreceptors to respiratory stimulators
location of chemoreceptors
medulla oblongata
aortic arch
carotid bodies
what is the greather ability for gas exchange with circulation in trained individuals due to
greather capillarization
larger lung volumes
greater alveolar ventilation rate
greater blood volume and hemoglobin levels
calculation for inspired ventilation
VE = VT(depth) * F(frequency)
calculation for alveolar ventilation
VA = (VT(depth) - VD(dead space) * F(frequency)
partial pressure O2/CO2 in atmosphere
159/0.3
relation of partial pressure O2/CO2 as air moves through body
difference decrease
when air expired, more CO2 than O2
calculation of partial pressure O2
Pb(barometric pressure) * [O2]
barometric pressure * 20.93%
calculation of partial pressure CO2
Pb * [CO2]
Pb at sea leavel
760 mmHg
pulmonary diffusion
capillaries open around arounud alveoli -> increase in O2 diffusion
why does a trained person have a greate pulmonary diffusion capacity
more capillaries around alveoli
increase in size of alveoli
increase in blood volume and hemoblobin levels
what is the diffusion path affected by
alveolar membrane interstitial fluid capillary membrane plasma RBCs
what does oxygen in blood depend on
ventilation pulmonary diffusion capacity, characteristics of diffusion pathway diffusion gradient and diffusion time altitude charcteristics of blood
how is the biggest amount of oxygen transported through the body
carried by hemoglobin
oxygen extraction
arterial - venous oxygen difference
we do not extract all the oxygen available
how much hemoglobin is in 100ml of blood
15.4 gm
how much oxygen can 1 hemoblobin molecule carry
4 O2 molecules
how much O2 can one gram of hemoglobin carry
1.34 ml
why do females have a lower hemoglobin level
due to the menstrual cycle
what is responsible for the drop of Po2 and increase Pco2 when going from atmospheric air to in alveoli
dilution with residual gases in alveoli of lungs
Po2 and Pco2 in arterial and venous blood
arterial: 100/40
venous: 40/46
what causes a decrease in pulmonary diffusion capacity
smoking
not enough H2O drinking
membrane damages through diabetes
decrease in blood and RBC volume
what does hemoglobin consist of
4 heme groups attached to globin
what does the hemoglobin-oxygen dissociation curve descrive
how much oxygen is bound to hemoglobin for a given partial pressure of oxygen
realtionship between Po2 and hemoglobin saturation
the higher the partial pressure of oxgen is the greater the saturation of hemoglobin with oxygen
not linear, rather sigmoidal relationship
what causes sigmoidal relationship between Po2 and hemoglobin saturation
the allosteric nature of hemoglobin
what enhances oxygen availability
two-fold characteristic of hemoglobin
binding and release is cooperative
what does it mean when binding and release of oxygen from hemoglobin is cooperative
binding of oxygen to one heme enhances enahnces binding of oxygen to other heme - same with release
with what does hemoglobin oxygen dissociation curve work in conjunction with
diffusion gradient
two states of hemoglobin
oxyhemoglob
deoxyhemoglobin
oxyhemoglobin
relaxed state
hemoglobin is highly satured with oxygen
deoxyhemoglobin
taut state
oxygen has difficult time binding to heme group
what shifts the hb O2 dissociation curve to the right
decrease in pH
increase in partial pressure of carbon dioxide
temperature
2,3-DPG levels
how does the shift of the hb O2 dissociation curve to the right affect the loading of hemoglobin with oxygen in the lung capillaries and the unloading in the muscle tissue capillaries
lung capillaries: minimal effects
unloading of O2 at muscle tissue capillaries: significant increase due to reduction in affinity
what does the bohr effect describe
enhancing oxygen availability during exercise to tissue due to higher levels of Pco2 and hydrogen ions
decrease in pH
what does the haldane effect describe
high Po2 in alveoli increases release of CO2 and H+ from hemoglobin in the lungs
increases removal of CO2 and H+ from body
why is endurance performance worse at high altitude
due to lower Pb, Po2 is lower -> hemoglobin saturation is reduced
when does altitude have an effect on maximal oxygen uptake rate
above 1,500m
every extra 1000m -> VO2max decreases by 10%
