Open AccessMitochondrial functional impairment with aging is exaggerated in isolated mitochondria compared to permeabilized myofibers
Author(s) -
Picard Martin,
Ritchie Darmyn,
Wright Kathryn J.,
Romestaing Caroline,
Thomas Melissa M.,
Rowan Sharon L.,
Taivassalo Tanja,
Hepple Russell T.
Publication year - 2010
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/j.1474-9726.2010.00628.x
Subject(s) - mitochondrion , biology , sarcopenia , mitochondrial permeability transition pore , bioenergetics , microbiology and biotechnology , context (archaeology) , myocyte , organelle , apoptosis , anatomy , biochemistry , programmed cell death , paleontology
Summary Mitochondria regulate cellular bioenergetics and apoptosis and have been implicated in aging. However, it remains unclear whether age‐related loss of muscle mass, known as sarcopenia, is associated with abnormal mitochondrial function. Two technically different approaches have mainly been used to measure mitochondrial function: isolated mitochondria and permeabilized myofiber bundles, but the reliability of these measures in the context of sarcopenia has not been systematically assessed before. A key difference between these approaches is that contrary to isolated mitochondria, permeabilized bundles contain the totality of fiber mitochondria where normal mitochondrial morphology and intracellular interactions are preserved. Using the gastrocnemius muscle from young adult and senescent rats, we show marked effects of aging on three primary indices of mitochondrial function (respiration, H 2 O 2 emission, sensitivity of permeability transition pore to Ca 2+ ) when measured in isolated mitochondria, but to a much lesser degree when measured in permeabilized bundles. Our results clearly demonstrate that mitochondrial isolation procedures typically employed to study aged muscles expose functional impairments not seen in situ . We conclude that aging is associated with more modest changes in mitochondrial function in sarcopenic muscle than suggested previously from isolated organelle studies.