quiz 5 start of exam 2 Flashcards
heat
direct calorimetry
O2 and CO2
indirect calorimetry
make fuel from
CHO, fat, and pro
40% of substrate energy =
ATP
60% of substrate energy =
heat
energy expenditure equation
fuel+ O2-energy +heat +CO2+h20
direct calorimetry
measures energy expenditure directly
indirect calorimetry
measures metabolic gases to measure energy expenditure indirectly
we use ____ to help burn fuel and produce ____ in that process
O2 and CO2
estimates total body energy expenditure based in O2 used and CO2 produced and measures ___
respiratory gas concentrations
CO2 produced: krebs cycle and PDH
O2 used : ETC
glycolysis in the
cytoplasm
krebs cycle in the
mitochondria
VO2
volume of O2 consumed per minute
-O2 used in tissues (final electron acceptor)
-rate of consumption= O2 used in ETC
calculating VO2
volume inspired O2-volume of expired O2 (inspired is always larger)
volume breathed IN
2.26 L/min
volume breathed OUT
1.24L/MIN
VO2 calculated =
1.02 VO2
relative VO2 =
ml/kg/min
why is O2 in larger than O2 out
arterial blood is highly oxygenated because tissues have not consumed oxygen out of it yet
venous blood has much lower O2 because
tissues have now consumed oxygen out of it
subtract arterial blood from venous blood =
get the amount of O2 consumed by your tissues
O2 =
volume of CO2 consumed per minute
CO2 is produced within bioenergetics
krebs cycle and PDH
rate of CO2 production units
l/min and ml/kg/min
volume of expired CO2 - volume of inspired CO2 =
VCO2
Why is CO2 breathed OUT larger than CO2 breathed IN?
Co2 production in bioenergetics and the extra Co2 enters the blood as a waste product
lowest while living =resting VO2
resting metabolic rate (RMR)
Respiratory exchange ratio
glucose = 1.0
fat = 0.70
RER = VCO2/VO2
ratio between rates of CO2 (VCO2) production and O2 usage (consumption)
more carbon atoms in molecules =
more O2 needed
more carbons = more acetyl CoA = more krebs spins=
more REs produced = more O2 needed
Fat “burns” using proportionately more O2:
Has more carbons which = more acetyl CoAs which = more krebs which = more RE’s which = more ETC
RER for 1 molecule of glucose =
1.0
RER for 1 molecule palmitic acid
=0.70
RER helps us determine
substrate use & kilocalories / O2 efficienc
RER for 1 molecule of glucose
1.0
RER for 1 molecule palmitic acid
0.70
fat RER range
0.6-0.8
mixed fuels (cho, fats, protein)
0.8-0.9
carbohydrates RER
> 0.9
as RER increases so does
RER equivalent
fat requires
more O2
cho requires
less O2
as RER changes
the energy per L O2 changes
everytime RER = 0.80
RER equivlant = 4.80 kcals/L O2
every time RER = 0,95
RER equivalent = 4.99 kcals/ L O2
measuring resting VO2 will be someones
lowest O2 consumption
maximal capacity for O2 consumption by the boy during maximal exertion
VO2 max
maximal capacity for O2 consumption by the boy during maximal exertion
VO2 max
at VO2 you will also
be at maximal energy expenditure/minute
maximal O2 uptake (VO2 peak)
point at which O2 consumption doesn’t increase with further increasing in intensity
VO2 max or VO2 peak
(a-v) O2 difference
arterial blood has
highest O2 concentration
venous blood has the
lowest O2 consumption
muscles extract O2 for energy use in the
ETC
VO2 max or VO2 peak is the best measurement
of aerobic fitness
training your VO2 peak you can
make more mitochondria
more hemoglobin
more myoglobin
more muscle capillaries
absolute VO2 peak
l/min
no units of body weight used
better used in non weight bearing activities
relative VO2 peak
ml/ O2/kg/min
units of body weights used
most accurate when comparing: body size, body comp, different sexes
normal ranges for untrained: young men
44 to 50 ml/kg/min
normal ranges for untrained: young women
38 to 42 ml/kg/min
criteria for reaching V\O2 max
- plateau in oxygen uptake
- > 95% of predicted heart rate
- RER of 1.10 or greater
2 of 3 most be made
plateau of oxygen uptake
< 2 ml/kg/min difference during last 2 minutes
ventilatory threshold
when talking becomes hard to do
breathing changes disproportionately
-point where Ve/VO2 begins to rise disproportionately and without a corresponding increase in VE/VCO2
glycolysis is cranked up
b/c its high intensity and need a lot of atp
PDH converts
pyruvate to actelyl COA
excess pyruvate that inst being consumed by the mitochondria, begins to accumulate in the cytosol and begins to be converted to
lactate accumulates in the cell
incomplete oxidation of glucose
pyruvate to lactate
sprinter would reach LT sooner than a marathoner
more mitochondria, more oxidative pathways,
sprinter= more glycolysis and few mitochondria
marathoner = few glycolytic enzymes and lots of mitochondria
fatigue after VT and LT
-increased acidity = decrease PH
- bioenergetics dysfunction
- breathing difficulty
