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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| Vydáno v: | Aging cell Ročník 17; číslo 2 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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England
John Wiley & Sons, Inc
01.04.2018
John Wiley and Sons Inc |
| Témata: | |
| ISSN: | 1474-9718, 1474-9726, 1474-9726 |
| On-line přístup: | Získat plný text |
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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 (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 (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. 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. 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 ( 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 (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. |
| 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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| 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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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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