Our intent was
to investigate the mechanisms driving the adaptive potential of
subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria in young (6
mo) and senescent (36 mo) animals in response to a potent stimulus for
organelle biogenesis. We employed chronic electrical stimulation (10 Hz, 3
h/day, 7 days) to induce contractile activity of skeletal muscle in 6 and
36 mo F344XBN rats. Subsequent to chronic activity, acute stimulation (1
Hz, 5 min) in situ revealed greater fatigue resistance in both age groups.
However, the improvement in endurance was significantly greater in the
young, compared to the old animals. Chronic muscle use also augmented SS
and IMF mitochondrial volume to a greater extent in young muscle. The
molecular basis for the diminished organelle expansion in aged muscle was
due, in part, to the collective attenuation of the chronic
stimulation-evoked increase in regulatory proteins involved in mediating
mitochondrial protein import and biogenesis. Furthermore, adaptations in
mitochondrial function were also blunted in old animals. However, chronic
contractile activity evoked greater reductions in mitochondrially-mediated
proapoptotic signaling in aged muscle. Thus, mitochondrial plasticity is
retained in aged animals, however the magnitude of the changes are less
compared to young animals due to attenuated molecular processes regulating
organelle biogenesis.