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KP322 > vo2max and training > Flashcards

vo2max and training Flashcards

1
Q

exercise vs training

A

exercise = single bout
training = repetitive bouts

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

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2
Q

FITT principle

A

frequency, intensity, time, type

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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
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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

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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

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6
Q

vo2peak

A

highest value on a max test

not necessarily highest possible value

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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

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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
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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

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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
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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

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12
Q

racial diffs in vo2max

A

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

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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%

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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
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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

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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

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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
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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
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19
Q

other ET adaptations

A

blood vol inc
total hemo content inc slightly

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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

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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

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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

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23
Q

RT enzyme changes

A

creatine kinase
PFK, hexokinase, LDH all inc

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24
Q

interval training

A

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

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25
Q

HIIT

A

high intensity interval training

brief bouts exercise w short recovery periods

26
Q

SIT

A

sprint interval training

“all out” at supramaximal efforts

i.e. sprints, wingate

27
Q

MICT

A

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
Q

fat loss with SIT

A

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
Q

HIIT and SIT health outcomes

A

similar to continuous i.e. CV fitness, body comp changes

also improves insulin sensitivity, glucose handling, appetite

30
Q

interval training adaptations

A

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
Q

resistance training

A

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
Q

muscular strength vs endurance

A

strength: max force a muscle can generate
- 1-RPM is 1 rep max

endurance: ability to make repeated contractions against submaximal load

33
Q

why is eating protein important

A

will have higher gains and lower losses when fasting

34
Q

neural system adaptations to RT

A
  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
Q

autogenic inhibition

A

muscle prevents itself from causing damage i.e. GTOs
- explains feats of strenght

36
Q

muscular system changes w RT

A

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
Q

myonuclear addition

A

myofibrillar proteins inc myofibre CSA

caused by RT

38
Q

transient vs chronic hypertrophy

A

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
Q

belgian blue

A

mutation of myostatin

undergo hyperplasia and get 2x muscle fibres

40
Q

metabolic changes with RT

A
  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
Q

CV sys changes w RT

A

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
Q

other adaptations with RT

A

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
Q

detraining

A

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
Q

retraining and vo2max

A

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
Q

interference of RT and ET

A

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
Q

why does RT/ET interference occur

A

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
Q

overtraining

A

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
Q

signs of overtraining

A
  • dec perf, strength, coordination
  • fatigue
  • irritable, anxious
  • depressed
  • dec motivation and mental conc
  • sleep disturbatnces
  • weight loss, appetite changes
49
Q

causes of overtraining

A

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
Q

muscular impact of overtraining

A
  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
Q

treating overtraining

A

best to avoid by ID signs

rest and recovery, fully remove stim…can take months

52
Q

what can training improve

A

health
body comp, immune sys, MSK health
dec disease i.e. CV, diabetes
dec risk of all cause mortality

53
Q

protein synthesis w training

A

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
Q

big picture of training adaptations

A

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
Q

primary signals

A
  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
Q

secondary messengers

A
  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
Q

training and messengers

A

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
Q

how does exercise initiate cascae

A

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
Q

ET and messengers

A

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
Q

RT and messenger

A

musc stretch
–> IGF-1
–> Akt
–> mTOR
–> protein synth

leads to musc hypertrophy

KP322 (9 decks)

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