Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

KP322 > vo2max and training > Flashcards

vo2max and training Flashcards

(60 cards)

Start Studying
1
Q

exercise vs training

A

exercise = single bout
training = repetitive bouts

exercise types: endurance/aerobic, resistance/anaerobic, interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

FITT principle

A

frequency, intensity, time, type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

principles of training

A
  1. overload: system worked beyond normal i.e. intensity
  2. reversibility: detraining, gains lost when overload removed
  3. specificity: muscle fibres and energy systems involved i.e. chest musc when bench press
    - type and velocity of contraction
  4. individuality: genetic susceptibility
  5. diminishing returns: less trained will improve faster
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

oxygen yptake

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

vo2max determinants

A
  1. o2 delivery to muscle - CV sys
  2. o2 utilization by musc - mito content

delivery is most important because limits vo2max

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

vo2peak

A

highest value on a max test

not necessarily highest possible value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

vo2max

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how to tell if vo2max is reached

A
  1. plateau in vo2…ideal
  2. RER > 1.15
  3. reach age predicted HRmax
  4. high blood lactate, 8x rest
  5. voluntary exhaustion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

vo2 tests

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

is vo2max the end all? factors of vo2

A
  1. genetics
  2. bio sex: women inc fat, hemo content, CV system i.e. Qmax and BF diffs
  3. age
  4. body size and composition
  5. training status
  6. mode of exercise i.e. endurance vs strength
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

OBLA/LT and vo2max

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

racial diffs in vo2max

A

african runners inc fatigue resistance, despite similar vo2max values
- have greater running economy
- perform better in heat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

why is vo2max important

A

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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

metabolic changes with ET

A
  1. increased capacity: for aerobic exercise
  2. inc guel storage: fuel changes i.e. 2x muscle glycogen content
    - inc IMTG stores
    - inc fat as fuel reliance
    - results in glycogen sparing
  3. glycogen sparing:
    - inc musc glycogen, inc glycolysis reliance
    - less glycogen used across all submax intensities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

mitochondrial content during ET

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

summary metabolic adaptations for trained ET

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

muscle changes with ET

A
  1. shift to type 1 fibres: fast to slow twitch shift
    - dec fast myosin, inc slow myo
    - degree of change depends on training and genetics
  2. less fatigue, handle metabolic differences better
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CV changes with ET

A
  1. 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
  2. inc a-vo2 diff: bcs of inc muscle BF, inc extraction
  3. inc BF redistribution: due to dec SNS activity and less vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

other ET adaptations

A

blood vol inc
total hemo content inc slightly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ET - CV adaptations summary

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

respiratory changes with ET

A
  1. inc resp muscle fatigue resistance
  2. inc breathing pattern: deep, less freq
  3. 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

overall summary ET adaptations, comparison to IT and RT

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

RT enzyme changes

A

creatine kinase
PFK, hexokinase, LDH all inc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

interval training

A

alternate periods of intense exercise w periods of low intensity or complete recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
HIIT
high intensity interval training brief bouts exercise w short recovery periods
26
SIT
sprint interval training "all out" at supramaximal efforts i.e. sprints, wingate
27
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
28
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
29
HIIT and SIT health outcomes
similar to continuous i.e. CV fitness, body comp changes also improves insulin sensitivity, glucose handling, appetite
30
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
31
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
32
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
33
why is eating protein important
will have higher gains and lower losses when fasting
34
neural system adaptations to RT
1. reduced neural inhibition: dec coactivation of agonist and antagonist...may be acute or chronic 2. MU firing rate: CNS fires the same MU more times, which inc output of muscle 3. 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
35
autogenic inhibition
muscle prevents itself from causing damage i.e. GTOs - explains feats of strenght
36
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
37
myonuclear addition
myofibrillar proteins inc myofibre CSA caused by RT
38
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
39
belgian blue
mutation of myostatin undergo hyperplasia and get 2x muscle fibres
40
metabolic changes with RT
1. immediate energy: inc PCr stores and resynthesis 2. glycolytic changes: inc content and function of PFK 3. oxidative changes: little change w RT, but can still inc
41
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
42
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
43
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
44
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
45
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
46
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
47
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
48
signs of overtraining
- dec perf, strength, coordination - fatigue - irritable, anxious - depressed - dec motivation and mental conc - sleep disturbatnces - weight loss, appetite changes
49
causes of overtraining
multifactoral 1. nutrition 2. psych factors 3. emotional stress 4. periods of excessive training 5. depressed immune function 6. disturbances in endocrine function 7. abnormal resp of ANS
50
muscular impact of overtraining
1. glycogen depletion 2. membrane damage 3. mitochondria dysfunction 4. reduced EC coupling 5. inc ROS 6. inflammation and cytokine signalling 7. creatine kinase efflux
51
treating overtraining
best to avoid by ID signs rest and recovery, fully remove stim...can take months
52
what can training improve
health body comp, immune sys, MSK health dec disease i.e. CV, diabetes dec risk of all cause mortality
53
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
54
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
55
primary signals
1. mechanical stress: force on fibre triggers adaptations i.e. mechanoreceptors 2. calcium: activates calmodulin dependent kinase (CAMK), which signals cascade 3. free radicals 4. phosphate: exercise inc AMP/ATP ratio, which causes cascade by activating AMPK
56
secondary messengers
1. AMPK: glucose uptake, FFA oxidation, mitochondrial biogenesis 2. PGC-1a: inc capillaries, mito, antioxidant enzymes - activated by ROS and AMPK 3. calcineurin: fibre growth, fast to slow fibre change 4. mTOR/IGF-1: musc growth from RT 5. NFkB: antioxidant enzymes, protects against free radicals
57
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
58
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
59
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
60
RT and messenger
musc stretch --> IGF-1 --> Akt --> mTOR --> protein synth leads to musc hypertrophy

KP322 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions