Cited by 215Cardiovascular and exercise physiologyAdipose Tissue and MetabolismExercise and Physiological Responses

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

Granata, Cesare, Oliveira, Rodrigo S. F., Little, Jonathan P., Renner, Kathrin, Bishop, David J.·2016·The FASEB Journal

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 ( W Peak )], high‐intensity interval training (HIIT; 4–7 × 4‐min intervals at ~90% W Peak ), or sublactate threshold continuous training (STCT; 20–36 min at ~65% W Peak ). 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 g 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.—Granata, C., Oliveira, R. S. F., Little, J. P., Renner, K., Bishop, D. J. 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. 30, 959–970 (2016). www.fasebj.org

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Crossref · 10.1096/fj.15-276907

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Authors
Granata, C., Oliveira, R. S. F., Little, J. P., Renner, K., & Bishop, D. J.
Affiliations
  • Victoria University (AU)
  • University of British Columbia, Okanagan Campus (CA)
  • University Hospital Regensburg (DE)
Corresponding author
Bishop, David J.
Venue
The FASEB Journal
Publisher
Wiley
Published
2015-11-16
Volume
30
Issue
2
Pages
959-970
ISSN
  • 0892-6638 (ISSN-L)
  • 1530-6860
OpenAlex
W2260205858
Cited by
215
References
37
Citations by year
2026: 18 · 2025: 19 · 2024: 20 · 2023: 12 · 2022: 19 · 2021: 27 · 2020: 22 · 2019: 23 · 2018: 22 · 2017: 19 · 2016: 14
FWCI
35.98
Type
journal article
Language
en
Open access
closed
Locations
  • The FASEB Journal (publishedVersion)
  • PubMed (publishedVersion)
  • Victoria University Research Repository (Victoria University) (submittedVersion)
  • University of Regensburg Publication Server (University of Regensburg) (submittedVersion)
Topics
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
Keywords
exercise intensity, mitochondrial respiration, mitochondrial biogenesis, PGC-1α, p53, high-intensity interval training, sprint interval training, continuous training, skeletal muscle, vastus lateralis, citrate synthase, TFAM, electron transport chain, exercise training
MeSH terms
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Adolescent, Adult, Antigens, Neoplasm, DNA-Binding Proteins, Humans, Male, Mitochondria, Muscle, Muscle Proteins, Oxygen Consumption, Transcription Factors, Biomarkers, Tumor, Exercise, Tumor Suppressor Protein p53, Muscle, Skeletal

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