03165nam 22003377a 4500008004200000022001400042024002900056040002000085099001300105245019100118251002900309252002900338253001500367260000900382260001100391266001500402520018300417520165700600546001202257650003402269651002802303656002702331657002002358700002202378700001802400790019002418856008102608942001702689952010602706999001502812180220s20182018 xxu||||| |||| 00| 0 eng d a1474-9718 a10.1111/acel.12716 [doi] aOvid MEDLINE(R) a29356348 aSkeletal muscle ex vivo mitochondrial respiration parallels decline in vivo oxidative capacity, cardiorespiratory fitness, and muscle strength: The Baltimore Longitudinal Study of Aging. aAging Cell. 2018 Jan 21 aAging Cell. 2018 Jan 21 aAging cell c2018 fFY2018 d2018-02-20 aCopyright 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. aMitochondrial 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. aEnglish aIN PROCESS -- NOT YET INDEXED aMedStar Harbor Hospital aClinical Research Unit aJournal Article aD'Agostino, Jarod aZukley, Linda aBecker KG, Bernier M, Chen B, Chia CW, Coen PM, D'Agostino J, de Cabo R, Diaz-Ruiz A, Fabbri E, Ferrucci L, Gonzalez-Freire M, Lehrmann E, Moore ZA, Scalzo P, Tanaka T, Zane A, Zukley L uhttps://dx.doi.org/10.1111/acel.12716zhttps://dx.doi.org/10.1111/acel.12716 cARTdArticle 001040708Articleaauthcatbauthcatd2018-02-20l0o29356348p29356348r2018-02-20w2018-02-20yART c3087d3087