Skeletal muscle ex vivo mitochondrial respiration parallels decline in vivo oxidative capacity, cardiorespiratory fitness, and muscle strength: The Baltimore Longitudinal Study of Aging.

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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DOI:
10.1111/acel.12725
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发表时间:
2018-04
期刊:
影响因子:
7.8
通讯作者:
Ferrucci L
Ferrucci L
中科院分区:
生物学1区
文献类型:
--
作者:
Gonzalez-Freire M;Scalzo P;D'Agostino J;Moore ZA;Diaz-Ruiz A;Fabbri E;Zane A;Chen B;Becker KG;Lehrmann E;Zukley L;Chia CW;Tanaka T;Coen PM;Bernier M;de Cabo R;Ferrucci L

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人类骨骼肌中的线粒体功能随着年龄的增长而下降。这种下降的大多数证据来自间接评估线粒体功能的研究,这种恶化对身体功能的影响尚未明确界定。我们假设,在透化的人肌纤维线粒体呼吸下降,随着年龄的增长,与磷酸肌酸运动后恢复率(KPCr),肌肉性能,有氧健身。在巴尔的摩老龄化纵向研究的38名参与者的股外侧肌活检中,通过高分辨率呼吸测定法评估了皂苷透化纤维的线粒体呼吸(BLSA; 21名男性,年龄24-91岁),他们也有来自跑步机测试的峰值耗氧量(VO 2 max)、不同任务中的步态速度、31 P磁共振波谱、等速膝关节伸展、和握力。结果表明,线粒体呼吸随年龄的增长而显著降低(p <0.05),这与其他潜在的混杂因素无关。线粒体呼吸能力也与VO 2 max、肌肉力量、kPCr和完成400 m步行的时间相关(p < .05)。在线粒体呼吸和BMI之间观察到显著性的负趋势(p = 0.074)。最后,转录谱显示线粒体基因网络的mRNA表达随着年龄的增长而减少(p <0.05)。总的来说,我们的研究结果加强了线粒体功能随年龄增长而下降的观点,并可能导致与年龄相关的肌肉性能和心肺功能的丧失。
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.
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发表时间: 2006-06-01
影响因子: 5.1
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发表时间: 2005-08-02
期刊: CIRCULATION
影响因子: 37.8
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