During
ischemia and some types of muscular contractions,
oxygen tension (Po(2)) declines to the point that mitochondrial
ATP synthesis becomes limited by
oxygen availability. Although this critical Po(2) has been determined in animal tissue in vitro and in situ, there remains controversy concerning potential disparities between values measured in vivo and ex vivo. To address this issue, we used concurrent heteronuclear magnetic resonance spectroscopy (MRS) to determine the critical intracellular Po(2) in resting human skeletal muscle in vivo. We interleaved measurements of
deoxymyoglobin using (1)H-MRS with measures of high-energy
phosphates and pH using (31)P-MRS, during 15 min of
ischemia in the tibialis anterior muscles of 6 young men.
ATP production and intramyocellular Po(2) were quantified throughout
ischemia. Critical Po(2), determined as the Po(2) corresponding to the point where PCr begins to decline (PCr(ip)) in resting muscle during
ischemia, was 0.35 ± 0.20 Torr, means ± SD. This in vivo value is consistent with reported values ex vivo and does not support the notion that critical Po(2) in resting muscle is higher when measured in vivo. Furthermore, we observed a 4.5-fold range of critical Po(2) values among the individuals studied. Regression analyses revealed that time to PCr(ip) was associated with critical Po(2) and the rate of
myoglobin desaturation (r = 0.83, P = 0.04) but not the rate of
ATP consumption during
ischemia. The apparent dissociation between
ATP demand and
myoglobin deoxygenation during
ischemia suggests that some degree of uncoupling between intracellular energetics and oxygenation is a potentially important factor that influences critical Po(2) in vivo.