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Luigi Ferrucci - One of the best experts on this subject based on the ideXlab platform.

  • Poor mitochondrial health and systemic inflammation? Test of a classic hypothesis in the Baltimore Longitudinal Study of Aging
    GeroScience, 2020
    Co-Authors: Marta Zampino, Richard G Spencer, Kenneth W Fishbein, Nicholas A. Brennan, Eleanor M. Simonsick, Luigi Ferrucci
    Abstract:

    Although a persistent inflammatory state has long been associated with aging and negative health outcomes, the underlying mechanisms remain unclear. Mitochondrial dysfunction has been proposed as a cause of inflammaging, but evidence of an association in humans is lacking. In this study, we analyzed the cross-sectional association between inflammatory biomarkers and mitochondrial oxidative capacity in skeletal muscle, assessed as post-exercise phosphocreatine Recovery Time Constant by phosphorus magnetic resonance spectroscopy, in a population of 669 adults (mean age 67 years) from the Baltimore Longitudinal Study of Aging. We observed that participants with lower mitochondrial oxidative capacity exhibited hallmarks of inflammation, specifically markedly higher levels of interleukin-6 and C-reactive protein, as well as increased erythrocyte sedimentation rate when compared with participants with better oxidative capacity, independent of age and sex. We speculate that this association reflects the observation that products of damaged mitochondria, such as mitochondrial DNA, activate multiple pathways that lead to inflammation. Furthermore, excess production of oxidative species (ROS) by dysfunctional mitochondria could trigger inflammation either directly via NF-κB or through oxidative damage to proteins, lipids, and nucleic acids. Longitudinal studies are necessary to ascertain whether and through which mechanisms mitochondrial dysfunction activate inflammation or whether both these phenomena derive from a common root.

  • greater skeletal muscle oxidative capacity is associated with higher resting metabolic rate results from the baltimore longitudinal study of aging
    Journals of Gerontology Series A-biological Sciences and Medical Sciences, 2020
    Co-Authors: Marta Zampino, Richard David Semba, Fatemeh Adelnia, Richard G Spencer, Kenneth W Fishbein, Jennifer A Schrack, Eleanor Marie Simonsick, Luigi Ferrucci
    Abstract:

    BACKGROUND: Resting metabolic rate (RMR) tends to decline with aging. The age-trajectory of decline in RMR is similar to changes that occur in muscle mass, muscle strength and fitness but while the decline in these phenotypes have been related to changes of mitochondrial function and oxidative capacity, whether lower RMR is associated with poorer mitochondrial oxidative capacity is unknown. METHODS: In 619 participants of the Baltimore Longitudinal Study of Aging, we analyzed the cross-sectional association between RMR (kcal/day), assessed by indirect calorimetry, and skeletal muscle maximal oxidative phosphorylation capacity, assessed as post-exercise phosphocreatine Recovery Time Constant (tauPCr), by phosphorous magnetic resonance spectroscopy. Linear regression models were used to evaluate the relationship between tauPCr and RMR, adjusting for potential confounders. RESULTS: Independent of age, sex, lean body mass, muscle density and fat mass, higher RMR was significantly associated with shorter tauPCr, indicating greater mitochondrial oxidative capacity. CONCLUSION: Higher RMR is associated with a higher mitochondrial oxidative capacity in skeletal muscle. This association may reflect a relationship between better muscle quality and greater mitochondrial health.

Richard G Spencer - One of the best experts on this subject based on the ideXlab platform.

