Skeletal muscle ex vivo mitochondrial respiration parallels decline in vivo oxidative capacity, cardiorespiratory fitness, and muscle strength: The Baltimore Longitudinal Study of Aging
Summary Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that m...
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| Vydané v: | Aging cell Ročník 17; číslo 2 |
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| Hlavní autori: | , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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England
John Wiley & Sons, Inc
01.04.2018
John Wiley and Sons Inc |
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| ISSN: | 1474-9718, 1474-9726, 1474-9726 |
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| Abstract | Summary
Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high‐resolution respirometry in saponin‐permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (BLSA; 21 men, age 24–91 years) who also had available measures of peak oxygen consumption (VO2max) from treadmill tests, gait speed in different tasks, 31P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (p < .05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with VO2max, muscle strength, kPCr, and time to complete a 400‐m walk (p < .05). A negative trend toward significance (p = .074) was observed between mitochondrial respiration and BMI. Finally, transcriptional profiling revealed a reduced mRNA expression of mitochondrial gene networks with aging (p < .05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age‐associated loss of muscle performance and cardiorespiratory fitness. |
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| AbstractList | Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (
kPC
r), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high‐resolution respirometry in saponin‐permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (
BLSA
; 21 men, age 24–91 years) who also had available measures of peak oxygen consumption (
VO
2max
) from treadmill tests, gait speed in different tasks,
31
P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (
p <
.05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with
VO
2max
, muscle strength,
kPC
r, and time to complete a 400‐m walk (
p
< .05). A negative trend toward significance (
p
= .074) was observed between mitochondrial respiration and
BMI
. Finally, transcriptional profiling revealed a reduced
mRNA
expression of mitochondrial gene networks with aging (
p
< .05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age‐associated loss of muscle performance and cardiorespiratory fitness. Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high-resolution respirometry in saponin-permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (BLSA; 21 men, age 24-91 years) who also had available measures of peak oxygen consumption (VO2max ) from treadmill tests, gait speed in different tasks, 31 P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (p < .05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with VO2max , muscle strength, kPCr, and time to complete a 400-m walk (p < .05). A negative trend toward significance (p = .074) was observed between mitochondrial respiration and BMI. Finally, transcriptional profiling revealed a reduced mRNA expression of mitochondrial gene networks with aging (p < .05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age-associated loss of muscle performance and cardiorespiratory fitness.Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high-resolution respirometry in saponin-permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (BLSA; 21 men, age 24-91 years) who also had available measures of peak oxygen consumption (VO2max ) from treadmill tests, gait speed in different tasks, 31 P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (p < .05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with VO2max , muscle strength, kPCr, and time to complete a 400-m walk (p < .05). A negative trend toward significance (p = .074) was observed between mitochondrial respiration and BMI. Finally, transcriptional profiling revealed a reduced mRNA expression of mitochondrial gene networks with aging (p < .05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age-associated loss of muscle performance and cardiorespiratory fitness. Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high‐resolution respirometry in saponin‐permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (BLSA; 21 men, age 24–91 years) who also had available measures of peak oxygen consumption (VO2max) from treadmill tests, gait speed in different tasks, 31P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (p < .05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with VO2max, muscle strength, kPCr, and time to complete a 400‐m walk (p < .05). A negative trend toward significance (p = .074) was observed between mitochondrial respiration and BMI. Finally, transcriptional profiling revealed a reduced mRNA expression of mitochondrial gene networks with aging (p < .05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age‐associated loss of muscle performance and cardiorespiratory fitness. Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high‐resolution respirometry in saponin‐permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (BLSA; 21 men, age 24–91 years) who also had available measures of peak oxygen consumption (VO 2max) from treadmill tests, gait speed in different tasks, 31P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (p < .05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with VO 2max, muscle strength, kPCr, and time to complete a 400‐m walk (p < .05). A negative trend toward significance (p = .074) was observed between mitochondrial respiration and BMI. Finally, transcriptional profiling revealed a reduced mRNA expression of mitochondrial gene networks with aging (p < .05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age‐associated loss of muscle performance and cardiorespiratory fitness. Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high-resolution respirometry in saponin-permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (BLSA; 21 men, age 24-91 years) who also had available measures of peak oxygen consumption (VO ) from treadmill tests, gait speed in different tasks, P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (p < .05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with VO , muscle strength, kPCr, and time to complete a 400-m walk (p < .05). A negative trend toward significance (p = .074) was observed between mitochondrial respiration and BMI. Finally, transcriptional profiling revealed a reduced mRNA expression of mitochondrial gene networks with aging (p < .05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age-associated loss of muscle performance and cardiorespiratory fitness. Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high-resolution respirometry in saponin-permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (BLSA; 21 men, age 24-91 years) who also had available measures of peak oxygen consumption (VO[sub.2max]) from treadmill tests, gait speed in different tasks, [sup.31]P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (p <.05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with VO[sub.2max], muscle strength, kPCr, and time to complete a 400-m walk (p <.05). A negative trend toward significance (p=.074) was observed between mitochondrial respiration and BMI. Finally, transcriptional profiling revealed a reduced mRNA expression of mitochondrial gene networks with aging (p <.05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age-associated loss of muscle performance and cardiorespiratory fitness. Summary Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Mitochondrial respiration was assessed by high‐resolution respirometry in saponin‐permeabilized fibers from vastus lateralis muscle biopsies of 38 participants from the Baltimore Longitudinal Study of Aging (BLSA; 21 men, age 24–91 years) who also had available measures of peak oxygen consumption (VO2max) from treadmill tests, gait speed in different tasks, 31P magnetic resonance spectroscopy, isokinetic knee extension, and grip strength. Results indicated a significant reduction in mitochondrial respiration with age (p < .05) that was independent of other potential confounders. Mitochondrial respiratory capacity was also associated with VO2max, muscle strength, kPCr, and time to complete a 400‐m walk (p < .05). A negative trend toward significance (p = .074) was observed between mitochondrial respiration and BMI. Finally, transcriptional profiling revealed a reduced mRNA expression of mitochondrial gene networks with aging (p < .05). Overall, our findings reinforce the notion that mitochondrial function declines with age and may contribute to age‐associated loss of muscle performance and cardiorespiratory fitness. |
| Audience | Academic |
