vo2max and training Flashcards
exercise vs training
exercise = single bout
training = repetitive bouts
exercise types: endurance/aerobic, resistance/anaerobic, interval
FITT principle
frequency, intensity, time, type
principles of training
- overload: system worked beyond normal i.e. intensity
- reversibility: detraining, gains lost when overload removed
- specificity: muscle fibres and energy systems involved i.e. chest musc when bench press
- type and velocity of contraction - individuality: genetic susceptibility
- diminishing returns: less trained will improve faster
oxygen yptake
represents ability to
1. take up: resp sys
2. utilize: metabolic sys
3. transport: CV sys
is an integration of systems
at max capacity, aka aerobic capcity, max o2 consumption
vo2 is highest vol o2 can take in and utilize
vo2max determinants
- o2 delivery to muscle - CV sys
- o2 utilization by musc - mito content
delivery is most important because limits vo2max
vo2peak
highest value on a max test
not necessarily highest possible value
vo2max
rigorous, defined criteria
- o2 intake during exercise so o2 intake reaches max…cannot inc w intensity
highest rate of oxidative metabolism
any higher causes rapid fatigue
how to tell if vo2max is reached
- plateau in vo2…ideal
- RER > 1.15
- reach age predicted HRmax
- high blood lactate, 8x rest
- voluntary exhaustion
vo2 tests
treadmill, cycling, bench step, swim, etc.
- can be continuous, 3-5min submax
- or progressive i.e. 8-10 min
subject ends test, needs motivation
vo2 is SINGULAR BEST measure of cardiorespiratory capacity
- if weigh more, higher vo2
world record 97.5ml/kg/min by cyclist
typically, cross country skiiers, runners, cyclists have highest vo2max
is vo2max the end all? factors of vo2
- genetics
- bio sex: women inc fat, hemo content, CV system i.e. Qmax and BF diffs
- age
- body size and composition
- training status
- mode of exercise i.e. endurance vs strength
OBLA/LT and vo2max
endurance training inc intensity at lactate threshold/OBLA w/o vo2max
also plays role in establishing LT:
- fibre type
- capillary density
- mito size and number
- enzyme conc
much different CV system, since functional capacity is determined by the muscle mass activated in exercise
racial diffs in vo2max
african runners inc fatigue resistance, despite similar vo2max values
- have greater running economy
- perform better in heat
why is vo2max important
for aerobic performance, %vo2max can determine sustainability and intensity of training
best indicator of health
if inc vo2 max by 1 MET:
- dec BGP by 5mmhg
- dec risk CVD by 15%
- dec all mortality by 13%
metabolic changes with ET
- increased capacity: for aerobic exercise
- inc guel storage: fuel changes i.e. 2x muscle glycogen content
- inc IMTG stores
- inc fat as fuel reliance
- results in glycogen sparing - glycogen sparing:
- inc musc glycogen, inc glycolysis reliance
- less glycogen used across all submax intensities
mitochondrial content during ET
in muscle: sarcolemmal mito are below sarcolemma
- intermyofibrillar mitochondria proteins surround contractile proteins, 80% of mito
mito content inc quickly thru training, especially during ET
- can inc 50-100% during first 6 weeks ET
inc endurance perf bcs of changes in muscle metabolism
intensity is key to gains, not just action of exercise
summary metabolic adaptations for trained ET
vo2max: inc at max
carb use: dec at rest/submax, inc at max
fat use: inc across all intensities
total energy: inc at max
fit will use fat faster, but use carbs at higher rate i.e. PCr to inc speed
muscle changes with ET
- shift to type 1 fibres: fast to slow twitch shift
- dec fast myosin, inc slow myo
- degree of change depends on training and genetics - less fatigue, handle metabolic differences better
CV changes with ET
- inc heart function:
- inc SV, bcs heart muscle/walls hypertrophy for inc contraction
- inc Q bcs of SV
- shorter duration training i.e. 4 months, inc in SV > inc in a-vo2 diff
- long training, inc a-vo2 > SV - inc a-vo2 diff: bcs of inc muscle BF, inc extraction
- inc BF redistribution: due to dec SNS activity and less vasoconstriction
other ET adaptations
blood vol inc
total hemo content inc slightly
ET - CV adaptations summary
vo2: same at rest/submax, inc at max
Q: inc at max
SV: increases at all intensities
HR: dec at rest/submax, normal at max
capillary density inc
respiratory changes with ET
- inc resp muscle fatigue resistance
- inc breathing pattern: deep, less freq
- inc gas exchange at lungs
VE dec at given intensity, inc gas exchange
no structural changes bcs ventilation isn’t a limiting facotr
- max vol ventilation > VE
submax: dec VE, freq, TV, and diffusion
max: inc VE, freq, TV, diffusion
inc mvmnt of air causes:
- inc breathing rate, lungs ability to expand
- inc BF and CSA for exchange, inc alveoli
overall summary ET adaptations, comparison to IT and RT
does not change fibre size, tho CSA of fibre type 1 can inc by 20%
no changes of neural recruitment patterns
main outcomes:
- fatigue resistance bcs inc vo2max, qmax, etc.
