Santanasto Adam J, Coen Paul M, Glynn Nancy W, Conley Kevin E, Jubrias Sharon A, Amati Francesca, Strotmeyer Elsa S, Boudreau Robert M, Goodpaster Bret H, Newman Anne B
Center for Aging and Population Health, Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, United States.
Department of Health and Physical Activity, School of Education, University of Pittsburgh, Pittsburgh, United States.
Exp Gerontol. 2016 Aug;81:1-7. doi: 10.1016/j.exger.2016.04.002. Epub 2016 Apr 12.
Age related declines in walking performance may be partly attributable to skeletal muscle mitochondrial dysfunction as mitochondria produce over 90% of ATP needed for movement and the capacity for oxidative phosphorylation decreases with age.
Participants were from two studies: an ancillary to the Lifestyle Interventions and Independence for Elders (LIFE) Study (n=33), which recruited lower functioning participants (Short Physical Performance Battery [SPPB], 7.8±1.2), and the Study of Energy and Aging-Pilot (SEA, n=29), which enrolled higher functioning (SPPB, 10.8±1.4). Physical activity was measured objectively using the Actigraph accelerometer (LIFE) and SenseWear Pro armband (SEA). Phosphocreatine recovery following muscle contraction of the quadriceps was measured using (31)P magnetic resonance spectroscopy and ATPmax (mM ATP/s) was calculated. Walking performance was defined as time (s) to walk 400m at a usual-pace. The cross-sectional association between mitochondrial function and walking performance was assessed using multivariable linear regression.
Participants were 77.6±5.3years, 64.2% female and 67.2% white. ATPmax was similar in LIFE vs. SEA (0.52±0.14 vs. 0.55±0.14, p=0.31), despite different function and activity levels (1.6±2.2 vs.77.4±73.3min of moderate activity/day, p<0.01). Higher ATPmax was related to faster walk-time in SEA (r(2)=0.19, p=0.02,); but not the LIFE (r(2)<0.01, p=0.74) cohort.
Mitochondrial function was associated with walking performance in higher functioning, active older adults, but not lower functioning, sedentary older adults.
与年龄相关的步行能力下降可能部分归因于骨骼肌线粒体功能障碍,因为线粒体产生超过90%的运动所需ATP,且氧化磷酸化能力随年龄增长而降低。
参与者来自两项研究:老年人生活方式干预与独立性(LIFE)研究的一项辅助研究(n = 33),该研究招募了功能较低的参与者(简短身体性能测试[SPPB],7.8±1.2);以及能量与衰老试点研究(SEA,n = 29),该研究招募了功能较高的参与者(SPPB,10.8±1.4)。使用Actigraph加速度计(LIFE)和SenseWear Pro臂带(SEA)客观测量身体活动。使用磷磁共振波谱测量股四头肌收缩后的磷酸肌酸恢复情况,并计算ATPmax(mM ATP/秒)。步行能力定义为以平常速度步行400米所需的时间(秒)。使用多变量线性回归评估线粒体功能与步行能力之间的横断面关联。
参与者年龄为77.6±5.3岁,64.2%为女性,67.2%为白人。尽管功能和活动水平不同(每天中等活动量分别为1.6±2.2分钟和77.4±73.3分钟,p<0.01),但LIFE组和SEA组的ATPmax相似(分别为0.52±0.14和0.55±0.14,p = 0.31)。在SEA组中,较高的ATPmax与更快的步行时间相关(r² = 0.19,p = 0.02);但在LIFE组中则不然(r²<0.01,p = 0.74)。
线粒体功能与功能较高、活跃的老年人的步行能力相关,但与功能较低、久坐的老年人无关。