While the most deleteriousmutations may be purged already in the
first generation, the organismmay protect itself against less severe mutations
by a number of molecular and functional adaptations. For example,
mice without Mb express more hypoxia-inducible factor and stress
proteins, display elevated nitric oxide metabolism, and shift from fatty
acid to glucose metabolism, probably to rescue the exercise capacity
of the animal (Grange et al., 2001; Flogel et al., 2005). It remains open
whether similar compensation mechanisms occur for marine mammals
with slightly impaired mutant Mb so as to improve their fitness.