Fig. 1. Oxygen-dependence of respiration at 20°C for superfused sartorius muscle and for skeletal muscle mitochondria isolated from the frog Rana temporaria. Measurements were made using high-resolution respirometry (Oroboros Oxygraph, Paar, Garz, Austria) that enables sensitive measurements of oxygen kinetics at low oxygen partial pressures (see St-Pierre et al., 2000c). Mitochondria show strict oxyregulation over a broad range of O₂ tensions, while skeletal muscle begins to oxyconform at P_O2 levels that are far in excess of the K_m of isolated mitochondria. Although oxyconformation is seldom seen in isolated cell preparations (see, however, Brand et al., 2000; Bishop and Brand, 2000; Guppy et al., 2000; Bishop et al., 2002), it does operate at the level of intact skeletal muscle (Hochachka and Guppy, 1987; West and Boutilier, 1998). One possibility is that the P_O2 of localised (hypoperfused) regions of tissue might fall below the critical P_O2 (P_crit) at which diffusion of oxygen to the mitochondria begins to limit oxidative phosphorylation. The metabolic rate of such localised regions could therefore become suppressed even though the mixed venous blood continues to exit the tissue at P_O2 levels higher than the P_crit. This so-called `diffusion limitation' could be one explanation for the well-known oxyconformation response seen in the intact skeletal muscle of cat (Whalen et al., 1973) and frog (Boutilier et al., 1997; West and Boutilier, 1998). Alternatively, oxyconformation could occur through some oxygen-sensing elements that trigger a reduction in the rate of mitochondrial respiration. From Boutilier (2001) with permission.