Molecular Adaptations To Exercise Flashcards
What mechanisms are responsible for molecular adaptations to endurance training?
Mitochondrial biogenesis,
AMPK-mediated signalling,
Ca2+ - Calmodulin dependant kinase/ calcineurin signalling
Give some examples of primary messengers
Mechanical stretch,
Calcium,
Redox potential,
Phosphorylation potential
Hypertrophy mechanisms
IGF-1 signalling pathway,
mTOR,
Satellite cell activation
Explain the ATP-dependant ubiquitin proteasome pathway
This pathway works by ubiquinating a protein which signals for their degradation via the proteasome. The proteasome degrades proteins via proteolysis.
When might you see atrophy in muscles?
Inactivity, ageing, disease, during regenerative remodelling (removing damaged proteins)
Why is concurrent training beneficial for distance runners?
Doing max strength training will improve the runners economy due to:
Better muscle fibre type recruitment pattern,
Greater muscle force generation capacity,
Increased proportion of type IIa fibres,
Reduced type IIb fibres and a shift towards a fatigue resistant yet more powerful muscle phenotype
Why is improving a runners economy beneficial?
Muscles are adapted so can work under higher intensities at the same effort
Why might concurrent training NOT be beneficial to endurance athletes?
Heavy resistance training doesn’t lead to mitochondrial biogenesis, and a larger CSA increases diffusion distance for O2 and substrates (unfavourable).
Why might concurrent training NOT be beneficial to strength athletes?
Endurance training doesn’t effect myofibril size and the higher levels of AMP/Ca2+ may negatively regulate PS and ability to generate force
What problems might occur as a result of concurrent training? Aside from at the cellular level for specific athletes
Carry over effects of fatigue due to: Impaired neural recruitment patterns, Reduced movement efficiency and increased EE, Increased muscle soreness, Reduced muscle glycogen
What is the interference effect?
The specific adaptations to the 2 exercise modes appear to be incompatible at the cellular level
What mechanisms mediate the interference effect?
AMPK-Akt hypothesis,
Divergent regulation of eEF2,
Divergent regulation of FoxO1
What may bring about the interference effect?
Certain modes of exercise bring about greater effect,
The muscles groups utilised,
Greater volume of endurance work performed,
Frequency of end training,
Sequencing of the sessions,
Intensity of the work,
Training status - elite sees greater effect