effects of aerobic and anaerobic training - week 9 Flashcards
what is training overload ?
when a physiological system is exercised at a level beyond its normally accustomed
what is specificity ? (4)
training being specific to …
- muscle fibres recruited
- energy system involved
- velocity of contraction
- type of contraction
what is reversibility ?
gains are lost when training ceases
what’s is involved in training to increase VO2 max ? (4)
large muscle groups, dynamic activity
20-60 mins
≥3 times a week
≥50% VO2 max
how much does VO2 max change with endurance training ? (2)
15-20% increase
if high VO2 already, increase is smaller
how does genetics impact VO2 max ?
heritability determines 50% in sedentary adults
also key role in determining training response
why does VO2 max change with training ?
due to changes in Cardiac output and stroke volume
- changes O2 consumption and VO2 max
how does training increase stroke volume ? (4)
increased preload
increased plasma volume
increased venous return
increased O2 uptake, improves systems, improves functions of heart
what is eccentric hypertrophy ? (2)
chamber size and wall thickness increase of heart
helps deal w increased volumes of heart so can pump more blood around - stronger heart
how does endurance training increase stroke volume ? (2)
increased blood, reduced resistance
increased contractility
- greater force produced
what factors influence stroke volume ? (3)
end diastolic volume (preload)
contractility
totally peripheral resistance (after load)
what factors influence end diastolic volume ? (3)
plasma volume
filling time + venous return
ventricular volume
what’s the equation for CO?
stroke volume x HR
what happens to max CO with training ?
increases !
mostly linear
increases efficiency of using O2
at sub-man workload HR is __ following trainmen due to increase in __ so __ can be achieved with fewer bpm
lower
stroke volume
CO
what happens due to increased muscle blood flow due to increased arteriovenous O2 difference from training?
decreased SNS vasoconstriction
increased diameter and compliance of arteries
what happens to improved ability of muscle fibres to utilise O2 due to increased arteriovenous O2 difference from training?
increased capillary density - increased diffusion due slower blood flow through muscle
increased mitochondria
transit time of RBCs _ due to bigger __ so they take longer to pass through
increase
capillary network
during sub-max exercise blood flow in trained muscles is lower _ the A-V difference is greater
because
during maximal exercise blood flow in trained muscles is higher _ the A-V difference is greater
and
what are the consequences of endurance training shifting fibre types ? (2)
reduction of fast fibres and increase in slow
magnitude of fibre type dependent on training, duration . genetics
what are the consequences of endurance training increasing capillaries surrounding muscle fibres ?
enhanced diffusion of oxygen
improved removal of waste
how does endurance training increase mitochondrial volume + turnover in muscles?
increased volume subsarcolemmal + intermyofibrillar mitochondria
greater capacity for oxidative phosphorylation
increased mitochondrial volume
- reduced systolic ADP so less lactate + H+ formation
how does endurance training change fuel utilisation ? (3)
increased plasma FFA transport and oxidation to muscle
transport of FFA from cytoplasm to mitochondria
mitochondria oxidation of FFA
- increased acetyl CoA formed
- slowed glycolysis
how does endurance training improve antioxidant capacity of muscle ? (3)
(when muscle contract they produce free radicals)
increases in endogenous antioxidant enzymes
- improved ability to remove radicals
- protects against oxidative damage + muscle fatigue
how does endurance training improve acid-base balance during exercise ? (3)
(lactate production creates H+ ions which can increase fatigue)
increased mitochondria - less carbs used- less pyruvate
increased NADH shuttles
- less NADh for lactate production
change in LDH isoform
- less lactate formation
how does training promote protein synthesis in fibres? (3)
‘stress’ activates gene transcription
contraction activates primary and secondary messengers
results in expression of genes and synthesis of new proteins
what are some of the primary signals for post exercise adaptations ?
mechanical stretch
calcium
AMP/ATP
free radicals
these drive proteins and enzymes that can shift/drive the adaptation
what is the secondary messenger AMP kinase ?
promotes glucose uptake and linked to gene expression by activation of transcriptional activating factors
what is the secondary messenger PGC-1a?
regulator of mitochondrial biogenesis, promotes angiogenesis and synthesis of antioxidant enzymes
- activated by AMPK
how does detraining effect body and vo2 max? (3)
rapid decrease in VO2 max
decrease in SV max
decrease in maximal a-v O2 difference
- less mitochondria
- less oxidative capacity of muscle
- type 2a fibres and increase type 2 x fibres