- changes of substrate use i.e. fat as fuel, carb sparing
RT enzyme changes
creatine kinase
PFK, hexokinase, LDH all inc
interval training
alternate periods of intense exercise w periods of low intensity or complete recovery
HIIT
high intensity interval training
brief bouts exercise w short recovery periods
SIT
sprint interval training
“all out” at supramaximal efforts
i.e. sprints, wingate
MICT
moderate intensity continuous training
v similar results to SIT
HIIT takes 1/40th time of training for same results
burns more calories than SIT
fat loss with SIT
improves aerobic performance but not Qmax
facilitates fat loss in women
2 mins of SIT elicits 24h o2 conusmption simialr to 30mins continuous ET/MICT
- inc post exercise metabolism
HIIT and SIT health outcomes
similar to continuous i.e. CV fitness, body comp changes
also improves insulin sensitivity, glucose handling, appetite
interval training adaptations
depends on interval protocol i.e. intensity, duration
can result in similiar adaptations to ET by inc aerobic metabolism
also improves anaerobic metabolism:
- inc glycolytic enzymes PFK and HK
- inc musc buffering capacity
- inc acid-base balance
resistance training
any training that uses resistance to inc force of muscle contraction
- aka strength training
based on progressive overload of muscles
percentage of gains is inversely proportional to initial strength (diminishing returns)
- genetic limitations to gains
- high resistance i.e. 2-10 RPM will inc strength
- low resistance i.e. 20+ RPM inc endurance
muscular strength vs endurance
strength: max force a muscle can generate
- 1-RPM is 1 rep max
endurance: ability to make repeated contractions against submaximal load
why is eating protein important
will have higher gains and lower losses when fasting
neural system adaptations to RT
- reduced neural inhibition: dec coactivation of agonist and antagonist…may be acute or chronic
- MU firing rate: CNS fires the same MU more times, which inc output of muscle
- MU recruitment: more muscle fibres produce more force
during regular RT set, a certain MU pool fires at constant rate to generate force
- as inc reps, fatigue occurs
- must either inc firing rate or MU recruitment to overcome loss of force
autogenic inhibition
muscle prevents itself from causing damage i.e. GTOs
- explains feats of strenght
muscular system changes w RT
hypertrophy: inc muscle fibre size (myofilaments) as result of training and diet
hyperplasia: inc muscle fibre number, mixed evidence
both will inc muscle CSA…genetics important role
- if have fewer fibres, won’t get as big despite training
fibre type alterations: training moves musc fibres to functional types
- i.e. strength athlete inc type 2
- detraining moves back to OG state
myonuclear addition
myofibrillar proteins inc myofibre CSA
caused by RT
transient vs chronic hypertrophy
transient hypertrophy: the “pump” caused by fluid accumulation
chronic hypertrophy: real gains in muscle mass, net muscle protein growth
- LT inc in protein synthesis
belgian blue
mutation of myostatin
undergo hyperplasia and get 2x muscle fibres
metabolic changes with RT
- immediate energy: inc PCr stores and resynthesis
- glycolytic changes: inc content and function of PFK
- oxidative changes: little change w RT, but can still inc
CV sys changes w RT
RT places different stress on CV than MICT
stimulates muscle capillarization, maintain cap density w dec muscle mass
inc in muscle size DOES NOT dec muscle endurance
other adaptations with RT
body composition changes: inc fat free mass i.e. musc, bone
- inc muscle leads to inc daily energy expenditure, inc calories to maintain
hormonal changes: acute changes
- chronic elevation in testosterone inc muscle size
- inc hormone sensitivty
detraining
when detraining occurs, it’s easier to retrain earlier than later
- dec perf, dec vo2max by 8% in 12 days, 20% after 84 days
decline in CV system: rapid dec in SVmax and blood volume
- dec a-vo2
- dec type 2a, inc type 2x
dec oxidative enzyme activity
