Recovery

Question 1

What are the mechanisms of recovery?

Answer 1

Signal, primary and secondary messengers, gens/proteins, fibre characteristics and phenotype

Question 2

Discuss skeletal muscle adaptation of training and adequate recovery

Answer 2

Improvements in exercise performance (capacity, power, speed), increased protein content due to increased MRNA and increased enzyme function (mitochondrial content and citrate synthase activity), repeated exercise bouts increase transcription and relative expression of genes (genes encoding cell proteins and enzymes)

Question 3

Explain the process of muscle breakdown and adaptation after resistance exercise

Answer 3

Increased motor unit recruitment when force is high therefore resistance exercise is damaging to muscles, leads to increased alpha and beta integrins, further leads to increased mTORC1 = increased p70S6K = protein synthesis = hypertrophy, can alter molecular response and potentially manipulate adaptation through diet, exercise and exposure to extreme conditions (CWI, massage)

Question 4

How does cold water immersion (CWI) affect recovery and adaptation?

Answer 4

CWI reduces p70S6K to baseline levels 24 hours post-exercise when usually it should stay elevated >48 hours post-exercise for increased protein synthesis and hypertrophy, this suggests CWI impairs activation of key signalling intermediates reducing adaptation from training, CWI reduces muscle mass gain compared to active recovery, CWI inhibits type II muscle fibre hypertrophy, CWI blunts strength gains in leg press and knee extension, CWI impairs rate of force development

Question 5

Discuss adaptation of endurance exercise

Answer 5

Increased alpha and beta integrins, production of FAK, AMPK leads to production of PGC1-alpha, results in mitochondrial biogenesis

Question 6

How does massage affect recovery and adaptation?

Answer 6

No effect on muscle lactate concentration, phosphorylates and activates FAK suggesting increased mechanical activation of muscles, increases PGC1-alpha in nucleus, no change in mTORC1 phosphorylation suggesting an activation of mitochondrial biogenesis as opposed to mTORC1 pathway, good for adaptation and recovery