what is one of the first major adaption to altitude after 48 hours
increase in 2,3-DPG levels -> increasing oxygen availability to tissue by 26-folds -> increasing endurance
calculation of cardiac output
Q = pressure gradient/resistance
or Q = SV * HR
what affects resistance
viscosity
length
vasodialation
what aids venous return flow
pressure head
muscle pump
intrathoracic pressure change
vasocontriction
systolic, mean, and diastolic pressure in the arteries, capillaries and veins
systolic starts at a little higher than 120 mmHg
mean at 100 mmHg
diastolic at 80 at a little higher than 80 mmHg
all 3 decrease to almost 0mmHg in veins
where do systolic, mean and diastolic pressure hit the same level
from arterioles to capillaries
what is the driving force of blood in circulatory system
mean blood pressure
how can cariac output be increase
by increasing pressure gradient and decreasing resistance
why does mean blood pressure tends to go up during exersice
due to an increase in systolic output
why does peripheral resistance with increasing exercise decrease
due to vasodialation of muscle tissue capillaries
why do untrained people have a greater cardiac output during submax exercise
greater SV and HR necessary to fullfil O2 demand
who has a greater maximal cardiac output
trained person
fick equation
VO2 = Q * O2 extraction rate
O2 extraction rate
arterial - venous O2 level
trained vs. untrained individual´s SV
trained individual has always a greater SV
relation between trained/untrained individual and SV with increasing workload
untrained SV plateaus at less work and at lower level (30%)
trained SV plateaus later and at 50% of max
Realtion between trained/untrained individual and HR with increasing workload
trained has lower resting and submax HR but no difference in max. HR
blood pressure characteristics with increasing workload
increase in systolic and mean BP
stable diastolic BP
calculation of SV
SV = End distolic volume - End systolic volume
what causes an increase in SV
increase in end diastolic volume (EDV) and a decrease in end systolic volume (ESV)
what affects end diastolic volume
anatomical voume (ventricular volume) return flow blood flow
what affects end systolic pressure
contractility
peripheral resistance
starling´s law
what does endurance training cause
increase in ventricular volume and blood volume -> increase in EDV
what does strength training cause
increase in wall thickness and contractility -> decrease in ESV
relation between trained/untrained individual´s Q and increasing workload
at rest both same Q
increases fast, but from submax to max slower increase due to plateau SV
at submax exercise higher Q in untrained individual
at max exercise greater Q in trained individual
O2 extraction rate following training
increasing maximal and submaximal values
internal influences on cardiorespiratory responses
increase in carebral coretex activity, kinesthetic feedback, chemoreceptor response, catecholamine release and temperature
relation between an increase in carebral coretex activity, kinesthetic feedback, chemoreceptor response, catecholamine release and temperature to ventilation, HR, SV, and blood vessels
ventilation, HR, SV, and blood vessels always increase as well
external influences on cariorespiratory responses
altitude
O2 enrichment
smoking
blood “doping”
what does an increase altitude lead to
decrease atmospheric pressue and a decrease in partial pressure O2
decrease in arterial O2 saturation
what causes an O2 enrichment
increase in arterial O2 saturation and VO2 max
what does smoking lead to
increase in airway resistance
decrease in pulmonary diffusion capacity
increase in [carbon monoxide] -> increase in Hb-CO2 -> decrease in O2 transportation
blood doping
infusion or reinfusion of RBCs -> increase in O2 carrying capacity
what does the ingestion of EPO lead to
bone marrow to produce RBCs -> increase in oxygen carrying capacity
main transportation of CO2 away from tissue
60-70% attached to RBCs
23-30% attached to hemoglobin
7-10% dissolved in plasma
main buffer of lactic acid in blood
sodium bicarbonate
what does buffering of lactic acid results in
formation of carbonic acid and sodium lactate
what are anaerobic threshold and VO2 max used for
prediction of cardiorespiratory fitness
