The DOI matches its Crossref record; 41 of the 42 references it cites were found in a registry or an index.
Skeletal Muscle Mitochondrial Energetics Are Associated With Maximal Aerobic Capacity and Walking Speed in Older Adults
Open accessAbstract
BACKGROUND: Lower ambulatory performance with aging may be related to a reduced oxidative capacity within skeletal muscle. This study examined the associations between skeletal muscle mitochondrial capacity and efficiency with walking performance in a group of older adults. METHODS: Thirty-seven older adults (mean age 78 years; 21 men and 16 women) completed an aerobic capacity (VO2 peak) test and measurement of preferred walking speed over 400 m. Maximal coupled (State 3; St3) mitochondrial respiration was determined by high-resolution respirometry in saponin-permeabilized myofibers obtained from percutanous biopsies of vastus lateralis (n = 22). Maximal phosphorylation capacity (ATPmax) of vastus lateralis was determined in vivo by (31)P magnetic resonance spectroscopy (n = 30). Quadriceps contractile volume was determined by magnetic resonance imaging. Mitochondrial efficiency (max ATP production/max O2 consumption) was characterized using ATPmax per St3 respiration (ATPmax/St3). RESULTS: In vitro St3 respiration was significantly correlated with in vivo ATPmax (r (2) = .47, p = .004). Total oxidative capacity of the quadriceps (St3*quadriceps contractile volume) was a determinant of VO2 peak (r (2) = .33, p = .006). ATPmax (r (2) = .158, p = .03) and VO2 peak (r (2) = .475, p < .0001) were correlated with preferred walking speed. Inclusion of both ATPmax/St3 and VO2 peak in a multiple linear regression model improved the prediction of preferred walking speed (r (2) = .647, p < .0001), suggesting that mitochondrial efficiency is an important determinant for preferred walking speed. CONCLUSIONS: Lower mitochondrial capacity and efficiency were both associated with slower walking speed within a group of older participants with a wide range of function. In addition to aerobic capacity, lower mitochondrial capacity and efficiency likely play roles in slowing gait speed with age.
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“Collectively, these age-related skeletal muscle deficits contribute to reductions in cardiorespiratory fitness (peak oxygen uptake [Vo2 peak]), exercise tolerance, and overall physical function (9, 10).”
From Combined Training Enhances Skeletal Muscle Mitochondrial Oxidative Capacity Independent of Age (2015) · cites this paper as [10]
In the citing paper
“recent studies have shown that loss of mitochondrial energetics in sub-optimal aging contributes to slower walking speed [[355], [356], [357], [358]], fatigability [359], multimorbidity [360], frailty [361] and sarcopenia [345,362].”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [356]
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“For instance, in a prospective cohort study, walking reduced the risk of dementia in a dose-dependent manner, with walking less than 0.25 miles per day compared to walking > 2 miles per day, controlling for other risk factors [356].”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [356]
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“For instance, in a prospective cohort study, walking reduced the risk of dementia in a dose-dependent manner, with walking less than 0.25 miles per day compared to walking > 2 miles per day, controlling for other risk factors [356].”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [356]
In the citing paper
“Thus, evidence to date strongly implicates the mitochondria as having a pivotal role in the pathogenesis of age-related functional decline,(Coen, Jubrias, Distefano, Amati, Mackey, Glynn, Manini, Wohlgemuth, Leeuwenburgh, Cummings, Newman, Ferrucci, Toledo, Shankland, Conley, and Goodpaster 2013) and reductions in autophagy appear to be a critical biological mechanism affecting the collective”
From Successful aging: Advancing the science of physical independence in older adults (2015) · cites this paper as Coen et al. 2013
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“AGING is associated with reduced mitochondrial capacity (1,2) and loss of muscle mass and strength (3,4), which could potentially predispose individuals to frailty and a slower preferential walking speed (5,6).”
