TY - JOUR
T1 - Muscle strength mediates the relationship between mitochondrial energetics and walking performance
AU - Zane, Ariel C.
AU - Reiter, David A.
AU - Shardell, Michelle
AU - Cameron, Donnie
AU - Simonsick, Eleanor M.
AU - Fishbein, Kenneth W.
AU - Studenski, Stephanie A.
AU - Spencer, Richard G.
AU - Ferrucci, Luigi
N1 - Funding Information:
This research was supported entirely by the Intramural Research Program of the National Institutes of Health, National Institute on Aging. The authors would like to thank Chee W. Chia for assistance with the OGTT protocol and data collection.
Publisher Copyright:
© 2017 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
PY - 2017/6
Y1 - 2017/6
N2 - Skeletal muscle mitochondrial oxidative capacity declines with age and negatively affects walking performance, but the mechanism for this association is not fully clear. We tested the hypothesis that impaired oxidative capacity affects muscle performance and, through this mechanism, has a negative effect on walking speed. Muscle mitochondrial oxidative capacity was measured by in vivo phosphorus magnetic resonance spectroscopy as the postexercise phosphocreatine resynthesis rate, kPC r, in 326 participants (154 men), aged 24–97 years (mean 71), in the Baltimore Longitudinal Study of Aging. Muscle strength and quality were determined by knee extension isokinetic strength, and the ratio of knee extension strength to thigh muscle cross-sectional area derived from computed topography, respectively. Four walking tasks were evaluated: a usual pace over 6 m and for 150 s, and a rapid pace over 6 m and 400 m. In multivariate linear regression analyses, kPC r was associated with muscle strength (β = 0.140, P = 0.007) and muscle quality (β = 0.127, P = 0.022), independent of age, sex, height, and weight; muscle strength was also a significant independent correlate of walking speed (P < 0.02 for all tasks) and in a formal mediation analysis significantly attenuated the association between kPC r and three of four walking tasks (18–29% reduction in β for kPC r). This is the first demonstration in human adults that mitochondrial function affects muscle strength and that inefficiency in muscle bioenergetics partially accounts for differences in mobility through this mechanism.
AB - Skeletal muscle mitochondrial oxidative capacity declines with age and negatively affects walking performance, but the mechanism for this association is not fully clear. We tested the hypothesis that impaired oxidative capacity affects muscle performance and, through this mechanism, has a negative effect on walking speed. Muscle mitochondrial oxidative capacity was measured by in vivo phosphorus magnetic resonance spectroscopy as the postexercise phosphocreatine resynthesis rate, kPC r, in 326 participants (154 men), aged 24–97 years (mean 71), in the Baltimore Longitudinal Study of Aging. Muscle strength and quality were determined by knee extension isokinetic strength, and the ratio of knee extension strength to thigh muscle cross-sectional area derived from computed topography, respectively. Four walking tasks were evaluated: a usual pace over 6 m and for 150 s, and a rapid pace over 6 m and 400 m. In multivariate linear regression analyses, kPC r was associated with muscle strength (β = 0.140, P = 0.007) and muscle quality (β = 0.127, P = 0.022), independent of age, sex, height, and weight; muscle strength was also a significant independent correlate of walking speed (P < 0.02 for all tasks) and in a formal mediation analysis significantly attenuated the association between kPC r and three of four walking tasks (18–29% reduction in β for kPC r). This is the first demonstration in human adults that mitochondrial function affects muscle strength and that inefficiency in muscle bioenergetics partially accounts for differences in mobility through this mechanism.
KW - 31P MRS
KW - bioenergetics
KW - in vivo
KW - muscle strength
KW - skeletal muscle
KW - walking speed
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U2 - 10.1111/acel.12568
DO - 10.1111/acel.12568
M3 - Article
C2 - 28181388
AN - SCOPUS:85011985653
SN - 1474-9718
VL - 16
SP - 461
EP - 468
JO - Aging Cell
JF - Aging Cell
IS - 3
ER -