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

早期 (1980之前)的研究 10周 肌力+心肺耐力訓練

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

mammalian target of rapamycin (mTOR) in muscle hypertrophy Baar 2014

mTOR pathway

Molecular responses after resistance training resistance exercise-induced muscle hypertrophy is completely dependent on mTOR mTOR phosphorylation  S6k phosphorylation

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

Role of PGC-1alpha PGC-1alpha coregulates the expression of respiratory genes, mitochondrial transcription factor A, GLUT4, fatty acid–oxidation enzymes

Role of PCG-1alpha

PGC-1alpha and gene expression

Review of strength, endurance, and concurrent training effects Wilson 2012

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)

Running concurrent vs cycling concurrent Wilson 2012

Dose-response relationship (day) of endurance in concurrent training Wilson 2012

Dose-response relationship (min) of endurance in concurrent training Wilson 2012

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

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

Wilson 2012

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

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

Conclusions coaches can incorporate strength training for individuals attempting to primarily increase endurance performance without interfering with their aerobic capacity Wilson 2012