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Aging alters Mitochondrial Respiratory Capacity and Function in Human Skeletal Muscle
Author(s) -
Porter Craig,
Hurren Nicholas,
Cotter Matthew,
Reidy Paul,
Dillon Edgar,
Durham William,
SheffieldMoore Melinda,
Sidossis Labros,
Rasmussen Blake,
Børsheim Elisabet
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.1036.16
Subject(s) - respiration , skeletal muscle , oligomycin , mitochondrion , respiratory system , medicine , endocrinology , senescence , ageing , biology , chemistry , anatomy , biochemistry , atpase , enzyme
Mitochondrial health is critical to physiological function, particularly in tissues with high ATP turnover, such a striated muscle. It has been postulated that derangements in mitochondrial function in skeletal muscle contribute to impaired physical function in older adults. Here, we determined mitochondrial respiratory capacity and function in m. vastus lateralis biopsies obtained from young and older adults. 21 young (28±5 yrs) and 27 older (63±9 yrs) adults were studied. Mitochondrial respiration was determined in permeabilized myofibers after the addition of substrates, inhibitors and uncouplers. Thereafter, flux control ratios and coupling control factors were calculated. Maximal coupled respiration (P) was higher in muscle from young vs. older subjects (58±3 vs. 44±3 pmol·mg ‐1 ·s ‐1 , P<0.01), as was maximal uncoupled respiration (E) (63±4 vs. 51±3 pmol·mg ‐1 ·s ‐1 , P<0.05). Oligomycin sensitivity was lower in older adults (P<0.05), as was the flux control ratio (P/E) (P<0.05). Calculation of respiratory function revealed lower respiration linked to ATP production (P<0.001) and greater residual respiration (P<0.01) in older adults. Mitochondrial respiratory capacity and function are altered in skeletal muscle of older individuals. In particular, ATP production is less efficient in muscle from older adults. These data suggest a role for skeletal muscle mitochondria dysfunction in senescence. NIH R01AG033761, R01AR049877, P30AG024832, P30AG028718, UL1TR000071, NIDRR H133P110012, Shriners 84090.