dec muscle glycogen
disturbed acid base balance
retraining and vo2max
mitochondria quickly adapt to training, double w/in 5 wks
is also lost quickly…dec 50% in 1 wk of detraining
takes 3-4 wks w retraining
interference of RT and ET
endurance = inc mitochondrial protein
resistance = inc contractile protein
strength WITH endurance leads to smaller strength gains…dec muscle hypertrophy
ET inhibits RT, but RT doesn’t inhibit ET
important to strength train to improve speed w ET
why does RT/ET interference occur
neural factors: impaired MU recruitment…limited evidence
low muscle glycogen content: due to successive bouts of ET
- dec intensity of subsequent RT
overtraining - no direct evidence
depressed protein synthesis: ET adaptations interfere w protein synthesis via INHIBITING mTOR
overtraining
produces an autonomic nervous system imbalance
SNS overdrive during rest, causes restlessness, weight loss, inc resting HR
PNS overdrive during exercise causes fatige and depression
- severe cases = exhaust endocrine system
causes inc cortisol, dec testosterone and thyroxine
mood states are sensitive to training, inc disturbances when overtrained
signs of overtraining
- dec perf, strength, coordination
- fatigue
- irritable, anxious
- depressed
- dec motivation and mental conc
- sleep disturbatnces
- weight loss, appetite changes
causes of overtraining
multifactoral
- nutrition
- psych factors
- emotional stress
- periods of excessive training
- depressed immune function
- disturbances in endocrine function
- abnormal resp of ANS
muscular impact of overtraining
- glycogen depletion
- membrane damage
- mitochondria dysfunction
- reduced EC coupling
- inc ROS
- inflammation and cytokine signalling
- creatine kinase efflux
treating overtraining
best to avoid by ID signs
rest and recovery, fully remove stim…can take months
what can training improve
health
body comp, immune sys, MSK health
dec disease i.e. CV, diabetes
dec risk of all cause mortality
protein synthesis w training
all training adaptations occur bcs of inc protein synth
RT will inc contractile proteins…leads to actin/myo
ET –> mito proteins
lasts for 2-4 days post training if dietary fibre and energy adequate
occurs when prim signal –> sensory protein –> kinase signaling cascade –> reg protein –> changed cellular function
big picture of training adaptations
training inc specific muscle proteins
- exercise stress activates transcription
- activates genes to make new proteins
musc contraction activates prim and secondary messengers
- peaks in 4-8hrs, back to baseline after 24hr
- why need freq exercise
- daily exercise cumulates effects and inc protein
primary signals
- mechanical stress: force on fibre triggers adaptations i.e. mechanoreceptors
- calcium: activates calmodulin dependent kinase (CAMK), which signals cascade
- free radicals
- phosphate: exercise inc AMP/ATP ratio, which causes cascade by activating AMPK
secondary messengers
- AMPK: glucose uptake, FFA oxidation, mitochondrial biogenesis
- PGC-1a: inc capillaries, mito, antioxidant enzymes
- activated by ROS and AMPK - calcineurin: fibre growth, fast to slow fibre change
- mTOR/IGF-1: musc growth from RT
- NFkB: antioxidant enzymes, protects against free radicals
training and messengers
RT: mTOR, results in hypertrophy
ET: CaMK and PGC-1a, cause mitochondria biogenesis
any reduction of musc strength training can be improved w rest b/w sessions
how does exercise initiate cascae
exercise results in homeostasis disturbance
metabolic:
- calcium: calmodulin dependent kinase/CaMK, calcineurin
- energy metabolis: AMPK, ROS
mechanica;: musc stretch or altered tension
- calcineurin
- IGF
- MAPK
ET and messengers
inc Ca:
–> inc calcineurin
–> fast to slow fibre shift
inc Ca:
–> inc camk
–> PGC-1a
–> mito biogenesis
inc AMP/ATP:
–> AMPK
–> PGC-1a
–> mito biogenesis
inc free radicals:
–> NFkB
–> synth of antioxidant enzymes
takes hours to activate PGC-1a
RT and messenger
musc stretch
–> IGF-1
–> Akt
–> mTOR
–> protein synth
leads to musc hypertrophy