| Author | Diaz‐Ruiz, Alberto Becker, Kevin G. Tanaka, Toshiko Zane, Ariel Fabbri, Elisa Zukley, Linda Bernier, Michel D'Agostino, Jarod Gonzalez‐Freire, Marta Coen, Paul M. Cabo, Rafael Moore, Zenobia A. Lehrmann, Elin Scalzo, Paul Chen, Brian Chia, Chee W. Ferrucci, Luigi |
| AuthorAffiliation | 6 Translational Research Institute for Metabolism and Diabetes Florida Hospital Orlando FL USA 4 Gene Expression and Genomics Unit National Institute on Aging Baltimore MD USA 1 Longitudinal Studies Section Translational Gerontology Branch National Institute on Aging Baltimore MD USA 2 Clinical Research Unit MedStar Harbor Hospital National Institute on Aging Baltimore MD USA 3 Experimental Gerontology Section Translational Gerontology Branch National Institute on Aging Baltimore MD USA 5 Diabetes Section Laboratory of Clinical Investigation National Institute on Aging Baltimore MD USA |
| AuthorAffiliation_xml | – name: 2 Clinical Research Unit MedStar Harbor Hospital National Institute on Aging Baltimore MD USA – name: 6 Translational Research Institute for Metabolism and Diabetes Florida Hospital Orlando FL USA – name: 4 Gene Expression and Genomics Unit National Institute on Aging Baltimore MD USA – name: 5 Diabetes Section Laboratory of Clinical Investigation National Institute on Aging Baltimore MD USA – name: 1 Longitudinal Studies Section Translational Gerontology Branch National Institute on Aging Baltimore MD USA – name: 3 Experimental Gerontology Section Translational Gerontology Branch National Institute on Aging Baltimore MD USA |
| Author_xml | – sequence: 1 givenname: Marta surname: Gonzalez‐Freire fullname: Gonzalez‐Freire, Marta email: marta.gonzalezfreire@nih.gov organization: National Institute on Aging – sequence: 2 givenname: Paul surname: Scalzo fullname: Scalzo, Paul organization: National Institute on Aging – sequence: 3 givenname: Jarod surname: D'Agostino fullname: D'Agostino, Jarod organization: National Institute on Aging – sequence: 4 givenname: Zenobia A. surname: Moore fullname: Moore, Zenobia A. organization: National Institute on Aging – sequence: 5 givenname: Alberto surname: Diaz‐Ruiz fullname: Diaz‐Ruiz, Alberto organization: National Institute on Aging – sequence: 6 givenname: Elisa surname: Fabbri fullname: Fabbri, Elisa organization: National Institute on Aging – sequence: 7 givenname: Ariel surname: Zane fullname: Zane, Ariel organization: National Institute on Aging – sequence: 8 givenname: Brian surname: Chen fullname: Chen, Brian organization: National Institute on Aging – sequence: 9 givenname: Kevin G. surname: Becker fullname: Becker, Kevin G. organization: National Institute on Aging – sequence: 10 givenname: Elin surname: Lehrmann fullname: Lehrmann, Elin organization: National Institute on Aging – sequence: 11 givenname: Linda surname: Zukley fullname: Zukley, Linda organization: National Institute on Aging – sequence: 12 givenname: Chee W. surname: Chia fullname: Chia, Chee W. organization: National Institute on Aging – sequence: 13 givenname: Toshiko surname: Tanaka fullname: Tanaka, Toshiko organization: National Institute on Aging – sequence: 14 givenname: Paul M. orcidid: 0000-0002-2805-2115 surname: Coen fullname: Coen, Paul M. organization: Florida Hospital – sequence: 15 givenname: Michel surname: Bernier fullname: Bernier, Michel organization: National Institute on Aging – sequence: 16 givenname: Rafael surname: Cabo fullname: Cabo, Rafael organization: National Institute on Aging – sequence: 17 givenname: Luigi surname: Ferrucci fullname: Ferrucci, Luigi email: FerrucciLu@grc.nia.nih.gov organization: National Institute on Aging |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29356348$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1152/japplphysiol.00583.2016 10.1111/acel.12604 10.1016/S0092-8674(04)00400-3 10.1093/gerona/glu096 10.1186/s40608-015-0070-4 10.1046/j.1532-5415.2001.4911247.x 10.1111/micc.12098 10.1016/j.bbabio.2016.02.014 10.1186/s13395-015-0059-1 10.1093/gerona/gls196 10.2337/db16-0754 10.1016/j.cmet.2007.01.008 10.2337/db15-0823 10.1159/000172832 10.1152/ajpendo.00125.2015 10.1016/S1525-1578(10)60455-2 10.1155/2012/194821 10.2337/db15-0809 10.1093/gerona/glv070 10.1016/j.cmet.2017.02.009 10.1093/geronj/21.4.575 10.1210/jc.2013-3983 10.1042/BJ20110366 10.3389/fnagi.2014.00208 10.1016/S0010-4825(01)00006-3 10.1093/gerona/61.6.534 10.1001/jama.295.17.2018 10.1161/JAHA.117.006604 10.1093/gerona/glu058 10.1111/acel.12568 10.1016/j.exger.2016.04.002 10.1161/CIRCULATIONAHA.105.545459 10.1186/1471-2105-6-144 10.1111/jgs.12653 10.1038/nature14614 10.1093/gerona/glw059 |
| ContentType | Journal Article |
