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FASEB J. 2016 Feb;30(2):959-70. doi: 10.1096/fj.15-276907. Epub 2015 Nov 16.

Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle.

Author information

1
*Institute of Sport, Exercise and Active Living (ISEAL), College of Sport and Exercise Science, Victoria University, Melbourne, Victoria, Australia; School of Health and Exercise Sciences, University of British Columbia Okanagan, Kelowna, British Columbia, Canada; and Department of Internal Medicine III, University Hospital of Regensburg, Regensburg, Germany.
2
*Institute of Sport, Exercise and Active Living (ISEAL), College of Sport and Exercise Science, Victoria University, Melbourne, Victoria, Australia; School of Health and Exercise Sciences, University of British Columbia Okanagan, Kelowna, British Columbia, Canada; and Department of Internal Medicine III, University Hospital of Regensburg, Regensburg, Germany david.bishop@vu.edu.au.

Abstract

Exercise training has been associated with increased mitochondrial content and respiration. However, no study to date has compared in parallel how training at different intensities affects mitochondrial respiration and markers of mitochondrial biogenesis. Twenty-nine healthy men performed 4 wk (12 cycling sessions) of either sprint interval training [SIT; 4-10 × 30-s all-out bouts at ∼200% of peak power output (WPeak)], high-intensity interval training (HIIT; 4-7 × 4-min intervals at ∼90% WPeak), or sublactate threshold continuous training (STCT; 20-36 min at ∼65% WPeak). The STCT and HIIT groups were matched for total work. Resting biopsy samples (vastus lateralis) were obtained before and after training. The maximal mitochondrial respiration in permeabilized muscle fibers increased significantly only after SIT (25%). Similarly, the protein content of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, p53, and plant homeodomain finger-containing protein 20 (PHF20) increased only after SIT (60-90%). Conversely, citrate synthase activity, and the protein content of TFAM and subunits of the electron transport system complexes remained unchanged throughout. Our findings suggest that training intensity is an important factor that regulates training-induced changes in mitochondrial respiration and that there is an apparent dissociation between training-induced changes in mitochondrial respiration and mitochondrial content. Moreover, changes in the protein content of PGC-1α, p53, and PHF20 are more strongly associated with training-induced changes in mitochondrial respiration than mitochondrial content.

KEYWORDS:

PHF20; TFAM; exercise; mitochondrial biogenesis; mitochondrial remodeling

PMID:
26572168
DOI:
10.1096/fj.15-276907
[Indexed for MEDLINE]

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