  • Poor mitochondrial health and systemic inflammation? Test of a classic hypothesis in the Baltimore Longitudinal Study of Aging
    GeroScience, 2020
    Co-Authors: Marta Zampino, Richard G Spencer, Kenneth W Fishbein, Nicholas A. Brennan, Eleanor M. Simonsick, Luigi Ferrucci
    Abstract:

    Although a persistent inflammatory state has long been associated with aging and negative health outcomes, the underlying mechanisms remain unclear. Mitochondrial dysfunction has been proposed as a cause of inflammaging, but evidence of an association in humans is lacking. In this study, we analyzed the cross-sectional association between inflammatory biomarkers and mitochondrial oxidative capacity in skeletal muscle, assessed as post-exercise phosphocreatine Recovery Time Constant by phosphorus magnetic resonance spectroscopy, in a population of 669 adults (mean age 67 years) from the Baltimore Longitudinal Study of Aging. We observed that participants with lower mitochondrial oxidative capacity exhibited hallmarks of inflammation, specifically markedly higher levels of interleukin-6 and C-reactive protein, as well as increased erythrocyte sedimentation rate when compared with participants with better oxidative capacity, independent of age and sex. We speculate that this association reflects the observation that products of damaged mitochondria, such as mitochondrial DNA, activate multiple pathways that lead to inflammation. Furthermore, excess production of oxidative species (ROS) by dysfunctional mitochondria could trigger inflammation either directly via NF-κB or through oxidative damage to proteins, lipids, and nucleic acids. Longitudinal studies are necessary to ascertain whether and through which mechanisms mitochondrial dysfunction activate inflammation or whether both these phenomena derive from a common root.

  • greater skeletal muscle oxidative capacity is associated with higher resting metabolic rate results from the baltimore longitudinal study of aging
    Journals of Gerontology Series A-biological Sciences and Medical Sciences, 2020
    Co-Authors: Marta Zampino, Richard David Semba, Fatemeh Adelnia, Richard G Spencer, Kenneth W Fishbein, Jennifer A Schrack, Eleanor Marie Simonsick, Luigi Ferrucci
    Abstract:

    BACKGROUND: Resting metabolic rate (RMR) tends to decline with aging. The age-trajectory of decline in RMR is similar to changes that occur in muscle mass, muscle strength and fitness but while the decline in these phenotypes have been related to changes of mitochondrial function and oxidative capacity, whether lower RMR is associated with poorer mitochondrial oxidative capacity is unknown. METHODS: In 619 participants of the Baltimore Longitudinal Study of Aging, we analyzed the cross-sectional association between RMR (kcal/day), assessed by indirect calorimetry, and skeletal muscle maximal oxidative phosphorylation capacity, assessed as post-exercise phosphocreatine Recovery Time Constant (tauPCr), by phosphorous magnetic resonance spectroscopy. Linear regression models were used to evaluate the relationship between tauPCr and RMR, adjusting for potential confounders. RESULTS: Independent of age, sex, lean body mass, muscle density and fat mass, higher RMR was significantly associated with shorter tauPCr, indicating greater mitochondrial oxidative capacity. CONCLUSION: Higher RMR is associated with a higher mitochondrial oxidative capacity in skeletal muscle. This association may reflect a relationship between better muscle quality and greater mitochondrial health.

  • 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
    Diabetes, 2017
    Co-Authors: Richard G Spencer, Kenneth W Fishbein, Elisa Fabbri, Chee W Chia, David Reiter, Donnie Cameron, Ariel Zane, Zenobia A Moore, Marta Gonzalezfreire
    Abstract:

    Whether individuals with insulin resistance (IR) but without criteria for diabetes exhibit reduced mitochondrial oxidative capacity is unclear; addressing this question could guide research for new therapeutics. We investigated 248 participants without diabetes from the Baltimore Longitudinal Study of Aging (BLSA) to determine whether impaired mitochondrial capacity is associated with prediabetes, IR, and duration and severity of hyperglycemia exposure. Mitochondrial capacity was assessed as the postexercise phosphocreatine Recovery Time Constant (τPCr) by 31P-magnetic resonance spectroscopy, with higher τPCr values reflecting reduced capacity. Prediabetes was defined using the American Diabetes Association criteria from fasting and 2-h glucose measurements. IR and sensitivity were calculated using HOMA-IR and Matsuda indices. The duration and severity of hyperglycemia exposure were estimated as the number of years from prediabetes onset and the average oral glucose tolerance test (OGTT) 2-h glucose measurement over previous BLSA visits. Covariates included age, sex, body composition, physical activity, and other confounders. Higher likelihood of prediabetes, higher HOMA-IR, and lower Matsuda index were associated with longer τPCr. Among 205 participants with previous OGTT data, greater severity and longer duration of hyperglycemia were independently associated with longer τPC. In conclusion, in individuals without diabetes a more impaired mitochondrial capacity is associated with greater IR and a higher likelihood of prediabetes.

