Recovery Flashcards
Describe the adaptation to contractile demand
Resistance training/endurance running
Signal:
Nerve stimulation
Contractile activity
Primary and secondary messengers: Alterations in force productions Alterations in energy charge of the cell Activation of mechanically - stimulated proteins Activation of energy sensing proteins
Increased expression of genes and functional proteins
Fibre characteristics and phenotype
Describe the molecular regulation of skeletal muscle adaptation
Improvements in exercise performance
Increased protein content and enzyme function
Repeated exercise bouts increase transcription and relative expression of genes
Describe what PGC1a mRNA and protein does
Regulator of mitochondrial biogenesis
Activates transcription factors
PGC1a mRNA - rapid increase then 24hrs later drops - general decreasing trend
PGC1a protein - gradual increase over time but starts to plateau after 3rd bout
More protein due to more transcription factors activated
Describe what CS does
Citrate synthase catalyses the first step in the krebs cycle - marker of mitochondrial biogenesis
CS mRNA increase after changes in PGC1a
CS maximal activity gradually increases over time
Changes in mRNA that occur 24hrs after 1st session takes 3 interval sessions to convert into functional protein
Resistance-type exercise does what type of damage?
Sarcomere damage (actin and myosin disrupted)
Z-disc damaged
Increase in myofibrilar proteins and sarcoplasmic proteins
Describe the adaptation to resistance-type training
Resistance exercise
Integrins a and b
mTORC1
Inhibits 4EBP1 (elf4E - freed) Activation of p70S6K
Protein synthesis
Hypertrophy
What is the evidence for this?
Given drug that inhibits mTORC1 no gains in protein synthesis after resistance exercise
mTOR regulates muscle protein synthesis. Blocking mTOR activity, inhibits induced increase’s in MPS
p70S6K increase (phosphorylation) direct correlation with increase in muscle mass
How can we manipulate the molecular response for optimal adaptation?
Diet
Exercise
Combination with exposure to extreme environments (cold water immersion)
Does cold water immersion help acute adaptation?
p70S6K phosphorylation and activation increase in both groups
In active recovery only p70S6K phosphorylation remained elevated above baseline for 48hrs
In cold water immersion p70S6K phosphorylation and activation returned to baseline after 24hrs
This suggests cold water immersion impairs activation of key signalling intermediates
Does cold water immersion help chronic adaptation?
Increase muscle mass after 12wks training when combined with active recovery (+309g)
Increase muscle mass after 12wks training when combined with active recovery (+103g)
Greater gains in muscle mass after active recovery suggests cold water immersion may blunt gains in muscle mass
Type II CSA was sig. larger after 12wks of training in the active recovery group
Both recovery interventions led to increase in leg press strength and knee extension strength but gains in active recovery were sig. greater
Rate of force development also impaired with cold water immersion
What conclusions can be drawn from cold water immersion?
Cold water immersion blunted or inhibited the acute molecular responses to strength training
Cold water immersion blunted the chronic adaptive response to strength training
Describe the adaptation to endurance exercise
Endurance exercise
Integrins a and b
FAK
PGC1a - AMPK and mitochondrial biogenesis
mTORC1 - Inhibits 4EBP1 (elf4E - freed) and Activation of p70S6K
Protein synthesis
Hypertrophy
Describe specifically the AMPK adaptation to endurance exercise
Reduced energy charge of the cell activates AMPK
This leads to activation of PGC1a
PGC1a is a co-activator of transcription factors
Activation of PGC1a leads to mitochondrial biogenesis and angiogenesis
What effect does massage therapy have?
Massage did not alter muscle lactate concentrations
Markers of muscle damage were increased after unaccustomed cycling
FAK phosphorylation suggests increased mechanical activation of the skeletal muscle after massage
Nuclear abundance of PGC1a was increased after massage but no change in mTOR phosphorylation
This suggests the activation of mitochondrial biogenesis signalling pathway and not mTORC1 pathway at the time points measured
How does inflammation lead to atrophy?
TNFa - binds with receptor on sarcolemma
NFKB pathway
Protein breakdown Necrosis
Atrophy
Explain the effect of massage therapy on inflammation
Massage therapy reduced the amount of TNFa
Massage therapy reduced activation of NFKB pathway
Markers of pro-inflammatory pathway are generally reduced with massage therapy
HSP27 also reduced
Explain the findings of the study that used rats to investigate massage therapy
Massive atrophy in hindlimb suspension
Adding massage after reambulation leads to greater gains in CSA
After 7 days with reambulation and massage 50% increased
What is the mechanism of this finding?
Total FAK concentration decrease due to hindlimb suspension
When massage therapy applied increase in activation state of FAK
Reductions in total FAK protein content with HS is consistent with a lack of mechanical stimulation of skeletal muscle
FAK phosphorylation and activation unchanged as a result of HS and RE
However reambulation plus cyclic compressor loading did increase FAK phosphorylation and activation
HS sig. reduce myofibrillar protein synthesis rates decrease 54%
Reintroduce PA increase protein synthesis rates but effect is amplified when you add massage
Same effect with mitochondrial protein synthesis (decrease 35%) but no diff between interventions
