The oxygen affinity of hemoglobin is critical for gas exchange in the lung and O2 delivery in peripheral tissues. In the present study, we generated model mice that carry low affinity hemoglobin with the Titusville mutation in the α-globin gene or Presbyterian mutation in the β-globin gene. The mutant mice showed increased O2 consumption and CO2 production in tissue metabolism, suggesting enhanced O2 delivery by mutant Hbs. The histology of muscle showed a phenotypical conversion from a fast glycolytic to fast oxidative type. Surprisingly, mutant mice spontaneously ran twice as far as controls despite mild anemia. The oxygen affinity of hemoglobin may control the basal level of erythropoiesis, tissue O2 consumption, physical activity, and behavior in mice.
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