Kenneth W Fishbein - One of the best experts on this subject based on the ideXlab platform.

  • Poor mitochondrial health and systemic inflammation? Test of a classic hypothesis in the Baltimore Longitudinal Study of Aging
    GeroScience, 2020
    Co-Authors: Marta Zampino, Richard G Spencer, Kenneth W Fishbein, Nicholas A. Brennan, Eleanor M. Simonsick, Luigi Ferrucci
    Abstract:

    Although a persistent inflammatory state has long been associated with aging and negative health outcomes, the underlying mechanisms remain unclear. Mitochondrial dysfunction has been proposed as a cause of inflammaging, but evidence of an association in humans is lacking. In this study, we analyzed the cross-sectional association between inflammatory biomarkers and mitochondrial oxidative capacity in skeletal muscle, assessed as post-exercise phosphocreatine Recovery Time Constant by phosphorus magnetic resonance spectroscopy, in a population of 669 adults (mean age 67 years) from the Baltimore Longitudinal Study of Aging. We observed that participants with lower mitochondrial oxidative capacity exhibited hallmarks of inflammation, specifically markedly higher levels of interleukin-6 and C-reactive protein, as well as increased erythrocyte sedimentation rate when compared with participants with better oxidative capacity, independent of age and sex. We speculate that this association reflects the observation that products of damaged mitochondria, such as mitochondrial DNA, activate multiple pathways that lead to inflammation. Furthermore, excess production of oxidative species (ROS) by dysfunctional mitochondria could trigger inflammation either directly via NF-κB or through oxidative damage to proteins, lipids, and nucleic acids. Longitudinal studies are necessary to ascertain whether and through which mechanisms mitochondrial dysfunction activate inflammation or whether both these phenomena derive from a common root.

  • greater skeletal muscle oxidative capacity is associated with higher resting metabolic rate results from the baltimore longitudinal study of aging
    Journals of Gerontology Series A-biological Sciences and Medical Sciences, 2020
    Co-Authors: Marta Zampino, Richard David Semba, Fatemeh Adelnia, Richard G Spencer, Kenneth W Fishbein, Jennifer A Schrack, Eleanor Marie Simonsick, Luigi Ferrucci
    Abstract:

    BACKGROUND: Resting metabolic rate (RMR) tends to decline with aging. The age-trajectory of decline in RMR is similar to changes that occur in muscle mass, muscle strength and fitness but while the decline in these phenotypes have been related to changes of mitochondrial function and oxidative capacity, whether lower RMR is associated with poorer mitochondrial oxidative capacity is unknown. METHODS: In 619 participants of the Baltimore Longitudinal Study of Aging, we analyzed the cross-sectional association between RMR (kcal/day), assessed by indirect calorimetry, and skeletal muscle maximal oxidative phosphorylation capacity, assessed as post-exercise phosphocreatine Recovery Time Constant (tauPCr), by phosphorous magnetic resonance spectroscopy. Linear regression models were used to evaluate the relationship between tauPCr and RMR, adjusting for potential confounders. RESULTS: Independent of age, sex, lean body mass, muscle density and fat mass, higher RMR was significantly associated with shorter tauPCr, indicating greater mitochondrial oxidative capacity. CONCLUSION: Higher RMR is associated with a higher mitochondrial oxidative capacity in skeletal muscle. This association may reflect a relationship between better muscle quality and greater mitochondrial health.

