The function Bax and/or Bak in constituting a gateway for mitochondrial 
apoptosis in response to apoptotic stimuli has been unequivocally demonstrated. 
However, recent work has suggested that Bax/Bak may have unrecognized 
nonapoptotic functions related to mitochondrial function in nonstressful 
environments. Wild-type (WT) and Bax/Bak double knockout (DKO) mice were used to 
determine alternative roles for Bax and Bak in mitochondrial morphology and 
protein import in skeletal muscle. The absence of Bax and/or Bak altered 
mitochondrial dynamics by regulating protein components of the organelle fission 
and fusion machinery. Moreover, DKO mice exhibited defective mitochondrial 
protein import, both into the matrix and outer membrane compartments, which was 
consistent with our observations of impaired membrane potential and attenuated 
expression of protein import machinery (PIM) components in intermyofibrillar 
mitochondria. Furthermore, the cytosolic chaperones heat-shock protein 90 
(Hsp90) and binding immunoglobulin protein (BiP) were markedly increased with 
the deletion of Bax/Bak, indicating that the cytosolic environment related to 
protein folding may be changed in DKO mice. Interestingly, endurance training 
fully restored the deficiency of protein import in DKO mice, likely via the 
upregulation of PIM components and through improved cytosolic chaperone protein 
expression. Thus our results emphasize novel roles for Bax and/or Bak in 
mitochondrial function and provide evidence, for the first time, of a curative 
function of exercise training in ameliorating a condition of defective 
mitochondrial protein import.