Effect of the time-average inlet perfusion pressure $P ¯ i n$ and MVI on the distribution of metabolic activation across the terminal vessels, F_mterm, for a terminal target flow, q_target, of 1.5 × 10⁻³ mm³/s. (A–L) With MVI (A–F) and without MVI (G–L). The capacity of metabolic regulation to maintain flow homogeneity is exhausted at low perfusion pressure (⁠$P¯in$ = 75 mmHg, A) under which all the vessels are maximally vasodilated with F_mterm = 1). It is completely suppressed at high perfusion pressure (⁠$P¯in$ = 165 mmHg) under which all the vessels are maximally vasoconstricted with F_mterm = 0).