BS277 Biology of Muscle. The response of muscle to strength

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Transcript BS277 Biology of Muscle. The response of muscle to strength

BS277 Biology of Muscle.
The response of muscle to strength
training.
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Objectives.
After these lectures and associated reading you should be
able to;
Describe the effects of strength training on muscle
structure, metabolism and function (phenotype).
Explain the regulation of muscle gene expression in the
hypertrophic response to strength and power training.
Explain how satellite cell proliferation and differentiation
are regulated and contribute to muscle growth.
Explain the role of muscle growth factors such as IGF-1
and myostatin in signalling changes in transcription and
translation.
Adaptations to resistance training
• Muscle fibre size increases
(mainly type 2)
• No evidence for type 1-2 switch
but type 2a might become more
type 2X-like in power training.
• Capillary density may decrease
• Creatine kinase increases
• Glycolytic enzymes increase (e.g.
PFK)
• ATP, CP and glycogen increase
• Ligament and tendon strength
increase
• BMD increases
Muscle strength is related to cross sectional area and strength
per unit area does not change much during puberty.
Total muscle size is subject to a number of influences.
Genetic, nutritional and endocrine
influence
• Number of fibres highly variable (Vastus lateralis
400,000 to 900,000 in 9 cadavers).
• Protein synthesis increased for ~48h post
resistance training (more in the untrained).
• Optimal hypertrophic resonse with mixed meal
post training and adequate protein in diet
(>0.8 <2 g.kg-1)
• Resistance training elevates thyroxine, GH and
testosterone (anabolic steroids) and reduces
resting cortisol.
Improvements in functional strength have a neural
as well as a muscular component.
Neural contribution to effects of
strength training
• Unilateral training of elbow flexors in
females produced 80% gain in 1RM in
trained arm and 9% in contralateral arm
(no hypertrophy by anthro.) with similar
improvements in rate of force development
(40-60%) and peak force (~35%).
Adamson et al. (2008)
Fig. 1 a Muscle
volumes of the trained
and untrained arms
before (pre-test) and
after (post-test) the
strength training
program, as determined
by anthropometry.
b 1RM of the trained
and untrained arms at
pre-test and post-test.
*, ** 2-way ANOVA
within-group differences
between pre-test and
post-test. # 1RM
increased with a greater
magnitude in the trained
than the untrained arm
The contribution of
hypertrophy to
strength gains
increases with the
duration of training.
Increases in muscle size are due to hypertrophy,
not hyperplasia. Myocyte nuclei are in Go so new
nuclei are derived from satellite cells.
Contribution of satellite cells to
hypertrophy
• A 10 cm long muscle fibre may have 412,000 nuclei.
• ~109 nuclei in the Vastus lateralis.
• 10 weeks of resistance training in women
increased satellite cells by 46% and nuclei
per muscle fibre by 70%.
• Respond to growth factors (upstream
signalling pathways not yet known?)
Gene expression in
satellite cells and
myonuclei might be
influenced by signals
associated with strength
training.
What is the nature of the
hypertrophic signal?
• Swelling (osmotic effect of metabolites)
increases amino acid transport, perhaps via an
integrin mediated signal (co-ordinates anabolic
effect?)
• Tension activation of titin kinase? Integrins via
cytoskeleton?
• Muscle damage? But not always associated
with hypertrophy (e.g marathon runners).
• Calcium? Increases specifically in recruited
motor units. Type 2 might be more susceptible
to a Ca++-related anabolic signal.
Muscles can respond to strength training even in the elderly.
(5x 68y males. Elbow flexors, 12 weeks training)
Roman et al. (1993) JAP 74, 750-754.
The hypertrophic response is mainly in type 2 fibres.
What is the diameter of a hypertrophied type 2 fibre?
(If SA = 6000 then D = 88µ. If SA = 8000 then D = 101µ
i.e. a 13% increase in diameter produces a 33% increase in area / volume)
Amplitude and latency of
Motor unit recruitment &
Tendon reflex following
resistance training.
(Indications that the
Alphamotoneurones
become more excitable;
latency shortens,tendon
reflex quicker(?), EMG
amplitude increases)