prediction of performance endurance capabilities
exercise prescription
setting long term work paces
setting tolerance for environmental extremes
how should anaerobic threshold and VO2 max be expressed
soccer and running - ml/kg/min
swimming and cycling - L/min
what are the 3 areas with an anaerobic threshold/breakaway
ventilation rate
carbon dioxide production rate
lactate production rate
what causes threshold in ventilation rate
increase in carbon dioxide production
increase in lactate -> decrease in pH
what causes threshold in carbon dioxide production rate
breakaway in lactate
what muscle fiber types and energy sources are used prior to an anaerobic threshold
SO, FOG
aerobic oxidative metabolism
what muscle fiber types and energy sources are used after an anaerobic threshold
FOG, FG
anaerobic metabolism
relation between Ant and VO2 max
AnT = 50 - 60% of VO2max in untrained AnT = 70 - 80% of VO2 max in trained
realtion between untrained/trained individual and VO2 with increasing workload
VO2 increases linearly
plateau at max exercise
VO2 lower at submax in trained
VO2 higher at max in trained
relationship in trained/untrained individuals and ventilation rate with increasing workload
both have breakaway with increasing workload
rest and submax: lower ventilation rate in trained
max ventilation greater in trained person
relationship in trained/untrained individuals and lactate production rate with increasing workload
both have breakaway with increasing workload
at rest even lactate values
submax lactate is lower in trained person
max trained person has higher lactate values
CHD risk factors
hypertension hypercholesterolemia smoking obesity hypertriglyceridemia diabetes stress physical inactivity age sex family history
potential effects of exercise on CHD
increase in colleteral circulation increase in vessel size increase in myocardial efficiancy, O2 transport decrease in dysrhythmias decrease in clot formation
relation between O2 deficit and debt
the greater the O2 deficit the greater the O2 debt
oxygen debt is greater than ixygen deficit
difference between trained and untrained O2 ventilation response
untrained a slower VO2 response
difference between trained and untrained O2 debt
untrained has a larger/slower O2 debt
alactacid phase of O2 debt
first part
fast decrease in VO2
faster in trained individual
lactacid phase of O2 debt
second part
slow decrease in VO2
what is oxygen uptake kinetics
rate of VO2 response
will influence rate or amount of O2 deficit use
what affects the maximal oxygen uptake deficit capacity
capacity of anaerobic energy system
phosphogen stores
Lactic Acid tolerance
reasons for greater oxygen debt compared to deficit
replace oxygen deficit
elevated breathing and HR
increased body temperature and metabolic rate
increased adrenaline and noradrenaline levels
when is fast-slow pacing appropriate
for high %ST , because of high [H-LDH]
when is slow-fast pacing appropriate
for high FT, because of good finishing “kick”
what is the best performance time
even pacing
how is lactate degredated
during lactacid phase through sweat and urine aminoacid production gluconeogenesis oxidation
how long doe sit take to replenish phophogen stores using passive recovery
50% within 30 sec
100% within 2-3 min
how long does it take to remove lactic acid using passive reovery
50% within 25-30 min
100% within 1-2 hours
how long does it take to remove lactic acid using active state
50% within 25-30 min
100% within 1/2 - 1 hour
characteristics of active recovery state
moderate intensity requires high rate of oxidative matabolism 50-60% of max HR in untrained 70-80% of may HR in trained ventilation rate under control work just below AnT
training implications from interval sprint training
shorter segments to complete greater total work
practice at competetive pace
no L.A. production
why is sprint interval training more effective
because it take longer to recover from high lactate levels than from phosphagen depletion
what does a training program need to include
training principles
program design
program phases
3 major training principles
overload - higher than normal demands
progression - increasing workloads
specificity- motor unit training
progrm design
task analysis
skill
strength
metabolic
training program phases