BackgroundSelf-citationMitochondrial dysfunction in the elderly: possible role in insulin resistance
Petersen, K. F., Befroy, D., Dufour, S., Dziura, J., Ariyan, C., Rothman, D. L., DiPietro, L., Cline, G. W., & Shulman, G. I. (2003) · Science · doi:10.1126/science.1082889 · Cited by 2,107
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Self-citationDecline in skeletal muscle mitochondrial function with aging in humans
Short, K. R., Bigelow, M. L., Kahl, J., Singh, R., Coenen-Schimke, J., Raghavakaimal, S., & Nair, K. S. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0501559102 · Cited by 1,333
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Cited by
Sorted by citations
Measuring biological aging in humans: a quest
Ferrucci, L., Gonzalez‐Freire, M., Fabbri, E., Simonsick, E., Tanaka, T., Moore, Z., Salimi, S., Sierra, F., & de Cabo, R. (2020) · Aging Cell · doi:10.1111/acel.13080 · Cited by 781
“…it has been demonstrated that the degree of oxidative phosphorylation declines with aging in humans in the heart, skeletal muscle, and other tissues (Coen et al., 2012; Consolini, Ragone, Bonazzola, & Colareda, 2017; Fabbri et al., 2016; Gonzalez-Freire et al., 2018; Holloway et al., 2018).”
BackgroundSelf-citationEvidence for the Domains Supporting the Construct of Intrinsic Capacity
Cesari, M., Araujo de Carvalho, I., Amuthavalli Thiyagarajan, J., Cooper, C., Martin, F. C., Reginster, J.-Y., Vellas, B., & Beard, J. R. (2018) · The Journals of Gerontology: Series A · doi:10.1093/gerona/gly011 · Cited by 745
“demonstrates the relationship between measures of mobility with subclinical pathophysiological modifications, such as increased atherosclerotic formation (60), decreased aerobic capacity (61), or inflammatory status (62).”
BackgroundMitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials
Marzetti, E., Calvani, R., Cesari, M., Buford, T. W., Lorenzi, M., Behnke, B. J., & Leeuwenburgh, C. (2013) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2013.06.024 · Cited by 627
“The impact of mitochondrial bioenergetic decline on muscle aging is witnessed by the existence of a correlation between ATP synthesis/O2 consumption and preferred walking speed in healthy elderly (Coen et al. 2013).”
Self-citationAndreux, P. A., Blanco-Bose, W., Ryu, D., Burdet, F., Ibberson, M., Aebischer, P., Auwerx, J., Singh, A., & Rinsch, C. (2019) · Nature Metabolism · doi:10.1038/s42255-019-0073-4 · Cited by 590
McGregor, R. A., Cameron-Smith, D., & Poppitt, S. D. (2014) · Longevity & Healthspan · doi:10.1186/2046-2395-3-9 · Cited by 532
“ciated with gait speed [56].”
Metadata
- Authors
- Coen, P. M., Jubrias, S. A., Distefano, G., Amati, F., Mackey, D. C., Glynn, N. W., Manini, T. M., Wohlgemuth, S. E., Leeuwenburgh, C., Cummings, S. R., Newman, A. B., Ferrucci, L., Toledo, F. G. S., Shankland, E., Conley, K. E., & Goodpaster, B. H.
- Affiliations
- University of Pittsburgh (US)
- University of Washington Medical Center (US)
- California Pacific Medical Center (US)
- University of Florida (US)
- National Institute on Aging (US)
- ORCID
- Venue
- The Journals of Gerontology: Series A
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-10-09
- Volume
- 68
- Issue
- 4
- Pages
- 447-455
- ISSN
- 1079-5006 (ISSN-L)
- 1758-535X
- PMC
- PMC3593613
- OpenAlex
- W2115546051
- Cited by
- 323
- References
- 42
- Citations by year
- 2026: 19 · 2025: 19 · 2024: 40 · 2023: 30 · 2022: 20 · 2021: 43 · 2020: 26 · 2019: 20 · 2018: 14 · 2017: 19 · 2016: 34 · 2015: 16 · 2014: 14 · 2013: 8 · 2012: 1
- FWCI
- 30.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journals of Gerontology Series A (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (acceptedVersion, other-oa)
- IRIS (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- University of Pittsburgh (P30-AG024827, UL1RR024153, RR024153)
- National Institutes of Health (UL1TR000005)
- National Institute on Aging (RC2AG036594, RC2AG036606, P30AG024827, P30AG028740)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR 41928, R01AR041928)
- National Center for Research Resources (RR-024153, UL1RR024153)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Keywords
- skeletal muscle mitochondria, mitochondrial respiration, maximal aerobic capacity, peak oxygen uptake, walking speed, older adults, mitochondrial efficiency, oxidative capacity, vastus lateralis, aging
- MeSH terms
- Age Factors, Aged, Biopsy, Energy Metabolism, Postural Balance, Female, Humans, Male, Mitochondria, Muscle, Muscle Contraction, Oxygen Consumption, Physical Endurance, Physical Fitness, Walking, Muscle, Skeletal, Quadriceps Muscle
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