| Copyright | Published 2018. This article is a U.S. Government work and is in the public domain in the USA. published by the Anatomical Society and John Wiley & Sons Ltd. Published 2018. This article is a U.S. Government work and is in the public domain in the USA. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. COPYRIGHT 2018 John Wiley & Sons, Inc. Copyright © 2018 The Anatomical Society and John Wiley & Sons Ltd. |
| Copyright_xml | – notice: Published 2018. This article is a U.S. Government work and is in the public domain in the USA. published by the Anatomical Society and John Wiley & Sons Ltd. – notice: Published 2018. This article is a U.S. Government work and is in the public domain in the USA. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. – notice: COPYRIGHT 2018 John Wiley & Sons, Inc. – notice: Copyright © 2018 The Anatomical Society and John Wiley & Sons Ltd. |
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| Keywords | aging muscle performance skeletal muscle mitochondria oxidative capacity |
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| License | Attribution http://creativecommons.org/licenses/by/4.0 Published 2018. This article is a U.S. Government work and is in the public domain in the USA. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| References_xml | – volume: 1857 start-page: 1284 year: 2016 end-page: 1289 article-title: The electrochemical transmission in I‐Band segments of the mitochondrial reticulum publication-title: Biochimica et Biophysica Acta – volume: 65 start-page: 561 year: 2016 end-page: 573 article-title: Altered skeletal muscle mitochondrial proteome as the basis of disruption of mitochondrial function in diabetic mice publication-title: Diabetes – volume: 55 start-page: 259 year: 2009 end-page: 268 article-title: Reproducibility of an isokinetic strength‐testing protocol of the knee and ankle in older adults publication-title: Gerontology – volume: 2012 start-page: 194821 year: 2012 article-title: Skeletal muscle mitochondria and aging: A review publication-title: Journal of Aging Research – volume: 437 start-page: 215 year: 2011 end-page: 222 article-title: Inhibiting myosin‐ATPase reveals a dynamic range of mitochondrial respiratory control in skeletal muscle publication-title: Biochemical Journal – volume: 2 start-page: 40 year: 2015 article-title: Relationships between mitochondrial content and bioenergetics with obesity, body composition and fat distribution in healthy older adults publication-title: BMC Obesity – volume: 121 start-page: 996 issue: 4 year: 2016 end-page: 1003 article-title: In vivo mitochondrial function in aging skeletal muscle: Capacity, flux, and patterns of use (2016) publication-title: Journal of Applied Physiology – volume: 5 start-page: 151 year: 2007 end-page: 156 article-title: Aging‐associated reductions in AMP‐activated protein kinase activity and mitochondrial biogenesis publication-title: Cell Metabolism – volume: 6 start-page: 144 year: 2005 article-title: PAGE: Parametric analysis of gene set enrichment publication-title: BMC Bioinformatics – volume: 71 start-page: 1638 year: 2016 end-page: 1645 article-title: 31P magnetic resonance spectroscopy assessment of muscle bioenergetics as a predictor of gait speed in the Baltimore longitudinal study of aging publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 64 start-page: 3737 year: 2015 end-page: 3750 article-title: Exercise and weight loss improve muscle mitochondrial respiration, lipid partitioning, and insulin sensitivity after gastric bypass surgery publication-title: Diabetes – volume: 16 start-page: 738 issue: 4 year: 2017 end-page: 749 article-title: Biochemical isolation of myonuclei employed to define changes to the myonuclear proteome that occur with aging publication-title: Aging Cell – volume: 70 start-page: 1394 year: 2015 end-page: 1399 article-title: Respirometric profiling of muscle mitochondria and blood cells are associated with differences in gait speed among community‐dwelling older adults publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 21 start-page: 131 year: 2014 end-page: 147 article-title: In vivo microscopy reveals extensive embedding of capillaries within the sarcolemma of skeletal muscle fibers publication-title: Microcirculation – volume: 25 start-page: 581 year: 2017 end-page: 592 article-title: Enhanced protein translation underlies improved metabolic and physical adaptations to different exercise training modes in young and old humans publication-title: Cell Metabolism – volume: 117 start-page: 399 year: 2004 end-page: 412 article-title: Foxo transcription factors induce the atrophy‐related ubiquitin ligase atrogin‐1 and cause skeletal muscle atrophy publication-title: Cell – start-page: 661 year: 1984 1984 – volume: 6 start-page: e006604 issue: 9 year: 2017 article-title: Lower mitochondrial energy production of the thigh muscles in patients with low‐normal ankle‐brachial index publication-title: Journal of the American Heart Association – volume: 5 start-page: 73 year: 2003 end-page: 81 article-title: Analysis of microarray data using Z score transformation publication-title: The Journal of Molecular Diagnostics: JMD – volume: 21 start-page: 575 year: 1966 end-page: 580 article-title: Activities and attitudes of participants in the Baltimore longitudinal study publication-title: Journal of Gerontology – volume: 16 start-page: 461 issue: 3 year: 2017 end-page: 468 article-title: Muscle strength mediates the relationship between mitochondrial energetics and walking performance publication-title: Aging Cell – volume: 68 start-page: 447 year: 2013 end-page: 455 article-title: Skeletal muscle mitochondrial energetics are associated with maximal aerobic capacity and walking speed in older adults publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 61 start-page: 534 issue: 6 year: 2006 end-page: 540 article-title: J Effects of exercise on mitochondrial content and function in aging human skeletal muscle publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 2 start-page: 209 year: 2003 end-page: 217 article-title: Application of z‐score transformation to Affymetrix data publication-title: Applied Bioinformatics – volume: 295 start-page: 2018 year: 2006 end-page: 2026 article-title: Association of long‐distance corridor walk performance with mortality, cardiovascular disease, mobility limitation, and disability publication-title: JAMA – volume: 205 start-page: 423 year: 2012 end-page: 432 article-title: The influence of age and aerobic fitness: Effects on mitochondrial respiration in skeletal muscle publication-title: Acta Psychologica – volume: 69 start-page: S21 issue: Suppl 1 year: 2014 end-page: S27 article-title: Recent progress in metabolic signaling pathways regulating aging and life span publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 81 start-page: 1 year: 2016 end-page: 7 article-title: The relationship between mitochondrial function and walking performance in older adults with a wide range of physical function publication-title: Experimental Gerontology – volume: 31 start-page: 269 year: 2001 end-page: 286 article-title: Java‐based graphical user interface for MRUI, a software package for quantitation of in vivo/medical magnetic resonance spectroscopy signals publication-title: Computers in Biology and Medicine – volume: 72 start-page: 535 year: 2017 end-page: 542 article-title: Chronological age does not influence ex‐vivo mitochondrial respiration and quality control in skeletal muscle publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 523 start-page: 617 year: 2015 end-page: 620 article-title: Mitochondrial reticulum for cellular energy distribution in muscle publication-title: Nature – volume: 49 start-page: 1544 year: 2001 end-page: 1548 article-title: Measuring fitness in healthy older adults: The Health ABC Long Distance Corridor Walk publication-title: Journal of the American Geriatrics Society – volume: 5 start-page: 35 year: 2015 article-title: A novel atlas of gene expression in human skeletal muscle reveals molecular changes associated with aging publication-title: Skeletal Muscle – volume: 6 start-page: 208 year: 2014 article-title: The neuromuscular junction: Aging at the crossroad between nerves and muscle publication-title: Frontiers in Aging Neuroscience – volume: 99 start-page: 1852 year: 2014 end-page: 1861 article-title: Skeletal muscle mitochondria in the elderly: Effects of physical fitness and exercise training publication-title: Journal of Clinical Endocrinology and Metabolism – volume: 66 start-page: 170 issue: 1 year: 2017 end-page: 176 article-title: Insulin resistance is associated with reduced mitochondrial oxidative capacity measured by 31P‐magnetic resonance spectroscopy in participants without diabetes from the Baltimore longitudinal study of aging publication-title: Diabetes – start-page: 38 year: 2009 end-page: 42 – volume: 112 start-page: 674 year: 2005 end-page: 682 article-title: Accelerated longitudinal decline of aerobic capacity in healthy older adults