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8/8/2019 Week 5 - Science of Hypertrophy
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Jon Cree
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What is hypertrophy?
Explain the physiological components ofhypertrophy
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Increase in size
Lean muscular mass Skeletal Muscle
Cardiac Muscle
Increase muscle cross-sectionalarea (sarcomeresin parallel)
Opposite Atrophy
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Contact sports Protection
Increase impact forces
Bodybuilding Competition
Increase in strength/power Pennation angle
Number of filaments
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Pennated muscle
Majority: skeletal
Attaches @ angle
Increased MF CSA
Increased A-M CBs
-VE:too much Hypertrophy
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Optimal Length-tension relationship increases number of cross bridges therefore STR
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Decreased ROM
Decreased performance
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Increase the number of A-M CBs
Satellite Cells
Found in sk
eletal muscle Aid growth, maintenance & repair
One nucleus
Become active due to trauma
Migrates to damaged area
Donates nucleus to muscle cell
Increases density of A-M cross bridges
48-H
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Increase in number of muscle fibers
Splitting
Found among animalpopulations
Unproven in human skeletal muscle
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Two mechanisms:
Increased muscle tension (Mechanical stress)
Intramuscular energy depletion (metabolic
stress)
(Nosaka etal. 2003;Stone etal. 2007; Zatsiorsky etal. 2006)
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Upstream signalling Downstream events
1. Mechanical & metabolic stress
2. Signalling from mechanical stress on musclefibers,hormonal response and inflammatory
response
3. Protein synthesis leading to hypertrophy
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Shown to be apowerful stimulantto muscle
growth
Eccentric contractions (over Iso & Concentric)
DOMS
Disruption of sacromeres
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Repeated exercise
Decreased function
Increased enzyme activity Breakdown of cell structure
Concentric over eccentric Concentric requires more energy
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Mechanical & metabilic stresses cause growth
signalling due to muscle contractions,
hormonaland inflammatory responses
1. Muscle Contractions2. Hormone Response3. Immune Response
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Directly signalprotein-kinase pathway
Increases protein synthesis
Therefore muscle growth
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Anabolic hormones stimulated during
resistance training
Hormones signaland promote growthby:
GH
TST
IGF
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Produced from pituitary gland
Aids production of muscle & bone
Also regulates blood glucose levels,
stimulates fattyacids from fat cells
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Helps to promoteGH responses bypituatory
gland
Promotes male sex characteristics
Influences structuralprotein synthesis
Therefore :Size and strength
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Hormone secreted by skeletal muscle
Produced in response toGH
Provides aprolific role in protein anabolism
Encourages satellite cellproduction
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Mechanical stress micro-trauma
Immediate infiltration of cytokines
Neutrophil & Macrophage production
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Concentric, eccentric, isometric
Greater levels of myofibrillar damage
Athletes: All 3 types Sports performance
Stabilization
Force production
Supramaximal loading
110% 1RM
Concentric,eccentric, isometric
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% of 1RM
50-75% (NSCA)
60-70%RM Beginner
70-80%RM Intermediate
70-100%RM Advanced
110%RM (keogh etal. 1999)
Kraemer & Ratamess (2004)
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Low moderate to begin with
Moderate high for advanced
Continuing low-moderate:Sarcoplasmic &
Type 1 muscle fibers (Bodybuilders)
Non-functional
(McDougall etal 1982; Fry 2004)
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TUT:Totaltime a muscle is under stress p/rep
Not widely researched
Written in 3 number sequence: Eg: 321 tempo (6 seconds p/rep)
3s descending; 2s pause; 1s ascending
Bird etal (2005) 2s Con; 2s Ecc, 1s Iso
Goto etal (2004) 1s Con, 5s EccGH production
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Total Vol:product of sets x reps
Vol load:Product of sets x reps xload
Hightotal vol & low rest & moderate load
Kreameretal: 10RM + 1 min rest
5RM + 3 min rest
Produced more resting anabolic hormones
(IGF,GH,TST)
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Important in dictating anabolic hormone
stimulation
Rest intervals
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Optimal stimulus for hypertrophy is 2-3
sessions per muscle per week
4-6 training sessions per week
Alternatively 2 sessions per day of 30-45 mins
Helps counteract catabolism if diet is correct
(Kraemer etal 2004; Wernbom etal 2007)
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Multi-joint exercises promote higher levels ofanabolic hormones
Fatigue in larger muscle groups prior tosmaller muscle groups: Stabilization Injuryprevention
Concurrent muscular usage
(Bird etal. 2005; Chiu &Barnes, 2003)
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