Oxidative power and intracellular distribution of mitochondria control cell oxygen regime when arterial hypoxemia occurs

The regulatory impact of the mitochondria spatial distribution and enlargement in their oxidative power on tissue oxygenation of skeletal muscle during hypoxia were studied. Investigations were performed by mathematical modeling of 3D O 2 diffusion-reaction in muscle fiber. The oxygen consumption rate and tissue were analyzed in response to a decrease in arterial blood oxygen concentration from 19.5 to 10 vol % at moderate load. Cells with evenly (case 1) and unevenly (case 2) distributed mitochondria were considered. According to calculations, owing to a rise in mitochondria oxidative power from 3.5 to 6.5 mL/min per 100 g of tissue it is possible to maintain muscle oxygen at a constant level of 3.5 mL/min per 100 g despite a decrease in O 2 delivery. The minimum value of tissue was about 0 and an area of hypoxia appeared inside the cell in case 1. Whereas hypoxia disappeared and minimum value of increased from 0 to 4 mmHg if mitochondria were distributed unevenly (case 2). The possibilities of such regulation depended on the relationship “the degree of hypoxemia — the level of oxygen delivery.” It was assumed that an increase in mitochondrial enzyme activity and their migration to places of the greatest oxygen consumption rate can improve the oxygen regime in the cell as it adapts to hypoxia.