Anoxia Tolerance

Animals living at high elevations where there is less oxygen must have adaptations to ensure that sufficient oxygen is delivered to the tissues. Since the total air pressure is reduced at high altitudes, the partial pressure of oxygen is also reduced, so hemoglobin may not be saturated and tissues would fail to get enough oxygen. In order to combat this, animals can alter the amount of oxygen carried in their bloodstream by increasing the concentration of hemoglobin, increasing the hematocrit, or by changing how well hemoglobin binds oxygen. Animals that travel from low elevations to higher ones usually increase the number of red blood cells and increase DPG concentrations so that hemoglobin binds oxygen less well (which increases delivery). However, this is not a good long term solution since high hematocrits also increase blood viscosity. These temporary changes are the result of phenotypic plasticity since they can happen in adulthood and are reversible. Animals that are permanently adapted to high altitudes instead have lower hematocrits and increased oxygen binding to increase hemoglobin saturation. In this study the authors wanted to see what the hematological parameters in high and low elevation deer mice, and to see if changes in oxygen binding are due to developmental plasticity (irreversible differences set from birth) or phenotypic plasticity. They found that high altitude mice had higher hemoglobin and DPG concentrations and higher hematocrits than lowland mice. But these decreased to be the same as lowland mice after 6 weeks at a lower elevation. When mice from either elevation were bred, the hematological parameters in F1 generation babies were all the same. This supports the concept that the hematological differences between lowland and mountain deer mice are not inborn but are the result of phenotypic plasticity. If the differences were permanent adaptations, they would not change when the mice were moved to a lower elevation and the babies would be the same as the parents.