4.6 Article

Training response of mitochondrial transcription factors in human skeletal muscle

期刊

ACTA PHYSIOLOGICA
卷 198, 期 1, 页码 71-79

出版社

WILEY-BLACKWELL PUBLISHING, INC
DOI: 10.1111/j.1748-1716.2009.02030.x

关键词

exercise; gene expression; mitochondrial biogenesis; regulation

资金

  1. Swedish National Centre for Research in Sports, Trygg-Hansa Foundation
  2. Ake Wiberg Foundation
  3. Magnus Bergvall Foundation
  4. Swedish Research Council

向作者/读者索取更多资源

Aim: Mitochondrial function is essential for physical performance and health. Aerobic fitness is positively associated with mitochondrial (mt) biogenesis in muscle cells through partly unknown regulatory mechanisms. The present study aimed to investigate the influence of exercise and training status on key mt transcription factors in relation to oxidative capacity in human skeletal muscle. Methods: The basal mRNA and protein levels of mitochondrial transcription factor A (TFAM), mitochondrial transcription factors B1 (TFB1M) or B2 (TFB2M), and mRNA levels of mitochondrial transcription termination factor (mTERF), were measured in a cross-sectional study with elite athletes (EA) and moderately active (MA) and the basal mRNA levels of these factors were measured during a 10-day endurance training programme with (R-leg) and without (NR-leg) restricted blood flow to the working leg. Results: TFAM protein expression was significantly higher in the EA than in the MA, while protein levels of TFB1M and TFB2M were not different between the groups. There was no difference between EA and MA, or any effect with training on TFAM mRNA levels. However, the mRNA levels of TFB1M, TFB2M and mTERF were higher in EA compared with MA. For TFB1M and TFB2M, the mRNA expression was increased in the R-leg after 10 days of training, but not in the NR-leg. mTERF mRNA levels were higher in EA compared with MA. Conclusion: This study further establishes that TFAM protein levels are higher in conditions with enhanced oxidative capacity. The mRNA levels of TFB1M and TFB2M are influenced by endurance training, possibly suggesting a role for these factors in the regulation of exercise-induced mitochondrial biogenesis.

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