  • 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
    Diabetes, 2017
    Co-Authors: Richard G Spencer, Kenneth W Fishbein, Elisa Fabbri, Chee W Chia, David Reiter, Donnie Cameron, Ariel Zane, Zenobia A Moore, Marta Gonzalezfreire
    Abstract:

    Whether individuals with insulin resistance (IR) but without criteria for diabetes exhibit reduced mitochondrial oxidative capacity is unclear; addressing this question could guide research for new therapeutics. We investigated 248 participants without diabetes from the Baltimore Longitudinal Study of Aging (BLSA) to determine whether impaired mitochondrial capacity is associated with prediabetes, IR, and duration and severity of hyperglycemia exposure. Mitochondrial capacity was assessed as the postexercise phosphocreatine Recovery Time Constant (τPCr) by 31P-magnetic resonance spectroscopy, with higher τPCr values reflecting reduced capacity. Prediabetes was defined using the American Diabetes Association criteria from fasting and 2-h glucose measurements. IR and sensitivity were calculated using HOMA-IR and Matsuda indices. The duration and severity of hyperglycemia exposure were estimated as the number of years from prediabetes onset and the average oral glucose tolerance test (OGTT) 2-h glucose measurement over previous BLSA visits. Covariates included age, sex, body composition, physical activity, and other confounders. Higher likelihood of prediabetes, higher HOMA-IR, and lower Matsuda index were associated with longer τPCr. Among 205 participants with previous OGTT data, greater severity and longer duration of hyperglycemia were independently associated with longer τPC. In conclusion, in individuals without diabetes a more impaired mitochondrial capacity is associated with greater IR and a higher likelihood of prediabetes.

Marta Zampino - One of the best experts on this subject based on the ideXlab platform.

  • Poor mitochondrial health and systemic inflammation? Test of a classic hypothesis in the Baltimore Longitudinal Study of Aging
    GeroScience, 2020
    Co-Authors: Marta Zampino, Richard G Spencer, Kenneth W Fishbein, Nicholas A. Brennan, Eleanor M. Simonsick, Luigi Ferrucci
    Abstract:

    Although a persistent inflammatory state has long been associated with aging and negative health outcomes, the underlying mechanisms remain unclear. Mitochondrial dysfunction has been proposed as a cause of inflammaging, but evidence of an association in humans is lacking. In this study, we analyzed the cross-sectional association between inflammatory biomarkers and mitochondrial oxidative capacity in skeletal muscle, assessed as post-exercise phosphocreatine Recovery Time Constant by phosphorus magnetic resonance spectroscopy, in a population of 669 adults (mean age 67 years) from the Baltimore Longitudinal Study of Aging. We observed that participants with lower mitochondrial oxidative capacity exhibited hallmarks of inflammation, specifically markedly higher levels of interleukin-6 and C-reactive protein, as well as increased erythrocyte sedimentation rate when compared with participants with better oxidative capacity, independent of age and sex. We speculate that this association reflects the observation that products of damaged mitochondria, such as mitochondrial DNA, activate multiple pathways that lead to inflammation. Furthermore, excess production of oxidative species (ROS) by dysfunctional mitochondria could trigger inflammation either directly via NF-κB or through oxidative damage to proteins, lipids, and nucleic acids. Longitudinal studies are necessary to ascertain whether and through which mechanisms mitochondrial dysfunction activate inflammation or whether both these phenomena derive from a common root.

  • greater skeletal muscle oxidative capacity is associated with higher resting metabolic rate results from the baltimore longitudinal study of aging
    Journals of Gerontology Series A-biological Sciences and Medical Sciences, 2020
    Co-Authors: Marta Zampino, Richard David Semba, Fatemeh Adelnia, Richard G Spencer, Kenneth W Fishbein, Jennifer A Schrack, Eleanor Marie Simonsick, Luigi Ferrucci
    Abstract:

