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 O 2 diffusion in regulating the intracellular O 2 flux, provided Mb diffusion can compete effectively with free O 2 diffusion. Pulsed‐field gradient NMR methods have now followed gradient‐dependent changes in the distinct 1 H NMR γ CH 3 Val E11 signal of MbO 2 in perfused rat myocardium to obtain the endogenous Mb translational diffusion coefficient ( D Mb ) of 4.24 × 10 −7 cm 2 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 O 2 diffusion coefficient ( K 0 ), myocardial Mb concentration and a partial pressure of O 2 that half saturates Mb ( P 50 ), the analysis yields an equipoise diffusion P   O   2of 1.77 mmHg, where Mb and free O 2 contribute equally to the O 2 flux. In the myocardium, Mb‐facilitated O 2 diffusion contributes increasingly more than free O 2 diffusion when the P   O   2falls below 1.77 mmHg. In skeletal muscle, the P   O   2must fall below 5.72 mmHg. Altering the Mb P 50 induces modest change. Mb‐facilitated diffusion has a higher poise in skeletal muscle than in myocardium. Because the basal P   O   2hovers around 10 mmHg, Mb does not have a predominant role in facilitating O 2 transport in myocardium but contributes significantly only when cellular oxygen falls below the equipoise diffusion P   O   2.