publication-title: Circulation – volume: 70 start-page: 1334 year: 2015 end-page: 1342 article-title: Reconsidering the role of mitochondria in aging publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 62 start-page: 230 year: 2014 end-page: 236 article-title: Difference in muscle quality over the adult life span and biological correlates in the Baltimore Longitudinal Study of Aging publication-title: Journal of the American Geriatrics Society – volume: 309 start-page: E224 year: 2015 end-page: E232 article-title: Mitochondrial respiratory capacity and coupling control decline with age in human skeletal muscle publication-title: American Journal of Physiology. Endocrinology and Metabolism – ident: e_1_2_9_20_1 doi: 10.1152/japplphysiol.00583.2016 – start-page: 661 volume-title: Normal human aging: The Baltimore longitudinal study of aging year: 1984 ident: e_1_2_9_37_1 – ident: e_1_2_9_10_1 doi: 10.1111/acel.12604 – ident: e_1_2_9_35_1 doi: 10.1016/S0092-8674(04)00400-3 – ident: e_1_2_9_41_1 doi: 10.1093/gerona/glu096 – ident: e_1_2_9_3_1 doi: 10.1186/s40608-015-0070-4 – ident: e_1_2_9_38_1 doi: 10.1046/j.1532-5415.2001.4911247.x – ident: e_1_2_9_28_1 – ident: e_1_2_9_15_1 doi: 10.1111/micc.12098 – start-page: 38 volume-title: Mitochondrial pathways and respiratory control year: 2009 ident: e_1_2_9_16_1 – volume: 205 start-page: 423 year: 2012 ident: e_1_2_9_22_1 article-title: The influence of age and aerobic fitness: Effects on mitochondrial respiration in skeletal muscle publication-title: Acta Psychologica – ident: e_1_2_9_29_1 doi: 10.1016/j.bbabio.2016.02.014 – ident: e_1_2_9_40_1 doi: 10.1186/s13395-015-0059-1 – ident: e_1_2_9_8_1 doi: 10.1093/gerona/gls196 – ident: e_1_2_9_12_1 doi: 10.2337/db16-0754 – ident: e_1_2_9_33_1 doi: 10.1016/j.cmet.2007.01.008 – ident: e_1_2_9_42_1 doi: 10.2337/db15-0823 – ident: e_1_2_9_19_1 doi: 10.1159/000172832 – ident: e_1_2_9_32_1 doi: 10.1152/ajpendo.00125.2015 – ident: e_1_2_9_6_1 doi: 10.1016/S1525-1578(10)60455-2 – ident: e_1_2_9_31_1 doi: 10.1155/2012/194821 – ident: e_1_2_9_9_1 doi: 10.2337/db15-0809 – ident: e_1_2_9_17_1 doi: 10.1093/gerona/glv070 – ident: e_1_2_9_34_1 doi: 10.1016/j.cmet.2017.02.009 – ident: e_1_2_9_39_1 doi: 10.1093/geronj/21.4.575 – ident: e_1_2_9_4_1 doi: 10.1210/jc.2013-3983 – ident: e_1_2_9_30_1 doi: 10.1042/BJ20110366 – ident: e_1_2_9_18_1 doi: 10.3389/fnagi.2014.00208 – ident: e_1_2_9_25_1 doi: 10.1016/S0010-4825(01)00006-3 – ident: e_1_2_9_23_1 doi: 10.1093/gerona/61.6.534 – ident: e_1_2_9_27_1 doi: 10.1001/jama.295.17.2018 – ident: e_1_2_9_2_1 doi: 10.1161/JAHA.117.006604 – volume: 72 start-page: 535 year: 2017 ident: e_1_2_9_11_1 article-title: Chronological age does not influence ex‐vivo mitochondrial respiration and quality control in skeletal muscle publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – ident: e_1_2_9_26_1 doi: 10.1093/gerona/glu058 – ident: e_1_2_9_43_1 doi: 10.1111/acel.12568 – ident: e_1_2_9_36_1 doi: 10.1016/j.exger.2016.04.002 – ident: e_1_2_9_13_1 doi: 10.1161/CIRCULATIONAHA.105.545459 – ident: e_1_2_9_21_1 doi: 10.1186/1471-2105-6-144 – ident: e_1_2_9_24_1 doi: 10.1111/jgs.12653 – ident: e_1_2_9_14_1 doi: 10.1038/nature14614 – volume: 2 start-page: 209 year: 2003 ident: e_1_2_9_5_1 article-title: Application of z‐score transformation to Affymetrix data publication-title: Applied Bioinformatics – ident: e_1_2_9_7_1 doi: 10.1093/gerona/glw059 |
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Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial... Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function... |
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| SubjectTerms | Adult Age Aged Aged, 80 and over Aging Cardiorespiratory fitness Cardiorespiratory Fitness - physiology Electron transport Exercise Female Gait Gene expression Humans Knee Longitudinal Studies Magnetic resonance spectroscopy Male Middle Aged Mitochondria Mitochondria, Muscle - metabolism Mitochondrial DNA muscle performance Muscle strength Muscle Strength - physiology Muscle, Skeletal - metabolism Muscles Musculoskeletal system Original Oxidation-Reduction oxidative capacity Oxygen consumption Oxygen Consumption - physiology Phosphocreatine Physical fitness Respiration Skeletal muscle Statistics Transcription Young Adult |
| Title | Skeletal muscle ex vivo mitochondrial respiration parallels decline in vivo oxidative capacity, cardiorespiratory fitness, and muscle strength: The Baltimore Longitudinal Study of Aging |
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