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 non-apoptotic functions related to mitochondrial function in non-stressful 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 IMF mitochondria. Furthermore, the cytosolic chaperones Hsp90 and 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.