Myoglobin translational diffusion in rat myocardium and its implication on intracellular oxygen transport

Current theory of respiratory control invokes a role of myoglobin (Mb)-facilitated O₂ diffusion in regulating the intracellular O₂ flux, provided Mb diffusion can compete effectively with free O₂ diffusion. Pulsed-field gradient NMR methods have now followed gradient-dependent changes in the distinct ¹H NMR γ CH₃ Val E11 signal of MbO₂ in perfused rat myocardium to obtain the endogenous Mb translational diffusion coefficient (D_Mb) of 4.24 × 10^-7 cm² s^-1 at 22°C. The D_Mb matches precisely the value predicted by in vivo NMR rotational diffusion measurements of Mb and shows no orientation preference. Given values in the literature for the Krogh's free O₂ diffusion coefficient (K₀), myocardial Mb concentration and a partial pressure of O₂ that half saturates Mb (P₅₀), the analysis yields an equipoise diffusion P_O2 of 1.77 mmHg, where Mb and free O₂ contribute equally to the O₂ flux. In the myocardium, Mb-facilitated O₂ diffusion contributes increasingly more than free O₂ diffusion when the P_O2 falls below 1.77 mmHg. In skeletal muscle, the P_O2 must fall below 5.72 mmHg. Altering the Mb P₅₀ induces modest change. Mb-facilitated diffusion has a higher poise in skeletal muscle than in myocardium. Because the basal P_O2 hovers around 10 mmHg, Mb does not have a predominant role in facilitating O₂ transport in myocardium but contributes significantly only when cellular oxygen falls below the equipoise diffusion P_O2.