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Lazy or Old: Mitochondria decline in vivo in human muscle similarly with inactivity and age.

Is inactivity or age responsible for the mitochondrial decline found in elderly humans?  We tested the role of lifestyle vs. age using innovative noninvasive tools to measure key mitochondrial functional properties in vivo.  Mitochondrial coupling (ATP/O2 or P/O), and phosphorylation capacity (ATPmax) were assessed in human vastus lateralis muscle (VL). Oxidative capacity was biochemically assessed in vitro from biopsies taken from the same site as the in vivo measures.  The chronic activity level was characterized in all subjects using a physical activity questionnaire and a VO2max test (active >40 ml O2 kg-1 min-1).  The assessed level was verified in a subset of subjects using a triaxial accelerometer.  Subjects were screened to be healthy and disease free.  The active (n=9) and sedentary (n=18) groups had a mean age of 30 yrs as compared to a mean age of 68 yrs for elderly subjects (n=30).  Mitochondrial coupling in active controls (2.3+0.20, mean+SE) corresponded with that in well-coupled mitochondria (2.3-2.5) but both sedentary (P/O=1.41+0.09) and elderly groups (P/O=1.69+0.11) were substantially uncoupled.  Similarly, active subjects had a higher ATPmax (1.11+0.08 mM ATP sec-1) than either sedentary (0.67+0.03) or aged groups (0.61+0.04).  Oxidative capacity was reduced in both groups by 25% relative to active adults.  These results demonstrate that mitochondrial properties in vivo drop substantially in sedentary adults to the level found in elderly subjects.  Thus inactivity as much as age accounts for the mitochondrial decline found in the elderly.  Supported by NIH R01 AG 030226, R01 AR 41928, 1RC2AG036606.

Kevin Conley, Sharon Jubrias, Sudip Bajpeyi, Magdalena Pasarica, Cedric Moro, Olga Sereda, David H. Burk, Alok Gupta, Lise Kjems, Kori Murray, Lori Arakaki, and Steven Smith

University of Washington Medical Center, Seattle, WA and Pennington Biomedical Research Center, Baton Rouge, LA