U4 VCE PE CHRONIC TRAINING ADAPTATIONS

aerobic training - respiratory, CV, muscular chronic adaptations, anaerobic training chronic adaptations, vo2 max, LIP vs lactate tolerance

acute responses vs chronic adaptations

acute responses → bodys immediate change to exercise and lasts for the duration of exercise.

chronic adaptations → long term training effects, occur due to bodies changing to better meet training demands. In response to

• type of training, intensity, duration, frequency, individual training status & capacity

aerobic based training methods vs anaerobic based training methods

aerobic → to improve vo2 max, LIP

• continuous

• long-interval

• HIIT

• fartlek

anaerobic → to improve muscular strength, muscular power, lactate tolerance, speed, force

• short interval

• intermediate interval

• resistance

• plyometric

• circuit (depending on time)

aerobic respiratory, cardiovascular, muscular st adaptations

all improve vo2 max and LIP

RESPIRATORY → inc uptake o2

• Inc TV

• inc V

• dec resting & submax RR

• inc alveolar and pulmonary diffusion

CARDIOVASCULAR → inc transport of o2 to working muscles, improve removal of wastes & metabolic by-products

• inc SV

• inc Q

• dec resting & submax HR

• inc heart capillarisation

• inc blood volume

• inc blood sent to muscles

MUSCULAR → inc utilisation of o2 by muscles to make aerobic ATP

• inc aerobic atp via inc mitochondrial density

• inc a-vo2 diff

• inc oxidative enzymes

• inc glycogen stores

• inc myoglobin

• inc fat oxidation

anaerobic muscular and neuromuscular adaptations

all improve lactate tolerance, force, speed, power, strength

MUSCULAR

• muscle hypertrophy

• inc anaerobic enzymes

• inc fuel stores

• imp anaerobic/glycolytic capacity

NEUROMUSCULAR

• inc motor unit recruitment

• imp synchronisation of motor units

• inc motor unit firing freq

• dec neural inhibition

respiratory ca aerobic - INC TIDAL VOLUME

amount of air breathed in and out per breath.

• how?diaphragm & intercostal muscles improve in efficiency (contract more forcefully & expand lung volume & rib cage)

• why? more air taken in for o2 to diffuse into capillaries surrounding alveoli.

• has finite capacity due to chest cavity expansion , then itll plateau

respiratory ca aerobic - INC PULMONARY AND ALVEOLAR DIFFUSION

gas exchange → swapping o2 & co2 from high to low conc. Pulmonary is lungs

• o2 in alveoli diffuse to capillaries and co2 come out of muscles exchange w o2 in cap and exhaled

• Size and no. alveoli in lungs inc from aerobic based training. → inc SA for o2 & co2 to diffuse.

• Why? to provide more o2 to working muscles and remove inc co2 lvls

alveolar capillary interface - alveoli & cap

tissue capillary interface - muscle cell & cap

respiratory ca aerobic - DEC RESTING & SUBMAXIMAL RESPIRATORY RATE

RR → no. breaths taken per min.

• lungs have inc efficiency by taking in larger amount of o2 at less energy = dec in RR cause fewer breaths taken per min for submax workload can be met.

• dec rate of fatigue, by working at higher aerobic workload with less o2 & fuel usage

• RR plateaus along with HR due to steady state (o2 demand is met with o2 supply)

  • trained athlete would have a lower steady state and reach it sooner (quicker) than an untrained

respiratory ca aerobic - INC MAXIMAL VENTILATION

VE/V → TVxRR=V, volume/how much air inspired and expired per min. L/min

• V continue to inc and when TV plateaus, RR continues inc.

• aerobic training → larger amounts of air inhaled/exhaled per min = more o2 available for diffusion to transport to working muscles

cv ca aerobic - INC STROKE VOLUME

sv → amount of blood ejected from left ventricle per beat

• heart muscle undergo hypertrophy and the ventricles INCREASE IN SIZE = greater capacity to take in & squeeze blood per beat & contract forcefully. → more o2 transport to working muscles & perform longer at higher intensities

• higher sv = can respond quicker to inc o2 demands and reach steady state sooner.

cv ca aerobic - DEC RESTING & SUBMAXIMAL HEART RATES

hr → no. heartbeats per min.

• heart pump out more blood then dont need to pump as frequently to supply muscles w o2 & fuels.

cv ca aerobic - INC HEART CAPILLARISAITON

Aerobic training leads to inc cross-sectional area of coronary arteries & capillaries that supply the heart

• Inc arterial size & capillary no. = more blood reaching the heart = more o2 feeding the heart to be pumped to working muscles

cv ca aerobic - INC CARDIAC OUTPUT

Q → amount of blood ejected out of left ventricle per min. HR x SV

• more blood = more oxygen pumped

cv ca aerobic - INC BLOOD VOLUME

inc in plasma → reduces blood viscosity so it can flow faster rate throughout the body, maintain thermoreg, remove wastes from cells.