    BACKGROUND: Resting metabolic rate (RMR) tends to decline with aging. The age-trajectory of decline in RMR is similar to changes that occur in muscle mass, muscle strength and fitness but while the decline in these phenotypes have been related to changes of mitochondrial function and oxidative capacity, whether lower RMR is associated with poorer mitochondrial oxidative capacity is unknown. METHODS: In 619 participants of the Baltimore Longitudinal Study of Aging, we analyzed the cross-sectional association between RMR (kcal/day), assessed by indirect calorimetry, and skeletal muscle maximal oxidative phosphorylation capacity, assessed as post-exercise phosphocreatine Recovery Time Constant (tauPCr), by phosphorous magnetic resonance spectroscopy. Linear regression models were used to evaluate the relationship between tauPCr and RMR, adjusting for potential confounders. RESULTS: Independent of age, sex, lean body mass, muscle density and fat mass, higher RMR was significantly associated with shorter tauPCr, indicating greater mitochondrial oxidative capacity. CONCLUSION: Higher RMR is associated with a higher mitochondrial oxidative capacity in skeletal muscle. This association may reflect a relationship between better muscle quality and greater mitochondrial health.

Gregg E. Trahey - One of the best experts on this subject based on the ideXlab platform.

  • acoustic radiation force impulse imaging of in vivo vastus medialis muscle under varying isometric load
    Ultrasonic Imaging, 2002
    Co-Authors: Kathryn R. Nightingale, Roger W. Nightingale, Deborah L. Stutz, Gregg E. Trahey
    Abstract:

    Acoustic Radiation Force Impulse (ARFI) imaging is a method for characterizing local variations in tissue mechanical properties. In this method, a single ultrasonic transducer array is used to both apply temporally short localized radiation forces within tissue and to track the resulting displacements through Time. Images of tissue displacement immediately after force cessation, maximum tissue displacement, the Time it takes for the tissue to reach its maximum displacement, and the Recovery Time Constant of the tissue are generated from the ARFI data sets. The information in each of these images demonstrates good agreement with matched B-mode images. The study presented here was designed to evaluate the relationship between changes in these ARFI parameters with known tissue mechanical properties in vivo. Utilizing a modified Siemens Elegra scanner with a 75L40 transducer array, ARFI images of vastus medialis muscle were generated in three of the authors under four levels of activation (0, 5.7, 14.5, and 23.3 N-m). Four ARFI datasets were acquired for each loading condition. The observed trends were that displacement magnitude, the Time it took for the tissue to reach its maximum displacement, and Recovery Time Constant decreased with increasing load (i.e., increasing muscle stiffness). Significant differences were observed between load levels and subjects for all parameters (p<0.01). The results indicate that ARFI imaging may be capable of quantifying tissue stiffness in real-Time measurements, although further investigation is required.

  • Acoustic radiation force impulse imaging of in vivo vastus medialis muscle under varying isometric load.
    Ultrasonic Imaging, 2002
    Co-Authors: Kathryn R. Nightingale, Roger W. Nightingale, Deborah L. Stutz, Gregg E. Trahey
    Abstract:

    Acoustic Radiation Force Impulse (ARFI) imaging is a method for characterizing local variations in tissue mechanical properties. In this method, a single ultrasonic transducer array is used to both apply temporally short localized radiation forces within tissue and to track the resulting displacements through Time. Images of tissue displacement immediately after force cessation, maximum tissue displacement, the Time it takes for the tissue to reach its maximum displacement, and the Recovery Time Constant of the tissue are generated from the ARFI data sets. The information in each of these images demonstrates good agreement with matched B-mode images. The study presented here was designed to evaluate the relationship between changes in these ARFI parameters with known tissue mechanical properties in vivo. Utilizing a modified Siemens Elegra scanner with a 75L40 transducer array, ARFI images of vastus medialis muscle were generated in three of the authors under four levels of activation (0, 5.7, 14.5, and 23.3 N-m). Four ARFI datasets were acquired for each loading condition. The observed trends were that displacement magnitude, the Time it took for the tissue to reach its maximum displacement, and Recovery Time Constant decreased with increasing load (i.e., increasing muscle stiffness). Significant differences were observed between load levels and subjects for all parameters (p