Recovery

Question 1

Describe the adaptation to contractile demand

Answer 1

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

Question 2

Describe the molecular regulation of skeletal muscle adaptation

Answer 2

Improvements in exercise performance
Increased protein content and enzyme function
Repeated exercise bouts increase transcription and relative expression of genes

Question 3

Describe what PGC1a mRNA and protein does

Answer 3

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

Question 4

Describe what CS does

Answer 4

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

Question 5

Resistance-type exercise does what type of damage?

Answer 5

Sarcomere damage (actin and myosin disrupted)
Z-disc damaged
Increase in myofibrilar proteins and sarcoplasmic proteins

Question 6

Describe the adaptation to resistance-type training

Answer 6

Resistance exercise

Integrins a and b

mTORC1

Inhibits 4EBP1 (elf4E - freed) Activation of p70S6K

Protein synthesis

Hypertrophy

Question 7

What is the evidence for this?

Answer 7

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

Question 8

How can we manipulate the molecular response for optimal adaptation?

Answer 8

Diet
Exercise
Combination with exposure to extreme environments (cold water immersion)

Question 9

Does cold water immersion help acute adaptation?

Answer 9

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

Question 10

Does cold water immersion help chronic adaptation?

Answer 10

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

Question 11

What conclusions can be drawn from cold water immersion?

Answer 11

Cold water immersion blunted or inhibited the acute molecular responses to strength training
Cold water immersion blunted the chronic adaptive response to strength training

Question 12

Describe the adaptation to endurance exercise

Answer 12

Endurance exercise

Integrins a and b

FAK

PGC1a - AMPK and mitochondrial biogenesis
mTORC1 - Inhibits 4EBP1 (elf4E - freed) and Activation of p70S6K

Protein synthesis

Hypertrophy

Question 13

Describe specifically the AMPK adaptation to endurance exercise

Answer 13

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

Question 14

What effect does massage therapy have?

Answer 14

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

Question 15

How does inflammation lead to atrophy?

Answer 15

TNFa - binds with receptor on sarcolemma

NFKB pathway

Protein breakdown Necrosis

Atrophy

Question 16

Explain the effect of massage therapy on inflammation

Answer 16

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

Question 17

Explain the findings of the study that used rats to investigate massage therapy

Answer 17

Massive atrophy in hindlimb suspension
Adding massage after reambulation leads to greater gains in CSA
After 7 days with reambulation and massage 50% increased

Question 18

What is the mechanism of this finding?

Answer 18

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