Facts and controversies in our understanding of how caloric restriction impacts the mitochondrion
Abstract
Caloric restriction (CR) has pronounced benefits in promoting healthy aging. Amongst the most frequently implicated physiological mechanisms implicated in this benefit is altered mitochondrial function. Whereas a reduction in mitochondrial reactive oxygen species (ROS) production is a widely consistent effect of CR, an increase in mitochondrial biogenesis, which is accepted by many as fact, is contradicted on several levels, most critically by a lack of increase in mitochondrial protein synthesis rate in vivo. Furthermore, an increase in PGC-1α protein and markers of mitochondrial content with CR is a highly variable observation between studies. On the other hand, deacetylation of several mitochondrial proteins by the sirtuin, Sirt3, is an increasingly reported observation and at least so far, this observation is consistent between studies. Notwithstanding this point, the controversies evident in the published literature underscore the significant questions that remain in our understanding of how CR impacts the mitochondrion and suggest we have yet to fully understand the complexities herein.
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Calorie restriction and endurance training improve mitochondrial function.
“In addition, the two most efficient non‐pharmacological strategies to attenuate the effects of ageing on skeletal muscle, calorie‐restriction (Mayhew et al. 1998; Baker et al. 2006; Hepple et al. 2006) and endurance training (Coggan et al. 1992; Song et al. 2006), are known to improve mitochondrial function (Gouspillou & Hepple, 2013).”
From Parkin overexpression protects from ageing‐related loss of muscle mass and strength (2019) · cites this paper as Gouspillou & Hepple, 2013
Exercise training and calorie restriction improve mitochondrial health.
“both well-known to improve mitochondrial health [28].”
From Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging (2021) · cites this paper as [28]
Calorie restriction improves mitochondrial health.
“and to improve mitochondrial health [28]”
From Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging (2021) · cites this paper as [28]
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Mitochondrial morphology is altered in atrophied skeletal muscle of aged mice
Leduc-Gaudet, J.-P., Picard, M., Pelletier, F. S.-J., Sgarioto, N., Auger, M.-J., Vallée, J., Robitaille, R., St-Pierre, D. H., & Gouspillou, G. (2015) · Oncotarget · doi:10.18632/oncotarget.4235 · Cited by 273 · see citing works
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Parkin overexpression protects from ageing‐related loss of muscle mass and strength
Leduc‐Gaudet, J., Reynaud, O., Hussain, S. N., & Gouspillou, G. (2019) · The Journal of Physiology · doi:10.1113/jp277157 · Cited by 119 · see citing works
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“Long-term caloric restriction (CR) is amongst the most efficient interventions to offset sarcopenia in rodents and CR is thought to exert its effects mostly through by improving mitochondria (see (Gouspillou and Hepple, 2013) for review).”
BackgroundSelf-citationMitochondrial function and diabetes: consequences for skeletal and cardiac muscle metabolism
Schrauwen-Hinderling, V. B., Kooi, M. E., & Schrauwen, P. (2016) · Antioxidants & Redox Signaling · doi:10.1089/ars.2015.6291 · Cited by 47 · see citing works
Mulvey, L., Sands, W. A., Salin, K., Carr, A. E., & Selman, C. (2017) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2016.09.001 · Cited by 16 · see citing works
Collaboration between mitochondria and the nucleus is key to long life in Caenorhabditis elegans
Chang, H.-W., Shtessel, L., & Lee, S. S. (2015) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.10.576 · Cited by 15 · see citing works
- Authors
- Gouspillou, G., & Hepple, R. T.
- Affiliations
- McGill University Health Centre (CA)
- Corresponding author
- Hepple, Russell T.
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 48
- Issue
- 10
- Pages
- 1075-1084
- ISSN
- 0531-5565 (ISSN-L)
- OpenAlex
- W2078444226
- Cited by
- 42
- References
- 118
- Citations by year
- 2026: 2 · 2025: 1 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 6 · 2017: 5 · 2016: 3 · 2015: 5 · 2014: 7 · 2013: 2
- FWCI
- 0.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (MOP57808, MOP119583)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- caloric restriction, mitochondrial function, healthy aging, mitochondrial biogenesis, mitochondrial reactive oxygen species, PGC-1α, SIRT3, mitochondrial translation, mitochondrial content
- MeSH terms
- Aging, Animals, Cardiolipins, DNA, Mitochondrial, Humans, Mitochondria, Reactive Oxygen Species, Caloric Restriction, Sirtuins, Rats, Mitochondrial Turnover
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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