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Using molecular biology to
maximize concurrent training
以分子生物學使
同時耐力與肌力訓練最佳化
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早期 (1980之前)的研究
10周 肌力+心肺耐力訓練
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Previous results
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cycling 3 day/week for 50 min at 70 %
VO2max NOT impair strength or
hypertrophy of concurrent strength training
4 day/week or the intensity > 80 % VO2max,
endurance exercise prevents the increase in
muscle mass and strength that occurs with
strength training
the primary effect of endurance exercise
↓resistance exercise-induced muscle
hypertrophy 肌肉生長  ↓ strength 肌力
mammalian target of rapamycin
(mTOR) in muscle hypertrophy
Baar 2014
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mTOR pathway
Molecular responses after
resistance training
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resistance exercise-induced muscle
hypertrophy is completely dependent on
mTOR
mTOR phosphorylation  S6k
phosphorylation
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Molecular response after
endurance exercise
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endurance adaptations are the result a variety of
metabolic signals and molecules
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Ca2+, free radicals, AMP, lactate, NAD, hormones
AMP  ↑ AMPK (AMP-activated kinase)
Low glycogen  ↑ mitogen-activated protein
kinase p38
lactate and NAD↑ NAD -dependent deacetylase
family of sirtuins (SIRT)
Epinephrine  cAMP  cAMP response element
binding protein (CREB)
All ↑ PGC-1alpha
?
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Role of PGC-1alpha
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PGC-1alpha coregulates the expression of
respiratory genes, mitochondrial transcription
factor A, GLUT4, fatty acid–oxidation
enzymes
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Role of PCG-1alpha
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PGC-1alpha and gene expression
Review of strength, endurance,
and concurrent training effects
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Wilson 2012
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Concurrent effects
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upregulation of translation initiation via the
PI3K-AKT-mTOR signaling pathway↓
when resistance training is performed after
glycogen depleting endurance exercise
moderate intensity endurance exercise
immediately acts to ↓ important elongation
factors (eef2, responsible for ↑protein
synthesis)
Running concurrent vs
cycling concurrent
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Wilson 2012
Dose-response relationship (day) of
endurance in concurrent training
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Wilson 2012
Dose-response relationship (min) of
endurance in concurrent training
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Wilson 2012
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Concurrent effects
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Basal and growth-related protein synthesis is
controlled by different mechanism
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Not affected by training/concurrent training
ctivated AMPK and CamK phosphorylate
histone deacetylases (HDAC) and permit
myocyte-enhancing factor (MEF) 2 binding
to the promoter of PGC-1alpha.
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↑expression of PGC-1alpha
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Concurrent effects
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TSC2 can be phosphorylated and activated
by AMPK
Activation of TSC2 by AMPK is dominant
over PKB-mediated inactivation
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leads to the inactivation of mTOR and ↓in the
rate of protein synthesis
Concurrent ↑ AMPK activity would
↓hypertrophy after resistance exercise
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Wilson 2012
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Conclusions
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overall power is the major variable, which is
affected by concurrent training.
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in sport requires maximal power or rate of force
development should limit concurrently training
for strength and endurance.
If focus is on maximal strength and
hypertrophy, then concurrent training may
NOT lead to significant decrements
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given the proper modality of endurance training
is selected.
Wilson 2012
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Conclusions
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select a modality of endurance exercise that
closely mimics their sport to avoid the
occurrence of competing adaptations.
Avoid long duration endurance exercise
(.20–30 minutes) at high frequency (>3
d/week).
athletes whose sport requires strength and
power should select endurance activity that is
performed at very high intensities
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Lower ↓ in hypertrophy, strength, and power.
Wilson 2012
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Conclusions
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coaches can incorporate strength training for
individuals attempting to primarily increase
endurance performance without interfering
with their aerobic capacity
Wilson 2012