• o2 transported to muscles faster to make aerobic ATP

• remove waste product by transporting it to liver, lungs, kidney, skin

• transport fuels, electrolytes & hormones

cv ca aerobic - INC MUSCLE CAPILLARISATION

capillaries = small blood vessels where diffusion occurs. Transfer blood to and from muscles.

capillarisation (capillaries supplying muscles inc in size & number).

high muscle capillary density = larger SA for muscle tissue capillary interface, oxygen can diffuse shorter distances = greater gas exchange, fuels and remove waste from muscles

• more quick waste removed = faster repair & recovery

• inc in blood flow to muscle = inc supply of o2 & fuel to produce energy

• muscles work at higher intensities aerobically longer w/o acc of fatiguing by-products.

cv ca aerobic - REDISTRIBUTION OF BLOOD

vascular shunt → process of redistributing blood via simultaneous vasoconstriction & vasodilation

• more blood = more o2 & fuel supplied & more waste removed to meet exercise demand and delay the onset of fatigue if blood is redistributed better

muscular ca aerobic - INC MITOCHONDRIAL DENSITY

mitochondria → responsible for producing energy from food fuels via aerobic respiration

• inc in size & no. mitochondria to meet aerobic demand on muscles (st fibres) = more use of o2 to make atp

inc in mitochondrial enzymes → make aerobic atp at a faster rate

muscular ca aerobic - INC ARTERIOVENOUS OXYGEN DIFFERENCE

a-vo2 diff → measure of amount of o2 taken up from blood by tissues. Its the diff in o2 conc in arterial blood vs venous blood per 100mL. Diff in o2 conc between arterioles & venules. (arterial always higher)

• aerobic training lets muscles extract more o2. A-vo2 diff inc submaximally and maximally (avo2 diff plateaus during steady state cause o2 demand met)

• an inc in avo2 can be due to → inc in myoglobin, inc mitochondria, inc ability of oxidative enzymes to make more aerobic atp, more capillaries at muscles

  • myoglobin stores o2 and transports it to mitochondria in muscle.

  • more capillaries = more o2 transported to muscle → more myoglobin can extract o2 from it and store o2 and give to mitochondria → more mitochondria can make aerobic atp and use oxidative enzymes to convert the fuels to atp

muscular ca aerobic - INC OXIDATIVE ENZYMES

oxidative enzymes - ATP SYNTHASE - convert adp & phosphate to atp in mitochondria.

• lesser extent glycolytic enzymes cause aerobic training targets fats as fuel source

• inc amount of aerobic atp being made → it dec the involvement of anaerobic energy systems to produce ATP

muscular ca aerobic - INC GLYCOGEN STORES

inc stores of muscle & liver glycogen in st fibres.

• carbs preferred exercuse fuel due to rapid breakdown & lower use of o2 than fats → any inc in availability = imp endurance performance

muscular ca aerobic - INC FAT OXIDATION

inc in intramuscular triglycerides and free fatty acids to fuel oxidative enzymes = in ability to oxidise fat.

• oxidise fat submaximally = conserve glycogen stores (GLYCOGEN SPARING)

• theres limited stores of liver glycogen and fat is rare to run out

• glycogen sparing allows endurance athlete to use more fat for aerobic atp whilst at steady state

  • extends carb availability

  • inc ability to use carb when working above LIP (surges to finish line)

muscular ca aerobic - INC MYOGLOBIN

myoglobin → transports o2 from bloodstream into muscle to mitochondria

• mitochondria density inc → so does need for o2 delivery to inc via capillaries and need more myoglobin to give o2

muscular ca ANAerobic - MUSCLE HYPERTROPHY

anaerobic training targets ft 2b fibres & 2a inc in cross-sectional area of myofibrils (makes up the muscle fibre) and inc in no. actin and myosin filaments (protein filaments responsible for muscle contractions)

muscular hypertrophy leads to inc contraction speed & force production

larger myofibrils → can store more anaerobic fuels (ATP, CP, glycogen) → this allows enzymes to be able to convert more fuels for energy as fast as possible.

muscular ca ANAerobic -INC ANAEROBIC ENZYMES

anaerobic enzymes that allow ATP and CP to be broken down rapidly → ATPase and creatine kinase. (think ATP & C)

• makes energy for explosive and powerful muscle contractions

GLYCOLTIC ENZYMES → responsible for production of atp from adp using glucose as food fuel.

muscular ca ANAerobic - INC FUEL STORES

ft fibres 2a & 2b need fuels to produce atp anaerobically (CP, ATP and CHO)

• these substrates have large myofibrils in which the fuels can be stored

• more atp & cp fuels means can use the anaerobic energy systems for longer

muscular ca ANAerobic - IMPROVED ANAEROBIC CAPACITY

ability to produce energy via 2 anaerobic energy systems → ATP-CP and anagly system.

