Assuming there isn't some other proteinaceous oxygen carrier in tissue that
hasn't been isolated yet, one possibility for how the tissues compensate
could be an increase in the amount of oxygenated substrates. Another
possibility might be an over-production of cytochromes, which can bind and
hold oxygen. Still another possibility might be the break-up of hemoglobin
into its subunits, which have structures similar to myoglobin.
None of these systems would probably count as true redundancies, but the
magic of metabolism is that a defect in one system can usually be
compensated for by "defects" in other systems.
Kevin L. O'Brien