-increasing buffering of H+ in blood
-increasing CO2 drives breathing
increased acidity
increased hydrogen ions : lactate production and ATPase activity
acidity inhibits enzymes
glycolysis, krebs, ETC
breathing difficulty
VE
increases buffering of H in blood
buffering uses bicarb and produces extra CO2
VO2
volume of O2 consumed
mitochondria consumes
O2
increase CO2 causes
hyperventilation
CO2
bioenergetics, H+ buffering and bicarb
VO2 max tests
fitness
VT and LT tests
performance
endurance training improves LT
increase in mitochondria
define improvement
right ward shift in LT
-run faster before lactate and H+ accumlates
RER inaccurate for protein oxidation
nitrogen removal requires energy above that within bioenergetics
lactate use as fuel produces RER above 1.0 due to
increase CO2 exhalation
gluconeogenesis
produces RER <0.70
1 L O2/min
5 kcals
1 met
3.5 mL O2/kg/min
1 kcal/kg/hour
1 met
METs
metabolic equivalents
-the ratio of a metabolic rate (VO2) during a specific activity to a reference metabolic rate
the reference metabolic rate is the average BMR
3.5 mlO2/kg/min
light intensity
< 3.0 MET
moderate intensity
3.0 -5.9 METS
high intensity
> 6.0 MET
metabolic rate
rate of energy use by body
BMR
rate of energy of use at rest
energy use to sustain life
supine
thermoneutral environment
after at least 8 hours sleep and fasting
metabolic rate energy expenditure
increases with exercise intensity
VO2 increases with
exercise intensity
O2 deficit
represents the difference between O2 consumption and O2 demand
pathways supplying energy
PCR and glycolysis
amount of O2 deficit depends on
-intensity of activity
-trained status of person
-genetics
O2 deficits equation
O2 required for ATP use - actual O2 consumed
Excess Post-exercise O2 Consumption
EPOC - represents the difference between O2 consumption and O2 demand
O2 consumed > O2 demand
in early recovery
duration of EPOC is typically dictated by
intensity prior to exercise
reasons for EPOC
HOTTIE
-elevated hormones (catecholamines)
-oxidizing lactate (higher intensity = more lactate = longer EPOC
-thermoregulation
-ion redistribution (NA+ - K pumps)
-elevated breathing and HR
O2 deficit and EPOC
O2 demand > O2 consumed in early exercise
-body incurs O2 deficit
- O2 required -O2 consumed
-occurs when anaerobic pathways used for ATP production
O2 consumed > O2 demand in early recovery
excess postexercise O2 consumption (EPOC)
-hormone elevation
-using and excess lactate
-thermoregulation
-ion distribution
-elevated ventilation and HR
economy of effort
as athlete practice more, use less energy for given pace
-high trained athlete has lower VO2 for same pace/intensity
economy increases once
muscles are warmed up and fully functional
increase VO2 =
more energy expenditure
fit people go back to baseline
faster
successful endurance athletes have
high VO2 max
-high lactate threshold (LT and VT)
-high economy of effort
-high percentage of type 1 muscle fibers
anaerobic sports =
high intensity
-short duration
-bioenergetics (PCR, glycolysis, usually incomplete glucose oxidation
lactate threshold
the point at which blood lactate accumlation increase markedly
- lactate production rate > lactate clearance rate
-integration of bioenergetics
-untrained people LT about ____ VO2 max
55%
endurance athletes about ___ VO2 max
75%
higher lactate threshold
better endurance performance
fatigue in exercise
decrements in muscular performance with continues effort, accompanied by sensations of tiredness
-inability to maintain required power output to continue muscular work at given intensity
fatigue and its causes
- inadequate energy delivery/metabolism
- accumulation of metabolic by products
- excessive heat
- altered neural control of muscle contraction
inadequate energy delivery/metabolism
phosphocreatine depletion
PCr depletion
supplementing with creatine will postpone
phosphocreatine depletion
glycogen depletion
“hitting the wall”
liver: 100 grams = about 400 cals.
muscle: 500 grams = about 2000 cals.
fibers recruited first are
depleted fastest
type 1 fibers are likely targets due to
orderly recruitment
orderly recuitment
type 1, type 2a, type 2x
as muscle glycogen decreases
liver glycogenolysis increases
-begin to rely more on liver glycogen to support blood glucose
acidosis
H+ accumulates during a brief, high-intensity exercise
-H+ accumulation causes decreases muscle Ph
buffers (bicarb) help muscle
ph
buffers minimize drop in ph and ph less than 6.9 =
inhibits glycolytic enzymes, ATP synthesis
causes of failure of NMJ
- decrease ACH synthesis and release
- altered ach breakdown in synapse
- increase in muscle fiber stimulus threshold (-55)
- if neural message is not inhibited on motor end plate then Ca+ release from SR will be inhibited