preseason - build specific fitness
in season - maintain specific fitness
postseason - maintain general fitness
volume and intensity in enducrance/strength training phases throughout the year
postseason: both high volume, low intensity
in pre-season: both moderate volume, moderate intensity
in season: both low volume, high intensity
technique level throughout season
line follows intensity line
which energy systems are used during events of various time lengths
phosphagen: 0:10 - 0:20 min
anaerobic glycolysis: 0:45 - 1:45 min
Oxidative: 3:45 - 135:00 min
when is energy production 50% anaerobic and 50% aerobc at maximal effort
after 3 - 4 min
e.g 1500m race
interval training guidelines for developing phosphagen energy system
work time: 0 - 30 sex
work recovery ratio: 1/3
type of recovery: passive
interval training guidelines for developing anaerobic glycolysis energy system
work time: 30-60 seconds, 60-120 seconds, 2-3 minute
work recovery ratio: 1/2
type of recovery: active
interval training guidelines for developing oxidative (aerobic) energy system
work time: 3-5 min
work recovery ratio:1/1
type of recovery: passive
target HR at work as well as between reps and sets during interval training
HR at work: 85-95% of max HR
HR for recovery between reps: 70% of max HR
HR for recovery between sets: 60% of max HR
endurance training intensity when trying to improve general fitness
> (or even) 75% of max HR
guidelines for endurance training intensity to improve competetive preperation
85-95% of max HR
endurance training compared to interval training
psychologicall and physiologically less demanding
used to develop general overall cardiorespiratory endurance
can be used in conjunction with interval training for competetive preperation
less specificity in training
duration guidelines for endurance training
minimum of 12 - 15 min(at high HR)
“practical maximum: 45 - 60 min
> 60min mainly beneficial to long distance competitors
what does endurance training longer than 60 min improve
fat metabolism
psychological benefits
frequency guidelines for endurance training
2/week minimum (high HR)
3-5/week need of most individuals
how long of detraining does it take to lose 50% of cardiorespiratory fitness
4 weeks
power
work/time
(force * distance)/time
force * velocity
strength
max force from one contraction
1 rep max
different types of muscle actions
idometric
concentric
eccentric
isokinetic
isometric muscle action
force = resistance
no movement can provide a max overload
concentric muscle action
force > resistance
movement in direction of force vector
eccentric muscle action
force < resistance
movement in direction of resistance verctor
overload can be max
isokinetic muscle sction
force > resistance
overload can be maximal
controlled speed may be fast or slow (machine)
muscular endurance
measure of work capacity under moderate to high resistance
depends on strength and anaerobic capabilities and function of relative load is involved
age predited max HR
220 - age in years
calculation of training intensity using HR max method
predicted max HR
multiply by training intensity of fitness level ( e.g. 0.7 or 0.8)
training target HR e.g. 140 - 160 bpm
what does muscular endurance not depend on
aerobic oxidative metabolism
anabolic
increase in lean tissue development and strength
androgenic
increase masculinization or feminization
potential side effects of exogenous intake
liver or kidney damage sterility closure of long bone growth severe acne musculization or feminization increase risk of cancer
what leads to greater lean body mass and strength in men after puberty
production of more anabolic hormones
guidelines for isometric training
100% of max effort
5 sec/ rep
5 reps/exercise
3-5 sessions per week
guidelines for muscular endurance training
15 -20 reps/set
up to as many as 30/40 reps/set
2-3 sets/exercise
3 sessions/week
guidelines for eccentric training
120% of 1 rep max
3-5 sets/exercise
6-8 reps/set
3-5 sessions/week
circuit training
6-15 exercise stations
30-40 sec/station
15/20 sec recovery between stations
what are results of circuit training
increase in strength, muscle endurance, cardiorespiratory endurance
decrease in fat
what causes accute muscle sourness
ischemia as blood flow is occluded
blockage of blood flow
