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Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1α in human skeletal muscle
Abstract
From a cell signaling perspective, short-duration intense muscular work is typically associated with resistance training and linked to pathways that stimulate growth. However, brief repeated sessions of sprint or high-intensity interval exercise induce rapid phenotypic changes that resemble traditional endurance training. We tested the hypothesis that an acute session of intense intermittent cycle exercise would activate signaling cascades linked to mitochondrial biogenesis in human skeletal muscle. Biopsies (vastus lateralis) were obtained from six young men who performed four 30-s “all out” exercise bouts interspersed with 4 min of rest (<80 kJ total work). Phosphorylation of AMP-activated protein kinase (AMPK; subunits α1 and α2) and the p38 mitogen-activated protein kinase (MAPK) was higher ( P ≤ 0.05) immediately after bout 4 vs. preexercise. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) mRNA was increased approximately twofold above rest after 3 h of recovery ( P ≤ 0.05); however, PGC-1α protein content was unchanged. In contrast, phosphorylation of protein kinase B/Akt (Thr308 and Ser473) tended to decrease, and downstream targets linked to hypertrophy (p70 ribosomal S6 kinase and 4E binding protein 1) were unchanged after exercise and recovery. We conclude that signaling through AMPK and p38 MAPK to PGC-1α may explain in part the metabolic remodeling induced by low-volume intense interval exercise, including mitochondrial biogenesis and an increased capacity for glucose and fatty acid oxidation.
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“there is evidence to suggest increased mitochondrial biogenesis with endurance training is prioritized over ribosome biogenesis (Morrison et al., 1989; Gibala et al., 2009)”
From Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities (2021) · cites this paper as Gibala et al., 2009
In the citing paper
“Moreover, the timing of skeletal muscle biopsies and therefore of the measurements of AMPK/mTORC1 activation is commonly referred as a limitation and a possible source of inconsistencies found between different studies (Gibala et al., 2009; Figueiredo et al., 2015; Stec et al., 2015).”
From Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities (2021) · cites this paper as Gibala et al., 2009
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Metadata
- Authors
- Gibala, M. J., McGee, S. L., Garnham, A. P., Howlett, K. F., Snow, R. J., & Hargreaves, M.
- Affiliations
- McMaster University (CA)
- ORCID
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2009-03
- Volume
- 106
- Issue
- 3
- Pages
- 929-934
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2163772556
- Cited by
- 427
- References
- 37
- Citations by year
- 2026: 15 · 2025: 30 · 2024: 22 · 2023: 19 · 2022: 21 · 2021: 23 · 2020: 17 · 2019: 21 · 2018: 23 · 2017: 29 · 2016: 31 · 2015: 33 · 2014: 30 · 2013: 25 · 2012: 25
- FWCI
- 61.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Victoria University Research Repository (Victoria University) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- high-intensity interval exercise, AMPK, p38 MAPK, PGC-1α, mitochondrial biogenesis, skeletal muscle, acute exercise, Akt signaling, vastus lateralis
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Bicycling, Heat-Shock Proteins, Humans, Male, Phosphorylation, Transcription Factors, Exercise, Gene Expression, Muscle, Skeletal, MAP Kinase Signaling System, p38 Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-akt, AMP-Activated Protein Kinases, Young Adult
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