Using molecular biology to maximize concurrent training

1. 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

2. 早期 (1980之前)的研究10周 肌力+心肺耐力訓練

3. Previous results • cycling 3 day/week for 50 min at 70 % VO2max NOT impairstrength or hypertrophy of concurrentstrength training • 4 day/week or the intensity > 80 % VO2max, endurance exercise preventsthe 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

4. mammalian targetof rapamycin (mTOR)in muscle hypertrophy Baar 2014

5. mTOR pathway

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

7. 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

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

9. Role of PCG-1alpha

10. PGC-1alpha and gene expression

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

12. 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)

13. Running concurrent vs cycling concurrent Wilson 2012

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

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

16. 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

17. 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

18. Wilson 2012

19. 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

20. 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

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