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Published byAgatha Wheeler Modified over 6 years ago
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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 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
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mammalian target of rapamycin (mTOR) in muscle hypertrophy
Baar 2014
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mTOR pathway
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Molecular responses after resistance training
resistance exercise-induced muscle hypertrophy is completely dependent on mTOR mTOR phosphorylation S6k phosphorylation
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Molecular response after endurance exercise
endurance adaptations are the result a variety of metabolic signals and molecules 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 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
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Review of strength, endurance, and concurrent training effects
Wilson 2012
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Concurrent effects 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)
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Running concurrent vs cycling concurrent
Wilson 2012
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Dose-response relationship (day) of endurance in concurrent training
Wilson 2012
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Dose-response relationship (min) of endurance in concurrent training
Wilson 2012
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Concurrent effects Basal and growth-related protein synthesis is controlled by different mechanism 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. ↑expression of PGC-1alpha
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Concurrent effects TSC2 can be phosphorylated and activated by AMPK
Activation of TSC2 by AMPK is dominant over PKB-mediated inactivation 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 overall power is the major variable, which is affected by concurrent training. 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 given the proper modality of endurance training is selected. Wilson 2012
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Conclusions 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 Lower ↓ in hypertrophy, strength, and power. Wilson 2012
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Conclusions coaches can incorporate strength training for individuals attempting to primarily increase endurance performance without interfering with their aerobic capacity Wilson 2012
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