Transcript Principles of Skeletal Muscle Adaptation

Principles of Skeletal
Muscle Adaptation
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Brooks ch 19 p 401-420
Outline
Myoplasticity
Protein turnover
Fiber Type
Training adaptations
Adaptations with inactivity, injury
Age associated changes
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Myoplasticity
• Altered gene expression - resulting
in an increase or decrease in amount
of specific protein
– tremendous potential to alter expression
in sk ms
– molecular basis for adaptations that
occur due to exercise tx in sk ms
proteins
• 20%of sk ms is protein, balance is
water, ions...
– All types of protein can be regulated by
altering gene expression
• Fig 19-1 cascade of regulatory
events - impacting gene expression
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Myoplasticity cont.
• myoplasticity - change either
quantity (amount) or quality (type)
of protein expressed
• Eg. Responses to training
• type IIb - hypertrophy (enlargement)
- inc amount of protein in fiber
– larger fast II b fiber
• Another fiber - hypertrophy
– also repress gene for fast II b myosin
HC, turn on fast IIa myosin HC
– not only enlarged, but change in
contractile phenotype
– larger, slower contracting fiber.
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Protein turnover
• Protein Turnover reflects 1/2 life of
protein - time frame for existence
– protein transcribed (DNA-mRNA)
– translated then degraded
• level of protein in cell governed by
– synthesis / degeneration ratio
– precise regulation of content through
control of transcription rate
– and/or degradation rate
• capacity to regulate structural and
functional properties of the ms
– applies to both structural and contractile
proteins and regulatory proteins
– as well as enzymes involved in
metabolism
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Adaptation
• Sk ms adaptation characterized by
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morphological
biochemical
molecular
variables that alter the functional
attributes of fibers in specific motor
units
• adaptations readily reversible when
stimulus is diminished or removed
• Fig 19-2 intracellular and extracellular
influences - reg gene pool expression
– stimuli of sufficient amount for
sufficient time- overload
– lead to changes in expression of
specific proteins - specificity
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Signals for Adaptation
• Insufficient energy balance
• nutrition can also influence
endocrine system - insulin
• endocrine system influence
independent of nutrition
– thyroid hormone
– IGF-1 - insulin like growth factor 1
– mediates Growth Hormone effects
• power developed by motor unit
– load against which fibers contract
– specific responses to demands
• each result in acute changes in
cellular environment
– changes can lead to altered rates of
protein synthesis and degradation
– changes [ ] or activity of proteins
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Hormonal Influences(cont)
• IGF-1 - GH stimulates release from liver
- 8-30 hours
– also muscle mediated release
• Autocrine/paracrine
• MGH - mechanogrowth factor
– Training inc IGF-1 mRNA expression
• GH dependant and independant
• Endurance Training
– GH- no change at rest
– Less dramatic rise during exercise
• Unless training above lactate inflection
• Resistance Training
– Testosterone and GH - two primary
hormones that affect adaptations
– Inc secretion with training
– Testosterone - augments GH release
• Inc muscle force production - Nervous
system influence
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Phenotype
• When protein structure of muscle is
altered - phenotype change
– outwardly observable characteristics of
muscle
– reflects underlying genes (genotype)
and their regulation by several factors
(exercise)
– altered phenotypes - affect cellular
environment as well
• eg. Receptors, integrating centers,
signal translocation factors and
effectors - mechanisms not fully
understood.
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Muscle Fiber Types
• Elite athletes - specialized fiber
typing
– sprinter II b, endurance I
• Fig 19-3 - elite - ends of spectrum
• genetics - strong influence on fiber
type disposition
• Training studies - alter biochemical
and histological properties - not fiber
type distinction - (myosin isoform)
• evidence, however, that intermediate
transitions can occur in MHC
expression - not detected with
conventional techniques
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Endurance Adaptations
• Occurs with large increase in
recruitment frequency and modest
inc in load
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minimal impact on X-sec area
significant adaptations to metabolic
Inc mitochondrial proteins
HK inc, LDH dec(cytosol), inc mito
• 2 fold inc in ox metabolism
– degree of adaptation depends on pre
training status, intensity and duration
• Table 19-1 Succinate DH (Krebs)
– response varies with fiber type involvement in training
– inc max blood flow, capillary density,
and potential for O2 extraction
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Adaptations to
Resistance Training
• Increased recruitment frequency and
load
• Hypertrophy - inc X-sec area
• Hyperplasia - inc cell number
– major adaptation is with hypertropyhy inc max force generating capacity
• Fig 17-28b - Force velocity after tx
– move sub max load at higher velocity
of shortening
– enhanced power capacity
• Fiber type specific adaptation
– inc X-sec area of both type I and II
– Fig 19-4 5-6 month longitudinal study
– II - 33% , I - 27% increase
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Resistance Training
• Fastest MHC’s repressed , inc in
expression of intermediate MHC
isoforms II x - II a
• mito volume and cap density
reduced with resistance tx
• Fig 19-5 - 25 % dec in mito protein
• Fig 19-6 - cap density dec 13%
• Adaptation with decreased activity
• large reduction in recruitment
frequency and /or load
• reduction in ms and ms fiber X-sec
area - dec in metabolic proteins
• Fig 19-8
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Injury and Regeneration
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Induced by a variety of insults
trauma, ischemia, excessive stretch
eccentric exercise, dennervation
active lifestyle - continuous
population of regenerating fibers
two phases
immediate - mechanical
secondary - biochemical - several
days
Gender differences
Table 19-2 - size and strength
Table 19-3 - strength vs. X-sec area
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