Week 9- effects of aerobic and anaerobic training Flashcards
What should you consider when training and performing?
-sources of energy and fibres used for force production
-contributions of the ATP-PC system, anaerobic glycolysis and aerobic metabolism during maximal effort
-muscle fibres recruitment in increased intensities
What are the principles of training?
-Overload
-Specificity
-Reversibility
When does training effects occur?
when physiological system is exercised at a level beyond which it is normally accustomed to
What is training effect specific to?
-muscle fibre recruitment during exercise
-energy systems involved
-velocity of contraction
-type of contraction
What is the definition of reversibility?
gains are lost when training ceases
What should your training be to increase VO2max?
20-60mins, >3x per week, >50% VO2max
How much of VO2max is determined by genetics?
50% in sedentary adults
What do low responders to exercising training VO2max improve to?
2-3%
what do high responders VO2max increase to following exercise?
by 50% with vigorous training
what is the average improvement to VO2max to exercise?
15-20%
What is the primary cause of differences in VO2max between individuals?
SVmax
How does short duration training increase VO2max?
increase in SV
How does longer duration training increase VO2max?
SV and a-VO2 increase
How does endurance training increase stroke volume?
-increase preload (EDV)
-increased plasma volume
-increase venous return
-increased ventricular volume
-decreased afterload
-decreased arterial constriction
increased maximal muscle blood flow with no change in arterial mean pressure
-increased contractility
When does 12-20% increase in plasma volume occur?
after 3-6 aerobic training sessions
What is eccentric hypertrophy?
when chamber wall and wall thickness is increased
With any given submaximal workload what effect does it have on HR following training?
lower heart rate due to an increase in stroke volume
What is the consequences of HR being lower after training?
-cardiac output is achieved in fewer beats
-vagal tone is increased
-allows for greater ventricle filling time (EDV)
What are the training-induced increases in arteriovenous O2 difference?
-muscle blood flow increased
-improved ability of muscle fibres to extract and utilise O2 from the blood
What causes the muscle blood flow to increase?
-decrease in SNS vasoconstriction
-increased diameter of compliant arteries
-increased arterial diameter is specific to limb being used
-permits greater ‘volume of flow per beat’ to limb
What allows for an improved ability of muscle fibres to extract and utilise oxygen from the blood?
-increased capillary density
-increased mitochondrial number/volume
What is the effect of increased number of capillaries?
shorter diffusion distance
After training, what results in improved oxidative capacity and ability to utilise fat as fuel?
increase in mitochondria in the muscle
How long does it take for muscle mitochondria number to double?
5 weeks
Why is blood flow in trained muscle lower?
A-V difference is greater and therefore better oxygen extraction
What is the ability to perform prolonged, submaximal exercise dependent on?
ability to maintain homeostasis
What does the training-induced improvements in homeostatic pressure result in?
-more rapid transition from rest to stead state
-a reduced reliance on limited liver and muscle glycogen stores
-numerous cardiovascular and thermoregulatory adaptations that assist in maintaining homeostasis.
What are the adaptations of endurance exercise training in muscle fibres that assist in maintaining homeostasis?
-shift in muscle fibre type (fast-to-slow) and increase in number of capillaries
-increased mitochondrial volume
-training-induced training in fuel utilisation
-increased antioxidant capacity
-improved acid base regulation
What is the difference between slow myosin isoform and fast myosin isoform?
slow myosin isoform have lower myosin ATPase activity but better efficiency
What determines the magnitude of fibre type change?
duration and intensity of training and genetics
What does the increased number of capillaries surrounding muscle fibres impact?
-enhanced diffusion of oxygen
-improved removal of wastes
What is mitochondrial turnover?
breakdown of damaged mitochondria and replaced with healthy mitochondria
What is the breakdown of damaged mitochondria termed?
mitophagy
What does the increase in mitochondrial volume result in?
-Greater capacity for oxidative phosphorylation
-decreased ADP due to increased ADP transporters in mitochondrial membrane
What does the decrease in cystolic (ADP) result in?
-less lactate and H formation
-less PC depletion
What is a result of high fat utilisation for energy production?
-spares plasma glucose and muscle glycogen
How does endurance training adaptations improve plasma FFA transport and oxidation?
- increased capillary density
-fatty acid binding protein and fatty acid translocase
-higher levels of carnitine palmitoyl transferase and FAT
-increased enzymes of b-oxidation
-increased rate of acetyl-CoA formation
-High citrate level inhibits PFK and glycolysis
What is a radical?
chemical molecule that contains unpaired electrons, making them highly reactive
What can radicals damage?
Proteins, cell membrane and DNA
What doe radicals promote?
oxidative damage and muscle fatigue
What does training increasing endogenous antioxidant enzymes improve and protect?
-improves the fibres ability to remove radicals
-protects against exercise induced oxidative damage and muscle fatigue
What happens if there is less carbohydrate utilisation?
less lactate formation
What does an increased NADH shuttles reduce?
the availability of NADH for lactic acid formation
What does endurance and resistance exercise training promote?
protein synthesis in fibres
What does exercise ‘stress’ activate?
gene transcription
What is the process of exercise-induced muscle adaptations?
-muscle contraction activates primary and secondary messengers
-results in expression of genes and synthesis of new proteins
-mRNA levels typically in 4-8 hours, back to baseline within 24hrs
-daily exercise require for training-induced adaptations
What are the primary signals for muscle adaptations?
-mechanical stretch (resistance training)
-calcium (endurance training)
-AMP/ATP
-Free radicals
What are the secondary messengers in skeletal muscles?
-AMP kinase
-Mitogen
-PGC-1a
-Calmodulin- dependent kinase
-Calcineurin (phosphates)
-Nuclear factor Kappa B (NFkB)
-mTOR
Why is AMPK important?
promotes glucose uptake and linked to gene expression by activation of transcriptional activating factors
What is PGC-1a the master regulator of?
mitochondrial biogenesis
promotes angiogenesis
synthesis of antioxidant enzymes
When is calmodulin-dependent kinase activated?
by increases in cytosolic Ca- promotes activation of PGC-1a
What does calcineurin participate in?
-fibre regeneration
-fast to slow fibre switch
What does NFkB promote?
synthesis of antioxidant enzymes
what does mTOR regulate?
protein synthesis and muscle size
What causes training-induced reductions in heart rate and ventilation?
-reduced ‘feedback’ from muscle chemoreceptors to cardiovascular control centre from group 3 and 4 nerve fibres
-reduced number of motor units recruited
What does improvement in muscle fibre oxidative capacity result in?
fewer motor units required for submaximal work
What are the consequences of detraining?
-rapid decrease in VO2max
-decrease in SVmax
-decrease in maximal a-vO2 difference
–decrease in mitochondria
–decrease in oxidative capacity
–decrease in type IIa fibres and increases Type IIx fibres
What is detraining primarily due to?
changes in mitochondria
When are the majority of the adaptations lost?
in two weeks
How long does it require of retraining to regain mitochondrial adaptations?
3-4 weeks
What muscle fibre types are recruited with anaerobic adaptation?
Type I and II
What does sprint training result in?
hypertrophy of type II muscle fibres and elevates enzymes involved in both ATP-PC system and glycolysis
What does high intensity interval training>30seconds promote?
mitochondrial biogenesis