• inc cp & glycogen stores & anaerobic enzymes → inc the rate & duration of anaerobic energy for events 400m

neuromuscular ca ANAerobic - INC MU RECRUITMENT, IMP SYNCHRONISATION OF MU, INC MU FIRING FREQUENCY, DEC NEURAL INHIBITION

imp MU recruitment

plyometrics, short-int and resistance training targets ft fibres and enhance body ability to recruit motor units.

• motor unit →a motor neuron and all the muscle fibres it stimulates

• more motor units recruited in muscle = greater force generated

• small motor units = lower force

imp synchronisation of MU

• MU recruited from small→large with st first.

• heavy load → st begin then ft take over. INC in load → the CNS recruit high threshold mu (if lighter load then recruit low threshold mu bc low intensity.

• resistance, short-int, inter-int training result in rapid involvement of high threshold mu & synchronise activation of more mu.

• plyo inc neuromuscular performance by inc set speed muscles perform

inc MU firing freq

• resistance & plyo inc firing rate of neural impulse to indiv mu. (rate coding = freq of mu discharge signals)

• rate coding only works if successive signals r sent to muscle fibre before it relax from previous one → leads to summation of impulses to produce higher contractile forces.

• more mu firing freq = more force and SPEED

dec neural inhibition

• tendons have built in protective mechanism receptors (golgi tendon organs) → when detects excessive tension there is a reflex and muscle force dec.

• resistance training dec. inhibitory signals sent so muscles generate more force and low injury risk.

what is vo2max

vo2 max → max amount of o2 that can be taken up, transported and utilised by muscles to produce ATP

absolute vo2 max → amount of o2 taken in per min. L/min

relative vo2 max → amount of o2 taken in per kg of body weight per min, measured in millilitres per kg per min mL/kg/min. Takes into account body weight for easier comparison

• doing aerobic training allows for greater vo2 max so athletes can take in/transport/utilise o2 more efficiently and effectively so they can work longer at higher intensities aerobically.

lactate inflection point vs lactate tolerance

LIP → intensity where blood lactate is at steady state. Lactate production is equal to lactate removal.

• aimed at delaying accumulation of H+ ions

• higher LIP = able to work at higher intensities aerobically w/o H+ accumulation

• aerobic based training

• working ABOVE LIP → sharp inc in lactate & h+ ion leading to fatigue

• trained athletes have higher LIP and because they have more o2 and higher vo2max they can clear lactate production and make aerobic atp so no h+ ion and lactate can be converted back into energy

• UNTRAINED LIP → 55-70% VO2MAX 70-80%MHR

• TRAINED LIP → 75-90%VO2MAX 85-95%MHR

• continuous and HIIT training improve LIP (hiit good for athlete).

• athletes should also train lactate tolerance for their surges at end of race. If they have a good lactate tolerance they can buffer out h+ ions and reduce fatigue so they can sprint to the end.

lactate tolerance → ability to buffer accumulating lactic acid so it doesnt interfere w muscle contractions.

• higher lactate tolerance = able to cope with H+ accumulation when working above LIP → good for surges

• anaerobic based training

• H+ acc incs acidity = dec muscle contraction forces bc neuromuscular system dont function well → slow down dec workload

• intermediate int training focuses on anagly system and this inc muscle buffers, exposing us to high lvls of H+ regularly and body adapts to it = buffer effect and inc lactate tolerance.

  • muscle buffering → ability of muscle to neutralise accumulating lactic acid in high intensity exercise → delaying onset of fatigue

  • this helps stabilise pH of muscles. After event there is high lactate lvls.

• allows athlete to work higher intensity for linger, imp energy production of anagly, more frequent high intensity effort w less fatigue,

• UNTRAINED LACTATE TOLERANCE → 80-95%MHR

• TRAINED LACTATE TOLERANCE → 95-100%MHR

lactate clearance

from inc LIP

• greater mitochondrial density to make aerobic atp and oxidise lactate to pyruvate

• inc transport of lactate from muscle to blood stream

• greater conversion of lactate back to glucose to produce more atp

heart

aerobic → bigger capacity so inc in overall size, more stroke volume

anaerobic → thickness of ventricle inc for greater force