Exercise training can induce robust changes in mitochondria that are beneficial for a range of metabolic health outcomes. However, a recent study suggests there might be an upper limit to the amount of high-intensity training that can be tolerated before disruptions to mitochondrial function and whole-body metabolic homeostasis occur.
This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
Design and implementation of load intensity monitoring platform supported by big data technology in stage training for women’s sitting volleyball
Scientific Reports Open Access 16 December 2023
Access options
Access Nature and 54 other Nature Portfolio journals
Get Nature+, our best-value online-access subscription
$29.99 / 30 days
cancel any time
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
Hawley, J. A. et al. Integrative biology of exercise. Cell 159, 738–749 (2014).
Perry, C. G. R. & Hawley, J. A. Molecular basis of exercise-induced skeletal muscle mitochondrial biogenesis: Historical advances, current knowledge, and future challenges. Cold Spring Harb. Perspect. Med. 8, a029686 (2018).
Holloszy, J. O. Biochemical adaptations in muscle. Effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity in skeletal muscle. J. Biol. Chem. 242, 2278–2282 (1967).
MacInnis, M. J. & Gibala, M. J. Physiological adaptations to interval training and the role of exercise intensity. J. Physiol. 595, 2915–2930 (2017).
Ruegsegger, G. N. & Booth, F. W. Health benefits of exercise. Cold Spring Harb. Perspect. Med. 8, a029694 (2018).
Hawley, J. A. et al. Maximizing cellular adaptation to endurance exercise in skeletal muscle. Cell Metab. 27, 962–976 (2018).
Flockhart, M. et al. Excessive exercise training causes mitochondrial functional impairment and decreases glucose tolerance in healthy volunteers. Cell Metab. https://doi.org/10.1016/j.cmet.2021.02.017 (2021).
Picard, M. et al. Mitochondrial functional impairment with aging is exaggerated in isolated mitochondria compared to permeabilized myofibers. Aging Cell 9, 1032–1046 (2010).
Granata, C. et al. Multi-omics reveal unexpected complexity of mitochondrial adaptations to training in human skeletal muscle. Preprint at bioRxiv https://doi.org/10.1101/2021.02.19.431993 (2021).
Granata, C. et al. Mitochondrial adaptations to high-volume exercise training are rapidly reversed after a reduction in training volume in human skeletal muscle. FASEB J. 30, 3413–3423 (2016).
Acknowledgements
Work in the authors’ laboratories is, in part, funded by an Australian Research Council grant DP160102176, “Molecular networks underlying exercise-induced mitochondrial biogenesis in humans”.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Competing interests
The authors declare no competing interests.
Rights and permissions
About this article
Cite this article
Hawley, J.A., Bishop, D.J. High-intensity exercise training — too much of a good thing?. Nat Rev Endocrinol 17, 385–386 (2021). https://doi.org/10.1038/s41574-021-00500-6
Published:
Issue Date:
DOI: https://doi.org/10.1038/s41574-021-00500-6
