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Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle.
FASEB J 2016; 30(2):959-70FJ

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.

Authors+Show Affiliations

*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.*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.*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.*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.*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.

Pub Type(s)

Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26572168

Citation

Granata, Cesare, et al. "Training Intensity Modulates Changes in PGC-1α and P53 Protein Content and Mitochondrial Respiration, but Not Markers of Mitochondrial Content in Human Skeletal Muscle." FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, vol. 30, no. 2, 2016, pp. 959-70.
Granata C, Oliveira RS, Little JP, et al. Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle. FASEB J. 2016;30(2):959-70.
Granata, C., Oliveira, R. S., Little, J. P., Renner, K., & Bishop, D. J. (2016). Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle. FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, 30(2), pp. 959-70. doi:10.1096/fj.15-276907.
Granata C, et al. Training Intensity Modulates Changes in PGC-1α and P53 Protein Content and Mitochondrial Respiration, but Not Markers of Mitochondrial Content in Human Skeletal Muscle. FASEB J. 2016;30(2):959-70. PubMed PMID: 26572168.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle. AU - Granata,Cesare, AU - Oliveira,Rodrigo S F, AU - Little,Jonathan P, AU - Renner,Kathrin, AU - Bishop,David J, Y1 - 2015/11/16/ PY - 2015/07/06/received PY - 2015/10/28/accepted PY - 2015/11/18/entrez PY - 2015/11/18/pubmed PY - 2016/6/18/medline KW - PHF20 KW - TFAM KW - exercise KW - mitochondrial biogenesis KW - mitochondrial remodeling SP - 959 EP - 70 JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology JO - FASEB J. VL - 30 IS - 2 N2 - 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. SN - 1530-6860 UR - https://www.unboundmedicine.com/medline/citation/26572168/Training_intensity_modulates_changes_in_PGC_1α_and_p53_protein_content_and_mitochondrial_respiration_but_not_markers_of_mitochondrial_content_in_human_skeletal_muscle_ L2 - http://www.fasebj.org/doi/full/10.1096/fj.15-276907?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -