Muscle myoglobin (Mb) can serve as an oxygen store during restricted blood flow and it can enhance intracellular oxygen transport by facilitated O₂ diffusion. Mb knockout mice proved Mb not to be essential for life, but compensatory adaptations indicate that Mb does play a role. Using morphological, metabolic and biochemical data, we applied the Krogh cylinder model to human heart muscle at maximal activity to quantitatively evaluate Mb functions. The spatial and temporal distribution of PO₂, MbO₂ and the amount of facilitated O₂ diffusion were calculated for continuous perfusion as well as for pulsatile blood flow assuming complete halt of left coronary artery perfusion during systole. At steady state conditions facilitated O₂ diffusion contributes only 5% to total O₂ diffusion within the tissue. When blood flow is stopped, the time until a PO₂ of 0 is reached at the outer circumference on the venous end of the Krogh cylinder is 150 ms, which is equivalent to the duration of a systole at a heart rate of 200/min. When Mb mobility is abolished and O₂ facilitation is lost, the time until local anoxia occurs is reduced to 120 ms. A reduction to 100 ms is calculated when no Mb is present in the tissue and the storage function is also lost. The model predicts that without Mb a heavily working human heart develops anoxic regions during the last third of the systole and it quantitatively explains the higher capillary densities and elevated hemoglobin concentrations observed in Mb knockout mice.