phenoytype, adaptive remodeling and metabolic drivers of resistance training adaptation. Flashcards
(46 cards)
What is pennation angle?
The arrangement of fasicles
Name the 4 type of pennation angle
- fusiform
- unipennate
- bipennate
- multipennate
What are the two types of CSA?
- anatomical - CSA runs perpendicular to the longitudinal axis of muscle itself
- physiological - CSA runs perpendicular to the longitudinal axis of the fascicles
Provide an overview of the muscle structure from macroscopic to ultrastructural level
Muscle –> fascicle –> myofiber –> myofibrils –> sarcomere
Provide a study that investigates whole-muscle CSA and RT
Aoki et al 2009
- Rodent study investigating the effects of RT on whole muscle growth
- Results: increased muscle length ~20% of the soleus
- Results: increased no of sarcomeres ~27%
This is only evident in animals
Provide study breaking down muscle growth as a whole
Roman et al, 1993
- 12-week RT on the elbow flexor
- Greatest increase in MPS is found in the belly of the muscle, not the distal ends ~23%
- Therefore muscle growth is not uniform
Explain the geometric model of CSA
Length = increased length due to increase no of fascicles, therefore CSA
+11% length = +14% fascicles, therefore +30% CSA
Radius = increased pennation angle, therefore CSA
+14% length = +15% pennation angle, therefore 30% CSA
Where defines the pennation angle?
- The point the fascicles emerge from the aponeurosis
What are the 3 proposed/assumptions of muscle?
What is the most likely mechanism in humans?
- Myofibril hypertrophy
- Fibre splitting
- Hyperplasia
Evidence for myofibril hypertrophy
Aagard et al 2001
- 16 weeks RT
- Results: Increased quad CSA, T2 fibres and pennation angle
Research into fibre splitting
Erikkson et al 2006
- steroid v no steroid use in powerlifters
- 3fold significant increase in fibre splitting in steroid users and without
Research into hyperplasia
Tamaki et al 1992
- Squat RT in rodent increased number of fibres, compared to sprint training and no training
- only evident in animals
Does sarcoplasmic hypertrophy contribute to overall muscle hypertrophy?
Dankel et al 2019 meta-analysis
- No evidence of disproportionate muscle swelling
- RT preserved T2 specific tension, therefore increased CSA is due to radial growth, not sarcoplasmic
Provide further evidence against sarcoplasmic hypertrophy assumption
MacDougall et al 1982
- 6 months RT in normal healthy trained displayed higher levels of myofibrillar density compared to cytoplasmic density
- this is opposite in bodybuilders
- also an increase in T2 muscle fibre area dismisses assumption
Describe how myofibers split
- New myofilaments grow around pre-existing myofibrils
- CSA reaches upper limit
- Myofibrils split into daughter myofibrils
- Cycle repeats
Describe the 5 step process of satellite cells
- Quiescent cell
- Exercise activates quiescent cell
- Quiescent proliferates, i.e. increase in number
- Commit to function
- Differentiate
What are the two proteins that must be present to allow differentiation of quiescent satellite cell?
MRF4 and myogenin
What are the acute and chronic roles of satellite cells?
Acute - repair of muscle tissue damage
Chronic - Maintain the myonuclear domain with hypertrophy, by increasing number of nucleuses, to support metabolic functions
How is muscle mass regulated?
- Balance of MPS and MPB
- Enhanced by AA and exercise, via promoting synthesis
How is protein made?
- Transcription: DNA in the nucleus is unzipped and exposes new mRNA sequence
- Translation: mRNA sequence leaves the cell to form AA chain and joined by peptides, consequently folded into new protein
What are the three steps of translation?
- Initiation: ribosome binds to mRNA sequence
- Elongation: AA are transported and joined together and begin to form new peptide chain
- Termination: ribosome is removed from mRNA sequence and new protein is formed
Define mTOR and what complex of mTOR regulates what?
- Mammalian target of rapamycin
- mTORC1 regulates muscle growth
Name 3 physiological stimuluses of mTOR, and 1 inhibitor
- GF
- AA
- Energy
- Stress or fasted state
How does mTORC1 regulate
- Physiological stimulus phosphorylates TSC2, becoming inactive, so increasing Rheb bound to GTP, therefore promoting MPS
- Stressor activates TSC2, so Rheb is bound to GDP, therefore inhibiting MPS